Biopsychology, 10th Edition John P J Pinel Solution Manual

Type:

Solution Manual

Resource:

Biopsychology

Edition:

10th Edition

Author(s):

John P. J. Pinel Steven Barnes

Instructor Resource Manual for

BIOPSYCHOLOGY Tenth Edition

John P. J. Pinel & Steven J. Barnes University of British Columbia

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1 Biopsychology as a Neuroscience: What Is Biopsychology, Anyway?

TABLE OF CONTENTS Chapter-at-a-Glance

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Learning Objectives

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Brief Chapter Outline

4

Teaching Outline

6

Lecture Launchers

14

Activities

16

Web Links

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Chapter 1: Biopsychology as a Neuroscience

CHAPTER-AT-A-GLANCE

Brief Outline A Personal Introduction Course Organization Four Major Themes of This Text (pp. 3–4) What Is Biopsychology? (pp. 4–5) What Types of Research Characterize the Biopsychological Approach? (pp. 5–9) What Are the Divisions of Biopsychology? (pp. 9–13) How Do Biopsychologists Conduct Their Work? (pp. 13–16) Critical Thinking about Biopsychological Claims (pp. 16–18)

Instructor’s Manual Resources

Lecture Launcher 1.1 Lecture Launcher 1.2 Lecture Launcher 1.7 Lecture Launchers 1.3, 1.8

Lecture Launcher 1.4 Lecture Launcher 1.5, Activity 1.1 Lecture Launcher 1.6

< Return to Table of Contents

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Biopsychology, Tenth Edition

LEARNING OBJECTIVES After completion of this chapter, the student should be able to: LO 1.1 LO 1.2 LO 1.3 LO 1.4 LO 1.5 LO 1.6 LO 1.7 LO 1.8 LO 1.9 LO 1.10 LO 1.11 LO 1.12 LO 1.13 LO 1.14 LO 1.15 LO 1.16

Define and discuss what is meant by biopsychology.

Discuss the origins of the field of biopsychology.

List the six fields of neuroscience that are particularly relevant to biopsychological inquiry.

Compare the advantages and disadvantages of humans and nonhumans as subjects in biopsychological research.

Compare experiments, quasiexperimental studies, and case studies, emphasizing the study of causal effects.

Compare pure and applied research.

Describe the division of biopsychology known as physiological psychology.

Describe the division of biopsychology known as psychopharmacology.

Describe the division of biopsychology known as neuropsychology.

Describe the division of biopsychology known as psychophysiology.

Describe the division of biopsychology known as cognitive neuroscience.

Describe the division of biopsychology known as comparative psychology.

Explain how converging operations has contributed to the study of Korsakoff’s syndrome.

Explain scientific inference with references to research on eye movement and the visual perception of motion.

Discuss Delgado’s bull-ring demonstration, emphasizing its flawed interpretation.

Describe the rise and fall of prefrontal lobotomy.

< Return to Table of Contents

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Chapter 1: Biopsychology as a Neuroscience

BRIEF CHAPTER OUTLINE

Lecture Launcher 1.1: First Impressions of Biopsychology 1. The Four Major Themes of This Text a. Thinking Creatively b. Clinical Implications c. The Evolutionary Perspective d. Neuroplasticity 2. What Is Biopsychology? a. Defining Biopsychology b. What Are the Origins of Biopsychology? c. How Is Biopsychology Related to the Other Disciplines of Neuroscience?

Lecture Launcher 1.2: Biopsychology Research—More than White Rats and Lab Coats Lecture Launcher 1.3: Ethical Issues in Animal and Human Research 3. What Types of Research Characterize the Biopsychological Approach? a. Human and Nonhuman Subjects b. Experiments and Nonexperiments c. Pure and Applied Research 4. What Are the Divisions of Biopsychology? a. Physiological Psychology b. Psychopharmacology c. Neuropsychology d. Psychophysiology e. Cognitive Neuroscience f. Comparative Psychology Lecture Launcher 1.4: Neuropsychology’s Case Studies versus Physiological Psychology’s Experiments 5. How Do Biopsychologists Conduct Their Work? a. Converging Operations: How Do Biopsychologists Work Together? b. Scientific Inference: How Do Biopsychologists Study the Unobservable Workings of the Brain?

Lecture Launcher 1.5: Studying Brain and Behavior from All Sides

Activity 1.1: Making Sense of Eye Movements 6. Critical Thinking About Biopsychological Claims a. Taming a Charging Bull with Caudate Stimulation b. Prefrontal Lobotomy Lecture Launcher 1.6: Chimpanzees and Mental Illness 4 ..

Biopsychology, Tenth Edition

7. End-of-Chapter Discussion a. What Was Wrong with Delgado’s Claims? b. What Was Wrong with Moniz’s Claims? < Return to Table of Contents

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Chapter 1: Biopsychology as a Neuroscience

TEACHING OUTLINE 1. A Personal Introduction Lend the course a personal perspective a. Training and Teaching Experience • How I first became interested in biopsychology (personal anecdotes) • Undergraduate training • Graduate training • Postgraduate experience • Other courses that I am currently teaching b. Research Experience • Thesis research • Past research • Current research interests (encourage students to speak with me about my work) The following information should also be included in the syllabus: c. Teaching Assistant (if possible, have the teaching assistant speak about himself/herself) Training, current research interests d. Availability of Instructor and Teaching Assistant • Office hours and location • Phone numbers/E-mail addresses/Web pages 2. Course Organization a. Who Is the Course For? Describe any prerequisites for the course (e.g., Introductory Psychology, Introductory Biology) b. Text and Ancillary Materials (bring these to class so the students can see them) • Biopsychology, Tenth Edition, by John P.J. Pinel • Any other assigned reading materials • Note use of other pedagogical tools, such as a Blackboard site for the course c. Lecture Format • Relation of lectures to text • Note if questions or comments are encouraged at any point in your lectures • If lecture notes are provided, note how they can be accessed d. Examination Format • Examination dates • General format of exams (multiple choice, short answer, essay, and/or figure identification) • Nature of final exam (Is it comprehensive or for the last block of material?)

• What to do if you think your examination has been graded incorrectly

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Biopsychology, Tenth Edition e. Major Assignments and Due Dates What are they? When are they due? f. Special Learning or Examination Requirements Provide information about your institution’s learning resource center g. Missed Examinations/Assignments Policy h. Final Grades Tell students how the final grades will be computed 3. The Four Major Themes of This Text a. Thinking Creatively • Novel approaches to research have led to progress in biopsychology b. Clinical Implications • Much has been learned through the investigation of brain damage and behavioral change c. The Evolutionary Perspective • Much has been learned by comparing and contrasting different species d. Neuroplasticity • The brain changes continuously throughout the life span 4. What Is Biopsychology? a. Defining Biopsychology LO 1.1 Define and discuss what is meant by biopsychology.

•

Brain and behavior are two of the most interesting subjects in science; biopsychology focuses on brain/behavior relationships (refer to Figure 1.1, showing a human brain, from Biopsychology, Tenth Edition).

b. What Are the Origins of Biopsychology?

LO 1.2 Discuss the origins of the field of biopsychology.

• • •

Biopsychology emerged as a distinct area in psychology at the end of the nineteenth century; Hebb’s The Organization of Behavior (1949) was a key factor in its development into a major neuroscientific discipline.

Biopsychologists study how the brain and the rest of the nervous system determine what we perceive, feel, think, say, and do.

This may be the ultimate challenge for the human brain: Does our brain have the capacity to understand something as complex as itself?

c. How Is Biopsychology Related to the Other Disciplines of Neuroscience?

LO 1.3 List six fields of neuroscience that are particularly relevant to biopsychological inquiry.

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Chapter 1: Biopsychology as a Neuroscience • •

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Neuroscience is the scientific study of the nervous system; neuroscience includes many different approaches, including neuroanatomy, neurophysiology, neurochemistry, neuroendocrinology, neuropharmacology, and neuropathology (see Figure 1.2).

Biopsychology is a discipline of neuroscience that integrates these various approaches.

Biopsychologists try to discover how the various phenomena studied by neurophysiologists, neuropharmacologists, neuroanatomists, and other neuroscientists relate to one another to produce psychological phenomena such as learning, memory, motivation, and perception.

Thus, biopsychology can be viewed as a bridge between psychology and neuroscience.

The first part of the course will examine the fundamentals of neuroanatomy, neurophysiology, neuropharmacology, genetics, and evolution; the rest of the course will focus on how these biological fundamentals are applied to the study of biopsychological phenomena.

What Types of Research Characterize the Biopsychological Approach?

• Biopsychologists use a variety of research approaches in their studies; to understand what biopsychology is, you must understand what biopsychologists do.

• This diversity can be illustrated by discussing three dimensions along which biopsychological research varies: – human vs. nonhuman subjects – experimental vs. nonexperimental studies – applied vs. pure research a. Human and Nonhuman Subjects LO 1.4 Compare the advantages and disadvantages of humans and nonhumans as subjects in biopsychological research.

Advantages of human subjects: • They can follow directions.

• They can report subjective experiences.

• They are often less expensive.

• They have a human brain.

Advantages of nonhuman subjects: • They have simpler nervous systems.

• Studying various species makes it possible to use the comparative approach.

• There are fewer ethical constraints (although the ethics of both human and animal research is carefully scrutinized by independent committees). b. Experiments and Nonexperiments LO 1.5 Compare experiments, quasiexperimental studies, and case studies, emphasizing the study of causal effects.

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Biopsychology research can involve experimental and nonexperimental studies.

Experiments • Used by scientists to determine cause-and-effect relationships.

• Usually a different group of subjects is tested under each treatment condition of an experiment; this is a between-subjects design.

• Sometimes the same group of subjects can be tested under multiple treatment conditions; this is a within-subjects design.

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Biopsychology, Tenth Edition • • • • •

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Independent variables are set or manipulated by the experimenter; these manipulations produce the different treatment conditions in an experiment.

Dependent variables reflect the subject’s behavior; this is what the experimenter measures.

The experimenter tries to conduct the experiment so that the independent variable is the only thing that varies between each treatment condition; the experimenter measures the effect of the independent variable on the dependent variable.

In a well-designed experiment, the experimenter can conclude that any differences in the dependent variable between the various treatment conditions were caused by the independent variable (it’s the only possibility).

Although the principle of good experimentation is conceptually simple, it is often difficult in practice to make sure that there is only one difference among conditions; unintended differences between conditions that can influence the dependent variable are called confounded variables.

The presence of confounded variables makes experiments difficult to interpret because it is impossible to tell how much of the effect on the dependent variable was caused by the independent variable and how much was caused by the confounded variable.

An example of a well-designed experiment is the experiment of Lester and Gorzalka (1988) on the Coolidge effect in female hamsters (refer to Figure 1.3 from Biopsychology).

Quasiexperimental Studies • Sometimes it is impossible to conduct controlled experiments (e.g., if human subjects are involved, it may be impossible for ethical or technical reasons to assign them to particular conditions and to administer the conditions).

• In a quasiexperimental design, researchers examine subjects in real-world situations who have self-selected into specific conditions (e.g., excessive alcohol intake); in a sense, these subjects have assigned themselves to treatment conditions.

• The major shortcoming of a quasiexperimental study is that although researchers can examine relations between the variables of interest (e.g., alcohol consumption’s relation to brain damage), a quasiexperimental study cannot control for potential confounding variables.

Therefore, it does not allow a researcher to establish direct cause-and-effect relationships.

Example:

Researchers cannot randomly assign humans to control and alcohol groups, and then expose one group to 10 years of chronic alcohol exposure to see if alcohol causes brain damage. Instead, they must compare the brains of alcoholics and non-alcoholics found in the real world.

Key Problem: Because subjects in the real world do not assign themselves to groups randomly, there are many other differences between the groups that could contribute to differences in the dependent measures. For example, the observation that alcoholics have far more brain damage than non-alcoholics does not mean that alcohol directly causes this difference, because alcoholics differ from non-alcoholics in many ways unrelated to their alcohol consumption (e.g., education, accidental head injury, diet, other drug use).

Case Studies • Case studies are scientific studies that focus on a single subject; for example, you will learn later in the course about how the in-depth study of one amnesic subject (H. M.) has contributed much to our understanding of the neural basis of memory.

• The main problem with case studies is their generalizability, or the extent to which their results tell us something about the general population.

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Chapter 1: Biopsychology as a Neuroscience

c. Pure and Applied Research LO 1.6 Compare pure and applied research.

• • •

Pure and applied research are defined by the motivation of the researcher.

Pure research is motivated primarily by the curiosity of the researcher to find out how things work; pure research focuses on establishing building blocks or basic concepts that may provide information salient to many problems.

Applied research is motivated by an attempt to directly use the building blocks of basic research to answer specific questions; human and animal problems are directly addressed.

6. What Are the Divisions of Biopsychology (see Figure 1.5 in Biopsychology)? a. Physiological Psychology LO 1.7 Describe the division of biopsychology known as physiological psychology.

• • •

It focuses on direct manipulation of the nervous system in controlled lab settings (e.g., lesions, invasive recording).

The subjects are usually laboratory animals.

There is a strong focus on pure research.

b. Psychopharmacology LO 1.8 Describe the division of biopsychology known as psychopharmacology.

• • •

Similar to physiological psychology, except that the nervous system is manipulated pharmacologically Focuses on drug effects on behavior and how these changes are mediated by changes in neural activity Many psychopharmacologists favor pure research and use drugs to reveal the nature of brainbehavior interactions, while others concentrate on applied questions (e.g., drug abuse, therapeutic drugs)

c. Neuropsychology LO 1.9 Describe the division of biopsychology known as neuropsychology.

• • •

Focuses on the behavioral effects of brain damage in humans, typically cortical damage Cannot be studied in humans by experimentation; research focuses on case studies and quasiexperimental studies Most applied of the six divisions of biopsychology; neuropsychological tests of brain-damaged patients facilitate diagnosis, treatment, and lifestyle counseling (e.g., the case of Mr. R. described in the text)

d. Psychophysiology LO 1.10 Describe the division of biopsychology known as psychophysiology.

• • •

It focuses on the relationship between physiological and psychological processes in human subjects.

Because human subjects are used, all brain recordings are noninvasive (i.e., from the surface of the head).

The usual measure of brain activity is the scalp electroencephalogram (EEG).

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Biopsychology, Tenth Edition •

Muscle tension, eye movement, heart rate, pupil dilation, and electrical conductance of the skin are other common psychophysiological measures.

Example: Eyetracking deficits in schizophrenics; refer students to Figure 1.6 from Biopsychology

e. Cognitive Neuroscience LO 1.11 Describe the division of biopsychology known as cognitive neuroscience.

• • • •

f.

Newest division of biopsychology Focuses on the neural bases of cognitive processes like learning/memory, attention, and perceptual processes Often employs human subjects—key methods are noninvasive, functional brain imaging techniques (refer students to Figure 1.7 from Biopsychology) Often involves collaborations between researchers with widely different backgrounds (e.g., biopsychology, cognitive psychology, computer science)

Comparative Psychology LO 1.12 Describe the division of biopsychology known as comparative psychology.

• • • •

Focuses on the biology of behavior Features comparative and functional approaches Features laboratory research, as well as studies of animals in their natural environments (ethology) Includes disciplines of evolutionary psychology (understanding behavior through its evolutionary origins) and behavioral genetics (understanding the genetic influences on behavior)

7. How Do Biopsychologists Conduct Their Work? a.

Converging Operations: How Do Biopsychologists Work Together?

LO 1.13 Explain how converging operations has contributed to the study of Korsakoff’s syndrome.

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a.

Each of the six approaches to biopsychological research is not without its weaknesses; thus, biopsychological issues are rarely resolved by a single experiment or study, or by any single approach.

Progress is greatest when several different approaches, each compensating for the shortcomings of the others, are used to solve the same problems; this is called converging operations.

Scientific Inference: How Do Biopsychologists Study the Unobservable Workings of the Brain?

LO 1.14 Explain scientific inference with reference to research on eye movement and the visual perception of motion.

• •

Science is a method of answering questions by direct observation; it is an empirical method.

However, brain activity is not directly observable (e.g., one cannot see a neuron firing or neurochemicals being released from neurons).

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Chapter 1: Biopsychology as a Neuroscience •

This situation is no different than other sciences (e.g., physicists cannot see gravity, chemists cannot see evaporation); the effects of the processes are observable, but not the processes themselves.

Question: How do scientists study the unobservable using a method (i.e., the scientific method) that is fundamentally observational?

Answer:

By scientific inference; scientists observe the consequences of unobservable processes and from these they infer the nature of unobservable processes.

8. Critical Thinking about Biopsychological Claims You might think it odd to begin a course on biopsychology by considering two bad examples of its science. This is done for two reasons: • because disciplines learn from their mistakes; understanding biopsychology’s previous errors help biopsychologists to avoid these mistakes in their own work; and • because it will make you a better consumer of scientific research—it will help you develop critical thinking about biopsychological research. a. Taming a Charging Bull with Caudate Stimulation LO 1.15 Discuss Delgado’s bull-ring demonstration, emphasizing its flawed interpretation.

• • • •

The biopsychologist Jose Delgado implanted an electrode into the caudate nucleus of a bull.

Each time the bull charged, Delgado used his hand-held transmitter to deliver an electrical stimulation to the caudate nucleus of the bull via the implanted electrode.

This stopped the charge and after a few attempts, the bull stood tamely as Delgado strode about the ring.

Delgado and the popular press declared this a major discovery, the discovery of the caudate taming center. It was even suggested that caudate stimulation might cure human psychopaths.

b. Prefrontal Lobotomy (use Figures 1.9, 1.10, and 1.11 from Biopsychology) LO 1.16 Describe the rise and fall of prefrontal lobotomy.

• • • • •

In 1949, Dr. Egas Moniz received a Nobel Prize for developing a novel treatment for mental illness: prefrontal lobotomy, a procedure that separates the prefrontal lobes from the rest of the brain.

Moniz based his technique on a report that a chimpanzee (Becky) was easier to handle after part of her prefrontal lobes had been destroyed as part of an experiment.

Various forms of the operation were devised, such as the transorbital lobotomy procedure, which was performed by inserting an ice pick-like device through the eye sockets, often in a doctor’s office.

Following the initial reports by Moniz of the operation’s benefits, it was performed on mentally-ill patients all over the world (over 40,000 in the United States alone).

Note the case of Howard Dully, the boy who was lobotomized at the insistence of his stepmother.

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Biopsychology, Tenth Edition End-of-Chapter Discussion Guide the discussion to the following points and issues: a. What Was Wrong with Delgado’s Claims?

• There are many ways that stimulation might stop a charging bull other than by taming it (e.g., the stimulation might have been painful, blinded the bull, made it sick, or made movement difficult).

• When there is more than one reasonable interpretation of a behavior, the general rule is to favor the simplest one; this rule is called Morgan’s Canon.

• In fact, analyses of the filmed record of this event strongly support a more simple interpretation: The left and right caudate are motor structures, and stimulating one side often causes an animal to walk in circles.

• This appears to be what happened in Delgado’s case; the bull was confused and incapable of charging, but not tamed. b. What Was Wrong with Moniz’s Claims?

• The surgery was based on the study of only one subject (Becky), and a nonhuman subject at that!

• It is difficult to see how one could conclude that an operation that would eliminate the adaptive defensive reactions of a chimpanzee to an experimenter would help the mentally ill.

• Moniz and others who prescribed prefrontal lobotomy were not in a position to be objective in its evaluation, nor were they trained to perform such evaluations. Early reports of the benefits of prefrontal lobotomy were based on poorly controlled studies focused on manageability and published by Moniz himself.

• After many thousands of people had been lobotomized, controlled studies by objective researchers revealed terrible side effects (e.g., “vegetable-like behavior,” urinary incontinence, epilepsy). < Return to Table of Contents

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Chapter 1: Biopsychology as a Neuroscience

LECTURE LAUNCHERS Lecture Launcher 1.1: First Impressions of Biopsychology Based on their reading of Chapter 1, and on preconceptions that they may have from other psychology classes, have your students discuss what THEY think biopsychology is—where it fits into psychology and where it fits into science. For background material to help you with this discussion, see the Web site for the International Society for the History of the Neurosciences at http://www.ishn.org.

Lecture Launcher 1.2: Biopsychology Research—More Than White Rats and Lab Coats Based upon lectures to this point, talk about another area of biopsychological inquiry in which experiments, quasiexperimental studies, and case studies complement one another to make valuable contributions to our understanding of brain/behavior relations (e.g., ask students to split into groups of three to five students to discuss how these three methods for studying brain/behavior relations could be used to study the neural bases of the behavioral changes that emerged following Phineas Gage’s accident).

Lecture Launcher 1.3: Ethical Issues in Animal and Human Research Biopsychology uses both human and nonhuman subjects, and there are different sorts of ethical issues associated with the use of each. Discuss the procedure of applying for ethics approval in your university or college. What are the factors that the ethics committees consider when determining whether to approve a particular experiment? Also, talk about what checks are in place in your country, state, or province to protect human and animal subjects.

Web sites for responsible use of nonhuman animal research: www.understandinganimalresearch.org.uk Go to http://www.apa.org/ and place “Guidelines for Animal Research” in the search box. Scroll down the page to “Guidelines for Ethical Conduct in the Care and Use of Animals” and click that link.

Go to http://www.the-aps.org/ and search for “APS and Animal Research.” Click “Introduction: APS and Animal Research.”

Web sites against the use of nonhuman animal research: www.uncaged.co.uk www.navs.org www.stopanimaltests.com Lecture Launcher 1.4: Neuropsychology’s Case Studies versus Physiological Psychology’s Experiments Neuropsychologists and physiological psychologists both study the effects of brain damage on their subjects. However, they use dramatically different methodologies: Neuropsychologists typically use case studies of human subjects, whereas physiological psychologists use experimental studies of nonhuman subjects. Given that neuropsychology can collect data directly from human subjects, why is it necessary to perform experiments on nonhuman subjects?

Lecture Launcher 1.5: Studying the Brain and Behavior from All Sides Consider the relative strengths and weakness of physiological psychology and neuropsychology.

Neuropsychology’s strength is that it deals with humans, but this is also its weakness because it precludes experimentation. In contrast, physiological psychology can bring the power of the experimental method and invasive neuroscientific techniques to bear on the question, but it is limited to the study of laboratory animals.

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Biopsychology, Tenth Edition Because the two approaches complement one another, together they can provide evidence for points of view that neither can defend individually. Read about the case of Jimmie G. to see the power of this approach in action.

Lecture Launcher 1.6: Chimpanzees and Mental Illness In the analysis of Case 2 (Beck, Moniz, and Prefrontal Lobotomy), it was pointed out that a treatment for mental illness was developed from the results of a single case study in a nonhuman animal. Moniz basing his conclusions on a single case study was problematic in itself, but what about the fact that the removal of an adaptive behavior in a nonhuman animal was taken as evidence for the viability of a treatment for a form of mental illness? To what degree are studies of nonhuman animals currently used as part of the process for developing treatments for mental illness? If they are similar, then how are the interpretations of the data obtained from these nonhuman animals different from that of Moniz?

Lecture Launcher 1.7: The History of the Brain Use the PBS Web site on the History of Research on the Brain to find events and illustrations for use in a classroom presentation. Images can often be copied from a Web site and inserted into a PowerPoint Presentation for use in class. (Make sure you keep a record of where the image came from.) This is not only good for legal defense of fair use, but it may allow you to find something again when you need it.

Web Link Web Link 1.1 History of the Brain Lecture Launcher 1.8: Research with Animals in Psychology “Psychologists undertake research with animals ‘...with a clear scientific purpose.’...There should be a reasonable expectation that the research will a) increase knowledge of the processes underlying the evolution, development, maintenance, alteration, control, or biological significance of behavior, b) increase understanding of the species under study, or c) provide results that benefit the health or welfare of humans or other animals.” (APA Guidelines for Ethical Conduct in the Care and Use of Animals, Section VI.A.) Web Links Web Link 1.4 Ethical Principles for Psychologists and Code of Conduct Web Link 1.5 Guidelines for Ethical Conduct in the Care and Use of Animals Web Link 1.6 Research with Animals in Psychology Web Link 1.7 PETA: People for the Ethical Treatment of Animals Lecture Launcher 1.9: Careers in Neuroscience Have a neuroscientist visit your classroom. The Society for Neuroscience has a listing of neuroscientists willing to make classroom visits. The list is organized by state. < Return to Table of Contents

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Chapter 1: Biopsychology as a Neuroscience

ACTIVITIES Activity 1.1: Making Sense of Eye Movements (refer students to Figure 1.6 from Biopsychology) Manually move your eye upward; the world appears to move downward. This is because the brain interprets movement across the retina as movement of the world, unless the eye movements are actively produced by the brain itself. < Return to Table of Contents

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Biopsychology, Tenth Edition

WEB LINKS Web Link 1.1: History of the Brain Place “Secret Life of the Brain” in your search engine. Select the clickable link from http://www.pbs.org.

On the left hand menu is a clickable link titled “History of the Brain.” Click that link to get to your final webpage destination.

“The history of our quest to understand the brain is certainly as long as human history itself. Use this extensive timeline to meander through some of the highlights (and lowlights) of this great journey of understanding.”

Web Link 1.2: Society for Neuroscience: Public Resources Go to http://www.sfn.org and click on the menu tab labeled “Public Outreach.” From that menu select the link “Brain Awareness Week” and click on that to reach the resources.

Neuroscience-related resources are intended to help you stay apprised of neuroscience research in its path from laboratory to bedside and to better understand the functions of the healthy brain. Links are provided to hundreds of sites related to neuroscience, including patient advocacy groups. Have a neuroscientist visit your classroom and learn about pursuing a career in neuroscience.

Web Link 1.3: Comparative Mammalian Brain Collection http://www.brainmuseum.org/ Web Link 1.4: Ethical Principles for Psychologists and Code of Conduct Go to http://www.apa.org and place “ethical conduct for psychologists” in the search box. Select the result titled “Ethical Principles of Psychologists and Code of Conduct” and click the link.

Web Link 1.5: Guidelines for Ethical Conduct in the Care and Use of Animals Go to http://www.apa.org/ and place “Guidelines for Animal Research” in the search box. Scroll down the page to “Guidelines for Ethical Conduct in the Care and Use of Animals” and click on that link.

Developed by the American Psychological Association’s Committee on Animal Research and Ethics (CARE) Web Link 1.6: Research with Animals in Psychology Go to http://www.apa.org/ and place “lab animal welfare” in the search bar. Select the first result titled “Lab Animal Welfare” and click on the link.

Suggestions from APA on why it is important to use animals in research.

Web Link 1.7: PETA: People for Ethical Treatment of Animals http://www.peta.org For another point of view, see information from the animal rights perspective.

Web Link 1.8: Career Counseling of College Students Go to http://www.apa.org and place “Career Counseling of College Students” in the search bar. Select the first result in the search titled “Career Counseling of College Students: An Empirical Guide to Strategies That Work.” < Return to Table of Contents 17 ..

Biopsychology, Tenth Edition

2 Evolution, Genetics, and Experience: Thinking About the Biology of Behavior TABLE OF CONTENTS Chapter-at-a-Glance

2

Learning Objectives

3

Brief Chapter Outline

4

Teaching Outline

5

Lecture Launchers

14

Activities

16

Web Links

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Chapter 2: Evolution, Genetics, and Experience

CHAPTER-AT-A-GLANCE

Brief Outline Chapter Introduction (p. 21) Thinking About the Biology of Behavior: From Dichotomies to Interactions (pp. 21–25) Human Evolution (pp. 25–36) Fundamental Genetics (pp. 36–44) Epigenetics of Behavioral Development: Interaction of Genetic Factors and Experience (pp. 44–47) Genetics of Human Psychological Differences (pp. 47–50)

Instructor’s Manual Resources Lecture Launchers 2.1, 2.2, 2.7 Activity 2.1 Lecture Launchers 2.3, 2.8 Lecture Launcher 2.4 Lecture Launcher 2.5

Lecture Launcher 2.6

< Return to Table of Contents

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Biopsychology, Tenth Edition

LEARNING OBJECTIVES After completion of this chapter, the student should be able to: LO 2.1 Explain the origins of dichotomous thinking.

LO 2.2 Explain why thinking about the biology of behavior in terms of traditional physiologicalpsychological and nature-nurture dichotomies is flawed.

LO 2.3 Describe the origins of evolutionary theory.

LO 2.4 Explain the evolutionary significance of social dominance and courtship displays.

LO 2.5 Summarize the pathway of evolution from single-cell organisms to humans.

LO 2.6 Describe nine commonly misunderstood points about evolution.

LO 2.7 Describe how research on the evolution of the human brain has changed over time.

LO 2.8 Discuss the field of evolutionary psychology and the study of mate bonding.

LO 2.9 Describe what Mendel’s work with pea plants tells us about the mechanisms of inheritance.

LO 2.10 Understand the structure and function of chromosomes.

LO 2.11 Outline the mechanisms of gene expression.

LO 2.12 Discuss several ways in which modern advances have changed out understanding of genetic processes.

LO 2.13 Define epigenetics, and explain how it is transforming our understanding of genetics.

LO 2.14 Discuss what insights into the genetics of behavior was gained from early research on selective breeding.

LO 2.15 Explain how classic research on phenylketonuria (PKU) has informed our understanding of the genetics of behavior.

LO 2.16 Describe how research on the ontogenetic development of birdsong has provided insight into the development of human language.

LO 2.17 Explain why it is important to distinguish between the development of individuals and the development of individual differences.

LO 2.18 Explain heritability estimates and how they are commonly misinterpreted.

LO 2.19 Describe two ways that twin studies can be used to study the interaction of genes and experience (i.e., nature and nurture). < Return to Table of Contents

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Chapter 2: Evolution, Genetics, and Experience

BRIEF CHAPTER OUTLINE Lecture Launcher 2.1: Opening Your Mind to the Biology of Behavior—It’s More Than Nature or Nurture!

Lecture Launcher 2.2: Are You a Dualist?

1. Thinking About the Biology of Behavior: From Dichotomies to Interactions a. The Origins of Dichotomous Thinking b. Problems with Thinking About the Biology of Behavior in Terms of Traditional Dichotomies Lecture Launcher 2.3: Understanding the Difference between Adaptations, Exaptations, and Spandrels 2. Human Evolution a. Darwin’s Theory of Evolution b. Evolution and Behavior c. Course of Human Evolution d. Thinking About Human Evolution e. Evolution of the Human Brain f. Evolutionary Psychology: Understanding Mate Bonding Lecture Launcher 2.4: Understanding the Significance of Mendelian Genetics 3. Fundamental Genetics a. Mendelian Genetics b. Chromosomes c. The Genetic Code and Gene Expression d. Human Genome Project e. Modern Genetics: Growth of Epigenetics Lecture Launcher 2.5: Humans and Birds Share the Same Singing Genes 4. Epigenetics of Behavioral Development: The Interaction of Genetic Factors and Experience a. Selective Breeding of “Maze-Bright” and “Maze-Dull” Rats b. Phenylketonuria: A Single-Gene Metabolic Disorder c. Development of Bird Song Lecture Launcher 2.6: Even If We Could, Should We Cure Stupidity?

5. The Genetics of Human Psychological Differences a. Development of Individuals Versus Development of Differences Among Individuals b. Heritability Estimates: Minnesota Study of Twins Reared Apart c. A Look into the Future: Two Kinds of Twin Studies 6. Themes Revisited < Return to Table of Contents

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Biopsychology, Tenth Edition

TEACHING OUTLINE 1. Thinking About the Biology of Behavior: From Dichotomies to Interactions a. The Origins of Dichotomous Thinking LO 2.1 Explain the origins of dichotomous thinking.

1. Is It Physiological or Is It Psychological?

• Emerged in Europe in the seventeenth century as science, and the Catholic Church struggled to describe the natural world.

• The French philosopher Descartes came up with a solution: The physical world could be the object of scientific study, while the mind could be the purview of the Church. This separation of mind and body became known as Cartesian dualism.

• This notion survives today: People agree with the idea that there is a category of human psychological activity that is independent of the human brain.

2. Is It Inherited, or Is It Learned?

• Also known as the nature/nurture controversy; debate on whether behavior is inherited through genetics or learned through experience.

• Epitomized by the struggle between early behaviorists and ethologists to adequately describe behavioral development. b. Problems with Thinking About the Biology of Behavior in Terms of Traditional Dichotomies LO 2.2 Thinking about the biology of behavior in terms of traditional physiologicalpsychological and nature-nurture dichotomies is flawed: Explain why.

1. Physiological-or-Psychological Thinking Runs Into Difficulty.

• Such dichotomies are overly simplistic and false; illustrate this by discussing the relationship between brain injury and psychological processes (see Figure 2.1 in Biopsychology) or the presence of “mind” in nonhuman species.

2. Nature-or-Nurture Thinking Runs Into Difficulty.

• The thought of nature-or-nurture is based on the premise that genetic factors and experiential factors combine in an additive fashion.

3. A Model of the Biology of Behavior.

• Behavior is best viewed as the product of genetic potential interacting with past experience and current situational factors, as illustrated by Figure 2.3 in Biopsychology.

2. Human Evolution a. Darwin’s Theory of Evolution LO 2.3 Describe the origins of evolutionary theory.

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Darwin published On the Origins of the Species (1859) and modern biology was born.

Darwin’s theory that species evolve (undergo gradual, orderly change) is the most influential in the biological sciences.

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Darwin was not the first to propose this idea, but he was the first to provide strong evidence for it from: 1) fossil records; 2) structural similarities among existing species; and 3) programs of selective breeding.

Even stronger evidence comes from modern genetic studies and from observations of evolution in progress (e.g., Grant’s (1991) study of changes in Galápagos finches after a oneyear drought—beak size increased in response to shortage of small seeds).

Darwin was also the first to suggest the mechanism by which evolution takes place: natural selection, in which normal variations in a characteristic that are associated with increased fitness (high rates of survival and reproduction) are most likely to be passed on to future generations.

The evidence for the theory of evolution is unassailable; it meets with no significant opposition from the biological community.

b. Evolution and Behavior LO 2.4 Explain the evolutionary significance of social dominance and courtship displays.

1. Social Dominance • Early studies of evolution focused on structure; behavior also plays an important role in determining an organism’s fitness.

• The contributions of some behaviors (e.g., eating, sexual behavior, predatory behavior) are obvious; others are less obvious, but no less important. Two examples are social aggression and courtship displays.

• Males of many species establish hierarchies of social dominance by combative encounters with other males.

• Social dominance influences evolution because dominant males (or females, in some species) are able to copulate more. Example: in a study of bull elephant seals, McCann (1981) found that the highest-ranking bull accounted for 37 percent of copulations; the lowest ranking bull accounted for only 1 percent.

2. Courtship Display • Courtship displays precede copulation in many species.

• Copulation is unlikely if one partner fails to respond appropriately to the displays of the other.

• Courtship displays are important to evolution because they can promote the formation of new species; the evolution of an idiosyncratic courtship display can form a reproductive barrier that is as effective as geographic separation. c. Course of Human Evolution LO 2.5 Summarize the pathway of evolution from single-cell organisms to humans.

1.

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Evolution of Vertebrates About 600 million years ago, the first multi-celled organisms evolved in the oceans.

About 450 million years ago, the first chordates (animals with dorsal nerve cords) evolved.

425 million years ago, the first chordates with backbones (i.e., vertebrates) evolved; they were bony fishes.

410 million years ago, bony fishes first ventured onto land to escape stagnant pools and take advantage of untapped food sources; the Florida walking catfish is a survivor of this stage.

2. Evolution of Amphibians 6 ..

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400 million years ago, the first amphibians evolved; they are born in water and spend their larval stage there, but as adults, they have legs and lungs and can survive on land.

3. Evolution of Reptiles • 300 million years ago, the first reptiles evolved from amphibians; they spend the first stage of their lives in the watery environment of a shell-covered egg; dry scales reduce water loss and allow adults to live away from water.

4. Evolution of Mammals • 180 million years ago, during the age of dinosaurs, a line of reptiles evolved that fed their young through mammary glands; eventually, mammals stopped laying eggs and nurtured their young in the watery environment of their bodies.

• Today, there are about 20 different orders of mammals; the one we belong to is primates; there are about 12 different families of primates. Five of the most widely-studied are the prosimians, old-world monkeys, new-world monkeys, apes, and hominids. The hominid family is composed of two genera: Homo and Australopithecus.

5. Emergence of Humankind • Four million years ago, Australopithecus evolved (we believe) from a species of African apes.

• Australopithecines were 1.3 meters (4 feet) tall, had small brains, had an upright walk, and became extinct about 1 million years ago.

• Two million years ago, the first Homo species evolved from Australopithecus; these hominids used tools and fire, but had a relatively small brain.

• 275,000 years ago, modern humans (homo sapiens) evolved.

• Interesting point: The human attributes of a big brain, upright posture, and free hands evolved hundreds of thousands of years ago, yet most uniquely human accomplishments occurred only within the last 40,000 years. Why? d. Thinking About Human Evolution (see Figure 2.12 in Biopsychology) LO 2.6 Describe nine commonly misunderstood points about evolution.

When thinking about human evolution, keep the following eight points in mind: • Evolution does not proceed in a straight line.

• Homo sapiens do not represent evolutionary supremacy.

• Evolution is not always a slow, gradual process.

• Present species represent a fraction of the species that have evolved on earth.

• Evolution is not a perfectionist.

• Evolution is not always adaptive; nonadaptive evolutionary byproducts are called spandrels.

• Sometimes structures or behaviors evolve in response to one type of evolutionary pressure, but later perform a different function; these types of changes are called exaptations.

• Similarities between species do not imply a common evolutionary origin. Keep in mind the differences between homologous structures (with a common evolutionary origin) and analogous structures (with different, but convergent evolutionary processes in their origins). e. Evolution of the Human Brain (see Figure 2.13 in Biopsychology) LO 2.7 Describe how research on the evolution of the human brain has changed over time.

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f.

Size is not the key to the intellectual power of the human brain; there is no relationship between size and intellectual capacity in humans, and human beings do not have the largest brains in the animal kingdom.

Three key points about the evolution of the human brain: – It has increased in size during the course of evolution.

– Most of this increase in size has occurred in the cerebrum.

– The increased size of the cerebrum has been accompanied by increased convolutions of the cortex.

The similarity between the brains of different species is more significant than the differences between them. All brains are composed of neurons; these neurons generally function in a similar fashion, and in most cases, similar structures can be found between species.

Evolutionary Psychology: Understanding Mate Bonding LO 2.8 Discuss the field of evolutionary psychology and the study of mate bonding.

• •

Evolutionary psychology seeks to understand human behaviors by considering the pressures that led to their evolution; much attention has focused on a comparison of promiscuity and the less common strategy of mate bonding (enduring mating relationships).

In mammals, this may be due to the fact that they produce relatively few young, and these young are helpless and slow to develop. Thus, it is adaptive for males to stay with females and promote the success of their young, and it is adaptive for females to evolve behaviors that will promote this type of bonding.

1. Polygyny and Polyandry • Polygyny (male bonds with multiple females) is the most common form of mate bonding.

The males of most species contribute little more than sperm to the development of the young; the investment of the female is much more substantial. Thus, in many species, the females evolved strategies to promote bonding with the most dominant males (to increase the likelihood their young will survive), whereas males mate with as many females as possible (resulting in polygyny).

• In species where the male’s contribution to reproduction outweighs the females, polyandry (female mates with multiple males) has evolved. (Example: In the seahorse, the males tend to the eggs and the young until they are mature enough to survive on their own.)

2. Monogamy • Where males helping to raise the young has enhanced the survival of offspring, monogamy (a single male bonds with a single female) has evolved as the optimal reproductive strategy.

• Developments in evolutionary psychology emphasize three key points: 1) evolutionary analyses can be applied to the most complex human behaviors; 2) humans are the product of evolution; and 3) humans are closely related to other animal species.

3. Thinking About Evolutionary Psychology • Men value youth and attractiveness while women value power and earning capacity.

• Physical attractiveness best predicts which women will bond with men of high occupational status.

• The major mate-attraction strategy of women is to make themselves more attractive, while for men it is displaying their power and resources.

• Men are more likely than women to commit adultery.

3. Fundamental Genetics 8 ..

Biopsychology, Tenth Edition a. Mendelian Genetics (see Figure 2.15 in Biopsychology) LO 2.9 Describe what Mendel’s work with pea plants tells us about the mechanisms of inheritance.

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• •

Darwin did not understand how structural or behavioral traits could be passed from generation to generation, or how conspecifics could differ from one another. These processes were first documented by Gregor Mendel, an Augustinian monk.

His success is that he studied dichotomous traits (characteristics that occur in one form or another, never a mix; Mendel studied the inheritance of the color of peas) and true-breeding lines (in which interbred members always produce offspring with the same trait).

Key finding: When true-bred brown and white peas are crossed, all the offspring from the first cross have brown seeds, whereas 25 percent of the offspring from the second cross have white seeds; this disproved the prevalent view that offspring inherit their parents’ exhibited traits.

Mendel proposed that each dichotomous trait was due to two kinds of inherited factors; these are called genes. Furthermore, each individual contains two genes for each dichotomous trait; these are called alleles.

These results led to Mendel’s concepts of: – dominant traits (appear in 100 percent of first crosses) and recessive traits (appear in about 25 percent of second crosses) – genotype (genetic traits passed on to offspring) and phenotype (observable genetic traits) – homozygous organisms (that possess identical genes for a trait) and heterozygous organisms (that possess different genes for a trait)

b. Chromosomes LO 2.10 Understand the structure and function of chromosomes.

1. Reproduction and Recombination.

• In the early 1900s, genes were localized to paired thread-like structures in the cell nucleus called chromosomes.

• Gametes (eggs and sperm cells) are produced when cells divide during meiosis. One chromosome from each chromosome pair in the parent cell goes to each of two gametes produced when that cell divides; thus, each gamete has half the usual number of chromosomes. When they combine during fertilization, the resulting zygote has the normal number of chromosomes (half from each parent).

• The strongest early evidence of this came from studies of linkage between various traits in a species (such that individuals expressing one trait usually expressed several other linked traits). In each species, the number of clusters of linked traits equals the number of pairs of chromosomes, suggesting that the traits were linked by their presence on the same chromosome.

• Crossing over (see Figure 2.18) explains why traits on a chromosome are not always linked (i.e., inherited together); crossing over is important because it allows increases in species diversity.

• Sex chromosomes are not found in matched pairs. Females have two X-chromosomes; males have an X- and a Y-chromosome. Sex-linked traits are traits associated with a sex chromosome; usually the X chromosome as the Y-chromosomes carries few genes other than those that cause a zygote to develop into a male.

2. Structure and Replication (see Figures 2.17, 2.18, and 2.19 in Biopsychology) 9 ..

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Each chromosome is a double-stranded molecule of deoxyribonucleic acid (DNA)—which is made up of 4 nucleotide bases: adenine, thymine, guanine, and cytosine. The sequence of those bases on each chromosome constitutes the genetic code.

Each strand of DNA is the complement of the other, as thymine is attracted to adenine and guanine is attracted to cytosine (see Figure 2.17). During replication, as the strands of DNA unwind, each base in a strand attracts its complement so that when unwinding is complete, two new strands of DNA are created.

DNA serves as a template for the transcription of messenger RNA (mRNA). It is called mRNA because it carries a code outside of the nucleus.

MRNA then attaches to a ribosome, moving along it to make a protein.

Three consecutive nucleotide bases (of the mRNA) make a codon.

Each codon instructs the ribosome to add 1 of 20 different amino acids to the protein.

Each amino acid is carried to the ribosome by transfer RNA.

3. Sex Chromosomes and Sex-Linked Traits Sex chromosomes are found in matched pairs. Females have two X-chromosomes; males have an X- and a Y-chromosome. Sex-linked traits are traits associated with a sex chromosome – usually the X chromosome because the Y-chromosome carries fewer genes. c. Genetic Code and Gene Expression LO 2.11 Outline the mechanisms of gene expression.

• • • • • • • • • • • •

Structural genes are genes that contain information for the synthesis of proteins.

Proteins are long chain of amino acids.

Structural genes compose a small portion of each chromosome.

The stretches of DNA that lack structural genes include portions called enhancers (or promoters).

The function of enhancers is to determine whether particular structural genes start the synthesis of proteins and at what rate.

Enhancers determine how a cell will develop and function.

Proteins that bind to DNA and influence gene expression are called transcription factors.

Transcription factors are influenced by signals received by the cell from the environment.

Messenger RNA carries the genetic code out of the nucleus of the cell.

Ribosomes translates the genetic code.

Codons are three consecutive nucleotide bases that instructs the ribosomes to add 1 of the 20 different kinds of amino acids available.

The process of gene expression involves transcription of the DNA to the RNA and the translation of the RNA base sequence code into a sequence of amino acids.

d. Human Genome Project LO 2.12 Discuss several ways in which modern advances have changed our understanding of genetic processes.

• •

Perhaps the most ambitious scientific project of all time; has mapped the base sequence of each of the 3,000,000,000 base letters that comprise the 46 chromosomes that human beings possess.

Many were surprised to note that the human genome includes only about 20,000 genes— about the same number as a mouse, and far fewer than corn! Human complexity appears to be due to refinements in gene expression, rather than in a huge increase in the number of genes 10 ..

Biopsychology, Tenth Edition

• • • •

involved. The function of the many bases found in human chromosomes that are not involved in classic protein synthesis remains a mystery.

Researchers have now generated a nearly complete map of the entire set of proteins encoded for by our genes called the human proteome.

It was initially hoped that genomic variations would be directly linked to human diseases.

The revealed relationships would then drive personalized medical treatments.

These hopes have not been realized because so many genes are involved with disease and they often account for a small portion of heritability.

Genome research is now focused on understanding the complex interactions between multiple genes, their variants, and experience.

e. Modern Genetics: Growth of Epigenetics LO 2.13 Define epigenetics, and explain how it is transforming our understanding of genetics.

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•

Epigenetics focuses on mechanisms that influence the expression of genes without changing the genes themselves.

Epigenetic mechanisms are responsible for the fact that a small number of genes are responsible for human development.

There are four factors that lead to the rise of epigenetics.

The assumption was that the function of DNA was to synthesize proteins.

Epigenetics focuses on mechanisms that influence the expression of genes without changing the genes themselves.

Epigenetic mechanisms are responsible for the fact that a small number of genes are responsible for human development.

There are four factors that lead to the rise in epigenetics. o The assumption was that the function of DNA was to synthesize proteins. o The portions of DNA that do not make proteins are referred to as junk DNA. Ninetynine percent of DNA regarded as junk DNA. o For decades we’ve known there is an interaction between genes and environment, but the mechanisms have been unknown. o New techniques for research discovered through the Human Genome Project.

Five advances The portions of DNA that do not make proteins are referred to as junk DNA. o It has been newly discovered that these active nongene DNA control structural gene expression. o Many types of RNA found, each with different functions. o Advances in gene expression o DNA methylation is an epigenetic mechanism whereby a methyl group is attached to DNA o Histone Remodeling is when DNA is coiled around proteins called histones (see Figure 2.21). Histones can change their shape, consequently increasing or decreasing adjacent gene expression. Remodeling is induced by environmental experiences. o RNA editing-changes incorporated from the environment o Epigenetic mechanisms are enduring o Transgenerational epigenetics is a subfield of epigenetics that examines the transmission of experiences via epigenetics mechanisms across generations.

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Chapter 2: Evolution, Genetics, and Experience 4. Epigenetics of Behavioral Development: Interaction of Genetic Factors and Experience • •

Ontogeny refers to the development of an individual through their lifespan; phylogeny refers to the evolutionary development of a species through the ages.

Behavioral development is a consequence of genetic potential interacting with the experience of an individual organism. To help you understand this idea, here are three examples:

a. Selective Breeding of “Maze-Bright” and “Maze-Dull” Rats (see Figures 2.21 and 2.22 in Biopsychology) LO 2.14 Discuss what insight into the genetics of behavior was gained from early research on selective breeding.

• •

Tryon raised maze-bright and maze-dull strains of rats; however, the maze-bright rats do better than the maze-dull rats only if both are raised in impoverished environments; if they are both raised in enriched environments, the differences disappear.

Maze-bright rats are not generally more intelligent, they do better because they are less emotional.

b. Phenylketonuria: A Single-Gene Metabolic Disorder LO 2.15 Explain how classic research on phenylketonuria (PKU) has informed our understanding of the genetics of behavior.

• • •

A form of mental retardation that results from the accumulation of phenylalanine in the body.

Due to absence of gene for phenylalanine hydroxylase, which converts phenylalanine to tyrosine.

Sufferers develop the disorder if they eat phenylalanine-rich foods during development. It is diagnosed by high levels of phenylpyruvic acid in urine; it is treated by keeping sufferers on a phenylalanine-free diet during childhood (though subtle cognitive deficits remain).

c. Development of Bird Song (see Figure 2.24 in Biopsychology) LO 2.16 Describe how research on the ontogenetic development of birdsong has provided insight into the development of human language.

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Some birds learn to sing by hearing conspecific songs early in life.

Research has revealed that birdsong develops in two stages: 1) a sensory phase, in which exposure to conspecific songs leads to memories that later guide song development and 2) a sensorimotor phase, in which birds must practice (and receive sensorimotor feedback) for songs to develop properly.

Zebra finches and white-crowned sparrows are age-limited learners, meaning that once a bird develops an adult song, it crystallizes, remaining unchanged for life. By contrast, male canaries are open-ended learners, meaning that they can add new songs to their repertoire each mating season.

Canary song circuit is remarkable in four ways: 1) it is lateralized to the left hemisphere (like human speech); 2) the vocal center is four times larger in males than in females; 3) in the spring, as new songs are acquired, the vocal centers double in size—only to shrink again in the fall; and 4) this growth is due to neurogenesis, a feat thought impossible in the adult vertebrate brain until very recently.

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Biopsychology, Tenth Edition 5. Genetics of Human Psychological Differences a. Development of Individuals Versus Development of Differences Among Individuals LO 2.17 Explain why it is important to distinguish between the development of individuals and the development of individual differences.

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To assess the relative contribution of genes and experience to the development of differences in psychological characteristics, researchers often study individuals with varying degrees of genetic similarity. For example, they might compare identical (monozygotic) twins (genetically identical) with fraternal (dizygotic) twins (no more genetically the same than any two siblings in a family).

b. Heritability Estimates: Minnesota Study of Twins Reared Apart LO 2.18 Explain heritability estimates and how they are commonly interpreted.

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Studies such as the Minnesota Study have found high correlations for a variety of complex human traits and behaviors for identical twins separated at birth; heritability estimates based on these range from 40 to 80 percent..

c. A Look into the Future: Two Kinds of Twin Studies LO 2.19 Describe two ways that twin studies can be used to study the interaction of genes and experience (i.e., nature and nurture).

1. Twin Studies of Epigenetic Effects.

• More recent twin studies have focused on epigenetic changes in humans, triggered by environmental experiences.

• Monozygotic twins are genetically identical at conception but their epigenetic profiles diverge with advancing age.

• Wong et al. (2010) examined DNA methylation and found that it is mainly a consequence of experiential factors.

2. Twin Studies of the Effects of Experience on Heritability.

• Turkheimer et al. (2003) found that heritability estimates of IQ in seven-year-old twins varied as a function of socioeconomic status (SES). In low SES families, the heritability estimate was near zero, while in high SES families, the heritability estimate approached 1.00.

– Discuss the implications of this finding to the idea that behavior is not a consequence of physiology or psychology, or of nature or nurture—instead, it is the product of neural activity shaped by interactions among genes, past experience, and an organism’s present situation. < Return to Table of Contents

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Chapter 2: Evolution, Genetics, and Experience

LECTURE LAUNCHERS Lecture Launcher 2.1: Opening Your Mind to the Biology of Behavior—It’s More than Nature or Nurture!

Spend some time discussing the commonly held notions that behavior is a function of physiology or psychology, or that behavior is learned or innate. This discussion is pretty easy to get rolling; for example, ask the class what the relationship between brain and mind is, or about the common observation that “They can’t help their behavior, they were born that way!”

Lecture Launcher 2.2: Are You a Dualist?

After reviewing Cartesian dualism, poll students about their personal philosophy. Are they monists, dualists, or unsure? Encourage students to reflect on their explanations of their own behavior. Do they view themselves as a ghost in the machine, somehow distinct from the biological reality of their brain?

Point out to students that a dualist philosophy might make it difficult for them to appreciate the remarkably complex chemical and cellular functions that produce all of their own behavior.

Lecture Launcher 2.3: Understanding the Difference between Adaptations, Exaptations, and Spandrels Students sometime have difficulty understanding the difference between an adaptation, an exaptation, and a spandrel. This is probably due, in part, to the fact that it is often difficult to determine what a particular anatomical structure might be. Provide the students with a list of anatomical structures and ask them whether that structure is an exaptation, an adaptation, or a spandrel. There might not be a correct answer for every particular structure; knowing this should help them understand this abstraction.

Lecture Launcher 2.4: Understanding the Significance of Mendelian Genetics Many students struggle with the basic ideas underlying Mendelian genetics, and the significance of these ideas to inherited contributions to behavior. You can use a combination of the resources available from the Genetic Science Learning Center at the University of Utah (http://learn.genetics.utah.edu/) to illustrate concepts like DNA/gene/chromosome, genetic mixing, and genetic and environmental interactions in the expression of behavioral traits.

Lecture Launcher 2.5: A Genetic Link between Human Language and Bird Song?

This chapter emphasizes the idea that human behavior has evolved from behaviors observed in other species. You can initiate a class discussion about this idea in this section, based on recent evidence that a gene known to be involved in human language is also important to the development of birdsong, at least in species where imitation is important to song acquisition. Background information can be found at on the BBC website. Go to http://www.bbc.com. Once there, click on the link to “earth” in the menu at the top of the page. Once on the “earth” website enter “language and birdsong” in the search bar. The first article that comes up from the search is is titled “songbirds may have helped us talk”. Click on that link for your article.

Lecture Launcher 2.6: Even If We Could, Should We Cure Stupidity?

Direct students to the New Scientist review of James Watson’s comments on using gene therapy to cure stupidity (found at http://www.newscientist.com/. Once on the main page place “DNA and stupidity” in the search field and select the first article). Use these comments to focus class discussion on the future role of genetic screening and gene therapy in determining human behavior. Video of Watson’s controversial comments can be found in the PBS video series “DNA, Episode 5: Pandora’s Box.”

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Biopsychology, Tenth Edition Lecture Launcher 2.7: The History of the Brain Use the PBS Website on the history of research on the brain to find events and illustrations for use in a classroom presentation. Images can often be copied from a Website and inserted into a PowerPoint presentation for use in class. (Make sure you keep a record of where the image came from. This is not only good for legal defense of fair use, but it may allow you to find something again when you need it.)

Web Link 2.1: History of the Brain Lecture Launcher 2.8 Basic Evolution Evolution is easily misunderstood. The Talk.Origins Website is an exceptional resource for basic evolutionary biology. Large parts of the Website, including the “Introduction to Evolutionary Biology” page, assume the reader has had little or no biology background. This makes it very accessible to most psychology majors.

Web Link 2.5: Talk.Origins Homepage < Return to Table of Contents

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Chapter 2: Evolution, Genetics, and Experience

ACTIVITIES Activity 2.1: Rene Descartes For advanced students, reading some of the original writings of some of the historical figures in the discipline can be useful. Chapters of the work of Descartes and Darwin are available online for easy access.

Web Link 2.2: Discourse on the Method of Rightly Conducting the Reason and Seeking for Truth in the Sciences—Rene Descartes (1637) Web Link 2.3:The Descent of Man (2nd ed.)—Charles Darwin (1874)

< Return to Table of Contents

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Biopsychology, Tenth Edition

WEB LINKS Web Link 2.1: History of the Brain http://www.pbs.org/wnet/brain/ (Once on the page for “The Secret Life of the Brain”, click on the link for the history of the brain.) “The history of our quest to understand the brain is certainly as long as human history itself. Use this extensive timeline to meander through some of the highlights (and lowlights) of this great journey of understanding.”

Web Link 2.2: Discourse on the Method of Rightly Conducting the Reason and Seeking for Truth in the Sciences, Rene Descartes (1637) Guide students to http://www.marxists.org. Once there, have students use the drop down menu on the left side of the homepage to select Rene Descartes. After arriving on the Rene Descartes webpage, have students select the article called “Discourse on Method”.

Source: Discourse on Method (1637). Cambridge University Press, edited by Haldane and Ross; first five parts.

Web Link 2.3: The Descent of Man (2nd ed.), Charles Darwin (1874) http://psychclassics.yorku.ca/ Once you arrive at the home page, click on the “author” link available on that page. Click on the “D” on the alphabetical bar at the top of the page. At the top of the page is the link for Charles Darwin and his article on “The Descent of Man”.

Web Link 2.4: The Origin of Species, Charles Robert Darwin http://www.bartleby.com/ Once you arrive at the home page, find the search by “author” link on the right hand side of the page. Click on “author”. Page down to the link for Charles Darwin and his “Origin of Species” article.

“Over fifteen years in the writing, this scientific treatise not only revolutionized every branch of the natural sciences with its theory of evolution, but influenced every literary, philosophical and religious thinker who followed.”

Web Link 2.5: Talk.Origins Homepage http://www.talkorigins.org/ “Talk.Origins is a Usenet newsgroup devoted to the discussion and debate of biological and physical origins.”

“The Talk.Origins Archive is a collection of articles and essays, most of which have appeared in Talk.Origins at one time or another. The primary reason for this archive’s existence is to provide mainstream scientific responses to the many frequently asked questions (FAQs) that appear in the Talk.Origins newsgroup and the frequently rebutted assertions of those advocating intelligent design or other creationist pseudosciences.”

Web Link 2.6: Introduction to Evolutionary Biology http://www.talkorigins.org/ Once on the home page, select “search the archive” from the menu on the left hand side of the page. Place “Introduction to Evolutionary Biology” in the search bar and select “search”.

Scroll down the page to the first link below the ads by Google. Click on the link.

Web Link 2.7: Comparative Mammalian Brain Collection http://www.brainmuseum.org/

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Chapter 2: Evolution, Genetics, and Experience Web Link 2.8: Sources of Human Psychological Differences: The Minnesota Study of Twins Reared Apart http://euvolution.com/ Once on the home page, select the “Science” link available on the left hand side of the page. From the Science page, select the link for the “Nature versus Nurture” debate. From the “Nature versus Nurture” debate page, select the link titled “Sources of Human Psychological Differences”.

Web Link 2.9: Heredity and Heritability http://plato.stanford.edu/ Once on the home page, type “heredity” in the search bar and click “search”.

After receiving the search results, click on the link for “heritability”.

Stanford Encyclopedia of Philosophy < Return to Table of Contents

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3 Anatomy of the Nervous System: Systems, Structures, and Cells That Make Up Your Nervous System TABLE OF CONTENTS Chapter-at-a-Glance

2

Learning Objectives

3

Brief Chapter Outline

4

Teaching Outline

5

Lecture Launchers

11

Activities

13

Demonstrations

15

Assignments

16

Web Links

18

Handout Descriptions

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Handouts

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Chapter 3: Anatomy of the Nervous System

CHAPTER-AT-A-GLANCE

Brief Outline Chapter Introduction (p. 53) 3.1. General Layout of the Nervous System (pp. 53–57) 3.2 Cells of the Nervous System (pp. 57–62) 3.3 Neuroanatomical Techniques and Directions (pp. 62–66) 3.4 Anatomy of the Central Nervous System (pp. 66–75)

Instructor’s Manual Resources Lecture Launchers 3.1, 3.2 Lecture Launcher 3.3 Lecture Launcher 3.4, Activity 3.1 Lecture Launchers 3.5, 3.6, 3.7, Activity 3.3, Demonstration 3.3 Lecture Launcher 3.8, Activities 3.2, 3.4, Demonstrations 3.1, 3.2, Assignments 3.1, 3.2, 3.3

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Biopsychology, Tenth Edition

LEARNING OBJECTIVES After completion of this chapter, the student should be able to: LO 3.1 List and describe the major divisions of the nervous system.

LO 3.2 Describe the three meninges and explain their functional role.

LO 3.3 Explain where cerebrospinal fluid is produced and where it flows.

LO 3.4 Explains what the blood-brain barrier is and what functional role it serves.

LO 3.5 Draw, label, and define the major features of a multipolar neuron.

LO 3.6 Describe four kinds of glial cells.

LO 3.7 Compare several neuroanatomical research techniques.

LO 3.8 Illustrate the neuroanatomical directions.

LO 3.9 Draw and label a cross section of the spinal cord.

LO 3.10 List and discuss the five major divisions of the human brain.

LO 3.11 List and describe the components of the myelencephalon.

LO 3.12 List and describe the components of the metencephalon.

LO 3.13 List and describe the components of the mesencephalon.

LO 3.14 List and describe the components of the diencephalon.

LO 3.15 List and describe the components of the telencephalon.

LO 3.16 List and describe the components of the limbic system and of the basal ganglia. < Return to Table of Contents

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Chapter 3: Anatomy of the Nervous System

BRIEF CHAPTER OUTLINE Lecture Launcher 3.1: Get Your Bearings: Relating the Nervous System to the Rest of the Body Lecture Launcher 3.2: The Latex Neuron 1. General Layout of the Nervous System a. Divisions of the Nervous System b. Meninges c. Ventricles and Cerebrospinal Fluid d. Blood-Brain Barrier Lecture Launcher 3.3: Name That Neuron Part 2. Cells of the Nervous System a. Anatomy of Neurons b. Glial: The Forgotten Cells Lecture Launcher 3.4: Jigsaw Brain 3. Neuroanatomical Techniques and Directions a. Neuroanatomical Techniques b. Directions in the Vertebrate Nervous System 4. Anatomy of the Central Nervous System a. Spinal Cord b. Five Major Divisions of the Brain c. Myelencephalon d. Metencephalon e. Mesencephalon f. Diencephalon g. Telencephalon h. Limbic System and the Basal Ganglia

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Biopsychology, Tenth Edition

TEACHING OUTLINE 1. General Layout of the Nervous System (see Figures 3.1 and 3.2 in Biopsychology) a. Divisions of the Nervous System LO 3.1 List and describe the major divisions of the nervous system.

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The nervous system can be divided into two divisions using several criteria: – CNS vs. PNS: the CNS lies within the bony skull and vertebral column.

– Brain vs. Spinal Cord: comprise the two parts of the CNS. – Somatic vs. Autonomic: comprise the two parts of the PNS. The somatic branch interacts with the external environment; the autonomic branch interacts with the internal environment.

– Efferent vs. Afferent: refers to whether nerves bring sensory information into the CNS (afferent) or carry motor commands away from the CNS (efferent).

– Sympathetic vs. Parasympathetic: the two branches of the autonomic division of the PNS. Convention suggests that the sympathetic branch activates an organism while the parasympathetic branch acts to conserve energy. Each autonomic target organ is innervated by both branches and sympathetic activation indicates arousal, while parasympathetic activation indicates relaxation.

The cranial nerves (see Appendix III in Biopsychology) are a special group of nerves that leave the CNS from the brain through the skull, rather than from the spinal cord. These have specific sensory and/or motor functions (see Appendix IV in Biopsychology); disruption of these functions allows neurologists to accurately determine the location and size of tumors and other kinds of brain pathology.

b. The Meninges (see Figure 3.4 in Biopsychology) LO 3.2 Describe the three meninges and explain their functional role.

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The brain and spinal cord are well-protected by the skull and vertebrae, and by three membranes called the meninges: the dura mater (tough mother; outside), the arachnoid mater (spidery mother; middle), and the pia mater (gentle mother; inside).

c. Ventricles and Cerebrospinal Fluid (see Figure 3.3 in Biopsychology) LO 3.3 Explain where cerebrospinal fluid is produced and where it flows.

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Cerebrospinal fluid (CSF) is manufactured by the choroid plexuses—capillary networks that protrude into the ventricles. CSF circulates through the ventricular system of the brain, the central canal of the spinal cord, and the subarachnoid space, and is absorbed into large channels called sinuses in the dura mater and then into the blood stream (see Figure 3.4 in Biopsychology).

When the flow of CSF is blocked, hydrocephalus results.

d. Blood-Brain Barrier LO 3.4 Explains what the blood-brain barrier is and what functional role it serves.

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Most blood vessels of the brain do not readily allow compounds to pass from the general circulation into the brain; this protection, called the blood-brain barrier, is due to the tightlypacked nature of the cells of these blood vessels.

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Chapter 3: Anatomy of the Nervous System •

Some large molecules (e.g., glucose) are actively transported through blood vessel walls and there are some areas of the brain that allow large molecules to pass through unimpeded.

2. Cells of the Nervous System (see Figures 3.5–3.10 from Biopsychology) The gross structures of the nervous system are made up of hundreds of billions of different cells that are either neurons or glia. a. Anatomy of Neurons LO 3.5 Draw, label, and define the major features of a multipolar neuron. i. External Anatomy of Neurons ii. Internal Anatomy of Neurons iii. Neuron Cell Membrane • •

These are the fundamental functional units of the nervous system; cells that are specialized for the reception, conduction, and transmission of electrochemical signals.

Most of you have seen a schematic drawing of a multipolar motor neuron; don’t be misled by its familiar shape, as neurons come in a wide variety of sizes and shapes. The following are its nine parts (see Figure 3.5 in Biopsychology):

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A semipermeable cell membrane: The cell membrane is semipermeable because of special proteins that allow chemicals to cross the membrane. This semipermeability is critical to the normal activity of the neuron. The inside of the cell is filled with cytoplasm.

– A cell body (soma), which is the metabolic center of the cell. The soma also contains the nucleus of the neuron, which contains the cell’s DNA. – Dendrites are shorter processes that emanate from the cell body and receive input from synaptic contacts with other neurons.

– A single axon that projects away from the cell body; this process may be as long as a meter.

– Axon hillock, the junction between cell body and axon, is a critical structure in the conveyance of electrical signals by the neuron.

– Multiple myelin sheaths: These are formed by oligodendroglia in the CNS and Schwann cells in the PNS; they insulate the axon and assist in the conduction of electrical signals.

– Nodes of Ranvier are the small spaces between adjacent myelin sheaths.

– Buttons are the branched endings of the axon that release chemicals that allow the neuron to communicate with other cells.

– Synapses are the points of communication between the neuron and other cells (neurons, muscle fibers). iv. Classes of Neurons • The type of neuron usually drawn in textbooks is called a multipolar neuron because it has multiple dendrites and an axon extending from soma. There are also unipolar neurons (one process that combines both axon and dendrites), bipolar neurons (two processes: a single axon and a single dendrite), and interneurons that have no axons. v. Neurons and Neuroanatomical Structure • Clusters of cell bodies in the central nervous system are called nuclei; while clusters of cell bodies in the peripheral nervous system are called ganglia.

• In the central nervous system bundles of axons are called tracts; in the peripheral nervous system, they are called nerves. b. Glia: The Forgotten Cells LO 3.6 Briefly describe four kinds of glial cells.

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The most common type of cells in the nervous system are glia.

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Biopsychology, Tenth Edition • •

There are four major types of glia with an expanding list of newly discovered subtypes.

One of the earliest recognized responsibilities of glia cells is to provide physical and functional support to neurons.

The glial cells that form the myelin sheaths of axons in the CNS and PNS are oligodendrocytes and Schwann cells respectively.

Microglia have immune system-like responsibilities in the brain, and they play a role in the regulation of cell death, synapse formation, and synapse elimination.

Astroglia are the largest of the glial cells; they support and provide nourishment for neurons and form part of the blood brain barrier. They also have the ability to contract or relax blood vessels throughout the brain.

Researchers are beginning to appreciate that astroglia play a key role in the function of the nervous system. They help send chemical signals between neurons, and establish and maintain connections between neurons.

• • • •

3. Neuroanatomical Techniques and Directions (see Figures 3.11–3.13 in Biopsychology) Research on the anatomy of the nervous system depends upon a variety of techniques that permit a clear view of different aspects of neural structure. a. Neuroanatomical Techniques LO 3.7 Compare several neuroanatomical research techniques.

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Golgi Stain: permitted individual neurons to be studied for the first time (see Figure 3.11).

Nissl Stain: highlights cell bodies of all neurons; allowed estimation of cell density in tissue (see Figure 3.12).

Electron Microscopy: allows visualization of the neuronal ultrastructure (see Figure 3.13).

Neuroanatomical Tracing Techniques: highlights individual axons; may be retrograde (trace back from terminal fields) or anterograde (trace from soma to terminal fields).

b. Directions in the Vertebrate Nervous System (see Figures 3.14–3.15 in Biopsychology) LO 3.8 Illustrate the neuroanatomical directions.

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First axis: anterior means toward the nose or front; posterior means toward the tail or back.

Second axis: dorsal is toward the surface of the back or top of the head (as in dorsal fin); ventral indicates the surface of the chest or bottom of the head.

Third axis: medial is toward the midline of the body; lateral indicates outside or away from the midline.

4. Anatomy of the Central Nervous System a. Spinal Cord (see Figure 3.16 in Biopsychology) LO 3.9 Draw and label a cross section of the spinal cord.

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In cross section, the gray matter (cell bodies) forms a butterfly inside of the white matter (myelinated axons).

The subcortical myelin gives the white matter its glossy white sheen.

The upper (dorsal; posterior) wings of the butterfly are called the dorsal horns; the lower (ventral; anterior) wings are called the ventral horns.

31 pairs of nerves are attached to the spinal cord. As they near the cord, they split into dorsal roots (sensory axons; cell bodies lie just outside the spinal cord in the dorsal root ganglia) or ventral roots (motor axons; cell bodies lie inside the ventral horns).

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Chapter 3: Anatomy of the Nervous System b. The Five Major Divisions of the Brain (a brain model is useful for teaching this section; see Figures 3.17 and 3.18 in Biopsychology) LO 3.10 List and discuss the five major-divisions of the human brain.

• There are five divisions of the mammalian brain; in general, higher structures are less reflexive and perform more complex functions, and they are also more recently evolved.

• The nervous system is first recognizable in the developing embryo as the neural tube.

• The brain develops from three swellings at one end of the neural tube: the hindbrain, the midbrain (mesencephalon), and the forebrain.

• The hind brain develops into the myelencephalon and the metencephalon; the forebrain develops into the diencephalon and the telencephalon (also called the cerebral hemispheres).

• The term “brain stem” refers to the stem on which the cerebral hemispheres rest (myelencephalon + metencephalon + mesencephalon + diencephalon = brain stem).

5. Major Structures of the Brain a. Myelencephalon (see Figure 3.19 in Biopsychology) LO 3.11 List and describe the components of the myelencephalon.

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The myelencephalon is commonly called the medulla; it is composed of major ascending and descending tracts and a network of small nuclei involved in sleep, attention, muscle tone, cardiac function, and respiration.

The core network of nuclei is the reticular formation; the reticular formation also composes the core of the hindbrain and midbrain. It is thought to be an arousal system and is sometimes called the reticular activating system (reticulum means “little net”).

b. Metencephalon (see Figure 3.19 in Biopsychology) LO 3.12 List and describe the components of the metencephalon.

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The metencephalon has two parts: the cerebellum (little brain) and pons (bridge).

The cerebellum has both sensorimotor and cognitive functions. The pons is visible as a swelling on the inferior surface and also contains the reticular formation.

Neural tracts ascend and descend through this area.

c. Mesencephalon (see Figure 3.20 in Biopsychology) LO 3.13 List and describe the components of the mesencephalon.

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The mesencephalon is composed of the tectum and tegmentum.

In mammals, the tectum consists of the superior colliculi (visual relay) and the inferior colliculi (auditory relay); in lower vertebrates, there is simply a single optic tectum.

The tegmentum contains the reticular formation, the red nucleus (sensorimotor), the substantia nigra (sensorimotor cell bodies here die in patients with Parkinson’s disease); and the periaqueductal gray (mediates analgesia).

d. Diencephalon (see Figures 3.21 and 3.22 and Appendix V in Biopsychology) LO 3.14 List and describe the components of the diencephalon.

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The thalamus and hypothalamus are the two main structures of the diencephalon.

The thalamus is the top of the brain stem; it is comprised of many different nuclei, most of which project to the cortex.

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Biopsychology, Tenth Edition • • • • • •

Some thalamic nuclei are sensory relay nuclei (e.g., lateral geniculate nuclei, vision; medial geniculate nuclei, audition; ventral posterior nuclei, touch).

There exists a reciprocal connection between the thalamic nuclei and the neocortex (new cortex).

The above sensory relay nuclei are not one-way streets. They all receive feedback from the very areas of the cortex to which they project.

The hypothalamus is just below the thalamus (“hypo” means below) and the pituitary gland (snot gland) is suspended from the hypothalamus. Together, the hypothalamus and pituitary play key roles in endocrine function and many motivated behaviors.

The mammillary bodies are two small bumps visible on the inferior surface, just behind the hypothalamus.

The optic chiasm is the X-shaped part of the optic nerves that lies just in front of the pituitary; it is the spot where axons that originate from the nasal half of each retina cross over (decussate) to the opposite side of the brain.

e. Telencephalon (see Figures 3.23–3.25 in Biopsychology) LO 3.15 List and describe the components of the telencephalon.

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Also called the cerebral hemispheres; characterized by the cortex (bark) with its many convolutions, which are referred to as gyri (like hills) or fissures (like valleys).

The telencephalon is the largest division of human brain. Large tracts called commissures connect the two hemispheres and the corpus callosum is the largest commissure.

The telencephalon mediates most complex cognitive functions.

About 90% of human cortex is neocortex, comprised of six cell layers of pyramidal cells and stellate cells.

The hippocampus is not neocortex; instead, it is a three-layer cortical area that lies in the medial temporal lobe.

The four lobes of the cerebral hemispheres are defined by the fissures of the cerebral cortex.

The four lobes are: – frontal lobe: superior to lateral fissure and anterior to central fissure.

– temporal lobe: inferior to lateral fissure.

– parietal lobe: posterior to central fissure.

– occipital lobe: posterior to temporal lobe and to parietal lobe.

Note the following useful neocortical landmarks: longitudinal fissure (between the hemispheres), precentral gyri (in frontal lobe; primary motor cortex), postcentral gyri (in parietal lobe; primary somatosensory cortex), superior temporal gyri (in the temporal lobe, auditory cortex), and prefrontal cortex (the nonmotor portion of the frontal lobe)

f. Limbic System and the Basal Ganglia LO 3.16 List and describe the components of the limbic system and of the basal ganglia.

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Most of the subcortical parts of the telencephalon are axonal pathways; however, two subcortical systems exist that play important roles in determining our behavior. These are: – The Limbic System (see Figure 3.26 in Biopsychology): Involved in regulation of motivated behaviors (including the “Four F’s!”); includes the mammillary bodies, hippocampus, amygdala, fornix, cingulate cortex, and septum.

– The Basal Ganglia (see Figure 3.27 in Biopsychology): Involved in movement; include the amygdala (again); the caudate and putamen (collectively called the striatum), and the globus pallidus.

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Chapter 3: Anatomy of the Nervous System < Return to Table of Contents

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Biopsychology, Tenth Edition

LECTURE LAUNCHERS Lecture Launcher 3.1: Get Your Bearings: Relating the Nervous System to the Rest of the Body If you have such a model available, bring a rack-mounted skeleton to class and ask your students what such a bony artifact might tell them about neuroanatomy. If you have a model of the vertebral column with the spinal cord in situ, bring that along, too. During this discussion, note that the skeleton can be used to define the difference between the CNS and the PNS, between the brain and spinal cord, and between the somatic and autonomic nervous system. (Here you will have to ask them to visualize the internal organs, muscles, and skin of the skeleton.) Depending on the level of detail you would like to go into, you can have your students palpate landmarks on their own bodies that will help them get oriented (e.g., external occipital protuberance, spinous process of C-7 vertebrae, temporal bones of skull).

Lecture Launcher 3.2: The Latex Neuron To help students learn neuroanatomy, bring an elbow-length latex glove to class (or better yet, a box of latex gloves so you can hand out gloves to each of your students). Inflate the latex glove and then use it as a model to help students visualize different parts of the neuron. The latex represents the neural membrane, the fingers represent the dendrites, the palm represents the soma, the wrist represents the axon hillock, the arm represents the axon, and the open end of the glove represents the terminal buttons. If you want to be more detailed, throw a colored marble into the glove to represent the nucleus. Want something even trickier?

Add some packing popcorn, cut into small pieces, into the glove before you inflate it. Shake the chips to the end of the “axon,” then allow some air to escape the glove. The chips that blow out can represent neurotransmitter being released during exocytosis (though caution students that terminal buttons don’t actually “spit out” the transmitter).

Lecture Launcher 3.3: Name That Neuron Part Use the “Neural Structure Quiz” available from Dr. John Krantz at the University of Hanover. Go to http://psych.hanover.edu/ and place “Krantz Neuron” in the search box. Once there, page down to a link that will be labeled “Neural Structure Quiz” to begin the quiz on your own. Ask your class to identify the eight different parts of the neuron shown in the quiz. After each part is named, ask your students to assign a function to the named part. Using the neuron, you can also illustrate the general flow of neural information (somato-dendritic to terminal button) in the cell, preparing your students for material in the next chapter.

Lecture Launcher 3.4: Brain Games Here is a fun diversion you can use in class to test your students’ neuroanatomical proficiency—a brain anatomy matching game, at http://anatomyarcade.com/. On the left hand side of the page, click on the “nervous” link. At the top of the page will be a link for the Match-a-Brain game.

At some point in your class, ask for volunteers to come to the front of the class and take a turn at matching anatomical terms to the diagrams.

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Chapter 3: Anatomy of the Nervous System Lecture Launcher 3.5: Why Is It Important to Learn Biological Terminology?

Discuss the importance of consistency in communication across languages and specialties. This is why many Latin and Greek terms remain in the sciences.

Handouts 3.1 Concept Maps of the Nervous System 3.2 Vocabulary Crossword Puzzle 3.6 Learning Medical Terms Lecture Launcher 3.6: What Are the Roots of the Names of Biological Structures?

Most biological names are not random. They tell where the structure is located relative to other structures, what the structure looks like, and sometimes hints at the function of the structure.

Web Links 3.8 Medical Mnemonics 3.9 Medical Mnemonics.com Lecture Launcher 3.7: Brain Animations Brain animations are available from several Websites and in video format. There are also software packages that allow interaction with brain diagrams from various points of view.

The Secret Life of the Brain is a companion site to the PBS series revealing the fascinating processes involved in brain development across a lifetime.

Web Links 3.5 The Secret Life of the Brain 3.6 Movies Lecture Launcher 3.8: 3-D Diagrams and Models The textbook is flat, yet the structures that are studied are three-dimensional.

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Sometimes it is difficult to make the transition between a flat diagram and a diagram from another point of view or a three-dimensional model. The student may have not been taught this skill and some coaching at the beginning can make it easier for everyone in the class.

Making your own models, looking for animations that rotate brain diagrams or models, and looking at diagrams from different points of view, are all good ways to make sense out of the diagrams.

One way to make your own model is to go to one of the Websites that has photos of a brain, either stained and sliced, or from MRI images.

Print out the series of images. You can print them onto heavy paper such as card stock, or glue The sections to foam core or other stiff material.

You can also use multiple colors of clay or Play-Doh to represent the central nuclei, cortex, and brainstem.

Either stack the series or arrange them in a slotted piece of folded paper so that they form a “brain.”

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Biopsychology, Tenth Edition

ACTIVITIES Activity 3.1: Digital Anatomist There are many digital anatomy Websites such as (www9.biostr.washington.edu/). Click the button for the neuroanatomy atlas. Select a specific part or orientation of the brain and quiz students on the parts by point them out with your hand. You could form teams and have them compete or call up several student contestants to play the game against each other. If possible, have them compete for a small prize that you bring to class (e.g., a small model of the human brain).

Activity 3.2: Bring Real Nervous Systems to Class Get a Real Brain, (Whole or Sectioned) If your department does not have a human brain, the biology department may have one you can borrow.

Seeing a real human brain does a great deal to disabuse students of many misconceptions about the characteristics of the brain, such as size or color.

Contact local butchers or slaughterhouses and request fresh cow or sheep brains. This is effective in helping the students understand the fragile nature of nervous system structures that preserved tissue disguises.

Activity 3.3: Use Metaphors to Create Mental Models Slice Fruit Students may have a great deal of difficulty with the orientation terms. Getting them comfortable with these terms will pay off as they refer to brain areas later in the course.

Bring apples and knives to class. (You can draw a face on one side with a permanent marker if you wish.)

Have the students work in groups to divide their apples sagitally, frontally, or horizontally. Then have the groups share the different views discussing how the slices look with different orientations. If you have maintained reasonable cleanliness in this process, you can encourage the students to eat the sectioned apples.

Bring in a Jell-O Brain Molds for making brains from Jell-O are available from anatomical model companies and novelty catalogs.

One will make a model of the top of the two hemispheres and the other makes a sagittal view. With the proper Jell-O flavor and food coloring, the brain looks good from a distance. The softness of the Jell-O reminds the students that brains are not hard like the models or preserved brains. This helps them understand the potential for injury to the nervous system. After the lecture you can pass out plastic spoons and cups and share the brain with the class. (Brain molds are available from a variety of sources, including http://www.partycity.com/. Once on the Party City Website, just search for the “Brain Gelatin Mold” to get you to the page you need.

Activity 3.4: Diagrams of the Nervous System An important part of understanding the nervous system is to be able to look at a diagram, x-ray, or model, and identify a structure. This is made more complicated by the lack of differences in the look of nervous system tissue that has different functions.

Even looking at diagrams can be confusing because they can be from many different points of view and may not look like the diagrams in the text, models you have used in class, or even dissections of real brains.

This makes a good in-class activity done in small groups of two to five students.

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Chapter 3: Anatomy of the Nervous System 3.4 Diagrams of the Nervous System < Return to Table of Contents

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Biopsychology, Tenth Edition

DEMONSTRATIONS Demonstration 3.1: Nervous System Tissue Preserved and fresh nervous system tissue is a valuable teaching tool. Brains are available both preserved in formalin or sectioned and embedded in plastic.

You can also use fresh nervous system tissue from domestic animals. This is effective in helping the students understand the fragile nature of nervous system structures that preserved tissue disguises.

Demonstration 3.2: Bring Real Nervous Systems to Class In-class Dissection of the Sheep Brain Purchase two sheep brains. Using a brain knife, section one brain along the midsagittal plane and cut the other brain using a series of coronal sections. Label the prominent features of the gross anatomy of the sheep brain using paper labels and pins.

The brains are packed in formaldehyde: be sure to thoroughly wash the brains prior to use and use gloves during handling.

For a pictorial guide to sheep brain dissection, consult Cooley and Vanderwoolf (1990), A Brief Manual Sheep Brain Dissection: The Anatomy of Memory, which is available at the Exploratorium Site. Go to http://www.exploratorium.edu/ and place “Sheep brain dissection” in the search box. Click on the first link labeled “sheep brain dissection” to start your tutorial.

Brains (and many other demonstration preparations) can be ordered from: Carolina Biological Supply Company: http://www.carolina.com Ward’s Natural Science: http://wardsci.com/ The Sheep Brain: A Basic Guide, is available from: A.J. Kirby Co. 301 Oxford Street West Box 24107, London, Ontario , Canada N6A 3Y6 ajkirbyco@pobox.com http://www3.sympatico.ca/ajkirbyco/ ] The Sheep Brain: A Basic Guide, by Richard K. Cooley and C. H. Vanderwolf, is an excellent manual that is used in many student laboratories. Purchase preserved brains that are complete, including the meninges and cranial nerves.

Web Links 3.10 Atlas of the Sheep Brain Demonstration 3.3: A “Handy” Model of the Human Brain This metaphor can be used to assist students with the three-dimensional aspect of the brain. If you are short on models or real brains for examination, having a brain model “at hand” can be very “handy.”

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Chapter 3: Anatomy of the Nervous System

ASSIGNMENTS Assignment 3.1: Vocabulary Crossword Puzzle This is one of the most vocabulary-rich chapters in your text, as well as within the discipline as a whole.

This can be a challenge.

Part of the assignment will require that the student knows the terminology used in describing the nervous system. I have created a crossword puzzle for this assignment. Crosswords provide cues in the length of the words and in letters determined from easier clues.

This can be used as an assignment, a test, or an in-class activity done in small groups of two to five students.

ANSWERS: ACROSS 1. SPINAL_CORD - Rope-like structure carrying information from the brain to the body 3. SUBSTANTIA_NIGRA - Name means “black stuff” 5. MEDULLA - You would have trouble breathing after damage to this area 6. CORTEX - Outer layers of brain or adrenal glands 9. PARIETAL - Lobe of cortex behind the central sulcus 10. LIMBIC - “System” involved in emotions 11. SENSORYMOTOR - Part of the nervous system responsible for sensory and motor functions 13. FRONTAL - Area of cortex responsible for decision making 14. SOMATOSENSORY - Area of cortex in the parietal lobe responsible for information from skin, muscles, and tendons 15. PARASYMPATHETIC - Digestion is controlled by this part of the peripheral nervous system DOWN 2. CORPUS_CALLOSUM - Contains fibers that connect the two halves of the cerebellum 4. TEMPORAL - Name of this area of cortex may remind you of a religious building 7. HIPPOCAMPUS - Involved in memory and part of the limbic system 8. STRIATUM - Striped part of the basal ganglia 12. AUTONOMIC - Part of peripheral nervous system that reacts “automatically Assignment 3.2: Labeling Diagrams of the Nervous System This handout provides a series of diagrams of nervous system structures to label. Some are very detailed and some are rough sketches. The student must look at the diagram carefully and determine if there are structures that he or she recognizes. From these it is possible to find and label other structures. This can be an in-class assignment done in groups.

Handout 3.4 Diagrams of the Nervous System

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Biopsychology, Tenth Edition Assignment 3.3: Fill in the Nervous System A hierarchical diagram provides spaces for the various parts of the nervous system. A few items are filled in for guidance.

Handout 3.5 Organizational Chart: Structure of the Nervous System < Return to Table of Contents

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Chapter 3: Anatomy of the Nervous System

WEB LINKS Web Link 3.1: Gray’s Anatomy

Go to http://www.bartleby.com/ and use the left search bar to select Gray’s Anatomy. In the search bar located on the right of the homepage, search for “neurology structure.” Click on the first link titled “IX. Neurology. 1. Structure of the Nervous System.” Gray’s Anatomy is available both in print and online. A classic text with many black and white illustrations of structures and cell types.

Makes an adequate coloring book.

Web Link 3.2: Nervous System

Go to http://www.kumc.edu/ and place “nervous system” in the search bar at the top of the page.

Select the first result titled “nervous system.”

Copyright © 1996, University of Kansas Medical Center. This document has pictures taken under a microscope of details of the nervous system structures. It is in more detail than you need but you might find it interesting.

Web Link 3.3: The Comparative Mammalian Brain Collections

http://brainmuseum.org/The Comparative Mammalian Brain Collections is a good source for images of sectioned brains.

Web Link 3.4: The Whole Brain Atlas

Place “The Whole Brain Atlas” in your search engine and click on the link associated with Harvard Medical School.

Web Link 3.5: The Secret Life of the Brain

Place “Secret Life of the Brain” in your search engine. Select the clickable link for http://www.pbs.org. The Secret Life of the Brain is a companion site to the PBS series revealing the fascinating processes involved in brain development across a lifetime. If you have Macromedia Flash installed, you can see a 3D brain model and rotate it.

Web Link 3.6: Movies

Go to http://hendrix.imm.dtu.dk/and click on the “movies” link. This site has movies illustrating brain structures and activation.

Web Link 3.7: Brain Model Tutorial

Go to http://www.ucf.edu and type “brain tutorial” into the search bar. Click on the link titled “brain model tutorial” to go to the site where you can search for many images of the whole brain.

The brain stem section is particularly useful, as it is unusual. There is also a set of images that you might find useful that includes diagrams, MRI, and brain sections, etc.

Web Link 3.8: Medical Mnemonics.com

http://www.medicalmnemonics.com/ Download a database for your PDA with Palm OS or download a PDF file of the mnemonics.

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Biopsychology, Tenth Edition Web Link 3.9 Atlas of the Sheep Brain

Go to http://www.msu.edu/ and place “sheep brain atlas” in the search bar. Click on the matching link.

Web Link 3.10 Brain Development

Go to http://www.brainfacts.org/ and click on the “Brain Basics” tab at the top of the page. Click the secondary link labeled “Brain Development” to get to the page you need.

A brief overview of brain development from the Brain Facts.org sponsored by the Society for Neuroscience.

Web Link 3.11 Brain Development

Go to http://faculty.washington.edu/ and place “Neuroscience for Kids Brain Development” in the search bar on the main page. Click on the first link about brain development.

Although this page is titled “Neuroscience for Kids,” it is a great and accessible overview of brain development. < Return to Table of Contents

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Chapter 3: Anatomy of the Nervous System

HANDOUT DESCRIPTIONS Handout 3.1: Concept Maps of the Nervous System You may find these concept maps a useful way to help students organize the terms that they are learning.

Handout 3.2: Vocabulary Crossword Puzzle Handout 3.3: A “Handy” Model of the Human Brain This metaphor can be used to assist students with the three-dimensional aspect of the brain. If you are short on models or real brains for examination, having a brain model “at hand” can be very “handy.”

Handout 3.4: Diagrams of the Nervous System This handout provides a series of diagrams of nervous system structures to label. Some are very detailed and some are rough sketches. The student must look at the diagram carefully and determine if there are structures that he or she recognizes. From these, it is possible to find and label other structures.

Handout 3.5: Organizational Chart: Structure of the Nervous System This Assignment Sheet provides the structure for a hierarchical map of the nervous system. It is a good way for students to test their understanding of relationships in the nervous system There are several correct versions, so try not to just give one set of correct answers for grades.

Handout 3.6: Learning Medical Terms A handout of medical terminology. < Return to Table of Contents

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HANDOUTS Handout 3.1 Concept Maps of the Nervous System

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Commented [LL1]: Above on the right-hand side is “Cerebran Aqueduct”, it should read “Cerebral Aqueduct.”

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Chapter 3: Anatomy of the Nervous System Handout 3.2: Vocabulary Crossword Puzzle Name: Section: Date: The Nervous System

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Biopsychology, Tenth Edition Across 1. Rope-like structure carrying information from the brain to the body 3. Name means “black stuff” 5. You would have trouble breathing after damage to this area 6. Outer layers of brain or adrenal glands 9. Lobe of cortex behind the central sulcus 10. “System” involved in emotions 11. Part of the nervous system responsible for sensory and motor functions 13. Area of cortex responsible for decision making 14. Area of cortex in the parietal lobe responsible for information from skin, muscles, and tendons.

15. Digestion is controlled by this part of the peripheral nervous system Down 2. Contains fibers that connect the two halves of the cerebellum 4. Name of this area of cortex may remind you of a religious building 7. Involved in memory and part of the limbic system 8. Striped part of the basal ganglia 12. Part of peripheral nervous system that reacts “automatically” Puzzle created with Puzzlemaker at DiscoverySchool.com.

< Return to Table of Contents

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Chapter 3: Anatomy of the Nervous System Handout 3.3: A Handy Model of the Human Brain Sometimes it is difficult to remember the major structures of the human brain and to understand their threedimensional relationship. Here are some ideas that might be helpful to you in your studies.

Mnemonic Devices Mnemonic devices have traditionally been the most effective tool for a student trying to put unfamiliar information into memory. Mnemonic devices build associations between the familiar and the new. These associations can then be used to cue memory.

Did your father always know when you were up to some type of mischief? Did he appear to have “eyes in the back of his head”? In one way, he did. The cortical area responsible for vision is at the back of the brain.

In Ancient Greece, the priestesses, called Oracles, would hear voices giving them important information about people and events. Most of the Oracles lived (or worked) in a temple. Under your temples (at the side of your head, under the temple of your glasses) is the temporal lobe. This part of the brain has cortex responsible for audition (or hearing).

Here is another mnemonic device to assist you in remembering the location of brain structures.

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Biopsychology, Tenth Edition A Brain Model The Two Hemispheres

First, imagine that each of your hands represents one of the two hemispheres of your brain. Fold your hands into fists and hold your hands in front of you with the thumbs on the outside. The place where your hands touch represents the corpus callosum, where the two halves of the brain are connected.

The right hand represents the left hemisphere and the left hand represents the right hemisphere.

This will help you to remember that the opposite side of the brain controls the movement and sensation from the body. The neurons cross at a level in the brain stem represented by your wrists.

This is called the decussation (or crossing) of the pyramids.

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Chapter 3: Anatomy of the Nervous System Why did you curl your hands into a fist?

Some of the structures inside the skull of a human being are curved in a “C” shape. This probably evolved through preference for infants with smaller skulls who still had the same density of neurons to support future learning. (Ask any mother if a small skull at birth is a good idea.) The more surface area a brain has on the cortex, or skin of the brain, the more neurons it can support. The C-shape of the cortex makes more surface area. So does the wrinkled surface of the brain.

The cortex has many wrinkles. The high part of each wrinkle is called a gyrus. The valley between two wrinkles is called a sulcus. If the valley is deep and long and divides major areas of the cortex, it may be called a fissure.

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Biopsychology, Tenth Edition Different areas on the skin of your hand can represent the different lobes of the cortex.

The fingers represent the Frontal Lobe. This part of the cortex is involved in complex thought and problem solving as well as emotional control.

The area at base of the fingers that is still within the frontal lobe represents that motor cortex. This area is responsible for voluntary movement below the neck.

The thumb represents the Temporal Lobe. Like the thumb, this area can be lifted away from the rest of the hand/brain, though it remains attached at the base, part of the C-shaped curve of the structures. This area has cells responsible for hearing and taste.

At the back of the hand is an area that represents the Occipital Lobe. The occipital lobe is responsible for basic vision.

The area remaining, the Parietal Lobe, appears to have cells responsible for complex relationships between other areas.

Underneath the occipital lobe at the back of the brain, is the Cerebellum, or little brain. (The large, mainbrain is referred to as the cerebrum.) You might imagine it as a bracelet around your wrist. The top of the bracelet is very detailed. The band going around your wrist can represent the fibers of the neurons in the cerebellum connecting the two hemispheres of the cerebellum at the front of the brain stem in two lumps called the Pons. < Return to Table of Contents

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Chapter 3: Anatomy of the Nervous System Handout 3.4: Diagrams of the Nervous System Name: Section: Date: An important part of understanding the nervous system is to be able to look at a diagram, x-ray, or model, and find a structure. This is made more complicated by the lack of differences in the look of nervous system tissue with different functions.

Even looking at diagrams can be confusing because they are from different points of view and may not look like the diagrams in the text, models you have used in class, or even dissections of real brains.

I will give you a series of diagrams of the nervous system to label. Some will be very detailed and some are rough sketches. You will need to look at the diagram carefully and determine if there are structures that you recognize. From these you can find and label other structures.

__ __ __ __ __ __ View

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__ __ __ __ __ __ View

__ __ __ __ __ __ View

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__ __ __ __ __ __ __ View

__ __ __ __ __ __ __ __ __ __ Nervous System

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Biopsychology, Tenth Edition Handout 3.5: Structure of the Nervous System Name: Section: Date:

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< Return to Table of Contents

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Chapter 3: Anatomy of the Nervous System Handout 3.6: Learning Medical Terms Capit – head Cephalo – head Cerebello – cerebellum (part of brain); “small brain” Cerebro – cerebrum (part of brain) Cranio – head Encephalo – brain Neuro – nerve

Cardi or cardio – heart

Glosso – tongue Laryngo – larynx Linguo – tongue Stoma – mouth Os – bone; or mouth

Arthro – joint Carpo – wrist Genu – knee (Latin) Osteo – bone

Naso – nose Rhino – nose

Orchio, orchido – testis Ovario – ovary

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Meningo – meninges (coverings of the brain and spinal cord) Derma – skin Pilo – hair Cilia – hair (Latin) Fibro – fibers

Ped – foot

Adeno – gland Adreno – adrenal gland

Myelo – bone marrow and spinal cord (Note: The use of this term will determine which tissue is meant.)

Myo – muscle (Note: The Latin word for muscle is mus.)

Chordo or Cordo – cord or string

Oto – ear

Oculo – eye

Hippo – horse; hippocampus (seahorse-shaped)

< Return to Table of Contents

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4 Neural Conduction and Synaptic Transmission: How Neurons Send and Receive Signals TABLE OF CONTENTS Chapter-at-a-Glance

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Learning Objectives

3

Brief Chapter Outline

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Teaching Outline

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Lecture Launchers

12

Activities

13

Web Links

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Chapter 4: Neural Conduction and Synaptic Transmission

CHAPTER-AT-A-GLANCE Brief Outline Chapter Introduction (p. 78) 4.1 Resting Membrane Potential (pp. 79–80) 4.2 Generation, Conduction, and Integration of Postsynaptic Potentials (pp. 80–84) 4.3 Conduction of Action Potentials (pp. 84–87) 4.4 Synaptic Transmission: Chemical Transmission of Signals among Neurons (pp. 87–94) 4.5 Neurotransmitters (pp. 94–97) 4.6 Pharmacology of Synaptic Transmission and Behavior (pp. 97– 100)

Instructor’s Manual Resources Lecture Launcher 4.1 Lecture Launcher 4.2 Lecture Launcher 4.3 Activity 4.1 Activity 4.2

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LEARNING OBJECTIVES After completion of this chapter, the student should be able to: LO 4.1 Describe how the membrane potential is recorded.

LO 4.2 Describe the resting membrane potential and its ionic basis, and describe the three factors that influence the distribution of Na+ and K+ ions across the neural membrane.

LO 4.3 Know the types of postsynaptic potentials and how they are conducted.

LO 4.4 Describe how postsynaptic potentials summate, and how action potentials are generated.

LO 4.5 Explain the ionic basis of an action potential.

LO 4.6 Explain how the refractory period is responsible for two important characteristics of neural activity.

LO 4.7 Describe how action potentials are conducted along axons—both myelinated and unmyelinated.

LO 4.8 Explain the shortcomings of the Hodgkin-Huxley model when applied to neurons in the mammalian brain.

LO 4.9 Describe the structure of different types of synapses.

LO 4.10 Describe how neurotransmitter molecules are synthesized and packaged in vesicles.

LO 4.11 Explain the process of neurotransmitter exocytosis.

LO 4.12 Describe the differences between ionotropic and metabotropic receptors.

LO 4.13 Explain how neurotransmitters are removed from a synapse.

LO 4.14 Describe the role of glia and gap junctions in synaptic transmission.

LO 4.15 Name the classes of neurotransmitters.

LO 4.16 Name and compare the different neurotransmitters.

LO 4.17 Provide a general overview of how drugs influence synaptic transmission.

LO 4.18 Describe three examples of how drugs have been used to influence neurotransmission. < Return to Table of Contents

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Chapter 4: Neural Conduction and Synaptic Transmission

BRIEF CHAPTER OUTLINE Lecture Launcher 4.1: Electrophysiology and Techniques for Cell Identification 1. Resting Membrane Potential a. Recording the Membrane Potential b. Ionic Basis of the Resting Potential Lecture Launcher 4.2: Passive and Active Transport across the Neural Membrane 2. Generation, Conduction, and Integration of Postsynaptic Potentials a. Generation and Conduction of Postsynaptic Potentials b. Integration of Postsynaptic Potentials and Generation of Action Potentials Lecture Launcher 4.3: Listening to Action Potentials Activity 4.1: Modeling the Benefits of Saltatory Conduction 3. Conduction of Action Potentials a. Ionic Basis of Action Potentials b. Refractory Periods c. Axonal Conduction of Action Potentials d. The Hodgkin-Huxley Model in Perspective Activity 4.2: Modeling Electrical and Chemical Signaling in Neurons Activity 4.3: Three Colossal Neurons 4. Synaptic Transmission: Chemical Transmission of Signals among Neurons a. Structure of Synapses b. Synthesis, Packing, and Transport of Neurotransmitter Molecules c. Release of Neurotransmitter Molecules d. Activation of Receptors by Neurotransmitter Molecules e. Reuptake, Enzymatic Degradation, and Recycling f. Glia, Gap Junctions, and Synaptic Transmission 5. Neurotransmitters a. Overview of the Transmitter Classes b. The Roles and Functions of Neurotransmitters 6. Pharmacology of Synaptic Transmission and Behavior a. How Drugs Influence Synaptic Transmission b. Behavioral Pharmacology: Three Influential Lines of Research < Return to Table of Contents

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TEACHING OUTLINE 1. Resting Membrane Potential a. Recording the Membrane Potential LO 4.1 Describe how the membrane potential is recorded.

• • • •

To learn how information is sent from the dendrites and soma of a neuron to its terminals, researchers study a neuron’s membrane potential (the difference in electrical charge between the inside and the outside of the neuron).

To record a membrane potential, two electrodes are needed: an intracellular electrode and an extracellular electrode.

Intracellular electrodes must be microelectrodes; they are usually made from saline-filled micropipettes by heating and pulling apart a fine glass tube with an electrode puller.

When intracellular and extracellular electrodes are outside a neuron, the difference between the electrical potentials at their tips is zero; when the intracellular electrode penetrates the neuron, the potential jumps to about -70 millivolts (the inside is 70 millivolts less than the outside). This is the resting potential of the neuron.

b. The Ionic Basis of the Resting Membrane Potential (see Figure 4.1 in Biopsychology) LO 4.2 Describe the resting membrane potential and the ionic basis, and describe the three factors that influence the distribution of Na+ and K+ ions across the neural membrane.

•

• •

• • • • • •

The resting potential exists because positively and negatively charged ions are distributed unequally on the two sides of the neural membrane: The concentration of Na+ is higher outside the neuron, and the concentration of K+ is higher inside the neuron.

Ions in solution are in random motion.

Thus, any time there is an accumulation of a particular class of ions in one area, the probability is increased that random motion will move ions out of this area (because there are more ions available to leave) and the probability is decreased that random motion will move more ions into this area (because there are fewer ions available to come in).

Like charges repel and opposite charges attract; therefore, electrostatic pressure disperses any accumulation of positive or negative charges in an area.

Ions pass through the cell membrane at special pores called ion channels.

When neurons are at rest, the membrane is resistant to the passage of Na + ions and only slightly resistant to the passage of K+ ions.

In 1950, neurophysiologists Hodgkin and Huxley provided the first evidence that an energyconsuming process is involved in the resting potential.

Active mechanisms in the neural membrane continuously transfer Na+ ions out of the neuron and K+ ions in.

This occurs at a ratio of three Na+ ions moved out for every two K+ ions moved in; thus, there is a loss of one positive charge every time the pump is activated.

2. Generation, Conduction, and Integration of Postsynaptic Potentials (see Figure 4.2 in Biopsychology) a. Generation and Conduction of Postsynaptic Potentials LO 4.3 Know the types of postsynaptic potentials and how they are conducted.

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• • • • •

Now that you understand the state of resting neurons, let’s see how electrical signals are created in a resting neuron.

Postsynaptic potentials are changes in the membrane potential produced by the action of neurotransmitters released by presynaptic neurons.

Excitatory postsynaptic potentials (EPSPs) are depolarizations; they increase the likelihood that a neuron will fire.

Inhibitory postsynaptic potentials (IPSPs) are hyperpolarizations; they decrease the likelihood that a neuron will fire.

Postsynaptic potentials have three important properties: – They are graded: Their amplitude is proportional to the intensity of the input; that is, stronger stimuli produce bigger EPSPs and IPSPs. – They are transmitted decrementally: As they passively spread from their site of generation, they get weaker as they go, like sound through air.

– They are transmitted rapidly: Like electricity through a cable, so rapidly that transmission is usually regarded as being instantaneous.

b. Integration of Postsynaptic Potentials and Generation of Action Potentials (see Figures 4.3– 4.4 in Biopsychology) LO 4.4 Describe how postsynaptic potentials summate, and how action potentials are generated.

• • • • •

•

Action potentials (APs; neuron firing) are triggered at the axon initial segment, which is immediately adjacent to the conical axon hillock.

An AP occurs when a neuron is depolarized to the point that the membrane potential at the axon hillock reaches about -70 mV—the threshold of excitation for many neurons.

Unlike EPSPs and IPSPs, APs are not graded; they are all-or-none (full-blown or not at all).

Most neurons receive hundreds of synaptic contacts—what happens at any one synapse has very little effect on the firing of the neuron. Whether or not a neuron fires is determined by the integration of what goes on at many neurons.

There are two kinds of neural integration: – Spatial summation, which can involve two or more EPSPs, two or more IPSPs, or both EPSPs and IPSPs. – Temporal summation, which can involve two or more EPSPs or two or more IPSPs. EPSPs and IPSPs cannot temporally summate due to the fact that just a single synapse is involved, and it must be either excitatory or inhibitory, but not both.

In a functioning neuron, spatial, and temporal summation go on continuously; synapses closer to the axon trigger zone often have a larger effect on firing due to the decremental transmission of postsynaptic potentials, although some neurons can amplify distal PSPs so that they are the same size when they reach the soma.

3. Conduction of Action Potentials (see Figure 4.5 in Biopsychology) a. Ionic Basis of Action Potentials LO 4.5 Explain the ionic basis of an action potential.

•

When the threshold of excitation (about -70mV) is reached, voltage-gated Na+ channels open momentarily, and Na+ ions rush into the neuron under tremendous pressure from their

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•

•

concentration and electrostatic gradients. This drives the membrane potential to about +50 millivolts.

At the same time, voltage-gated K+ channels slowly begin to open. Most of these channels open at about the time that the membrane potential is about +50 mV. At this point, K + ions are driven out by the +50 millivolt charge and their high internal concentration; this repolarizes the neuron and leaves it slightly hyperpolarized for a few milliseconds.

Because only a few ions adjacent to the membrane are involved in the generation of an action potential, the resting potential is readily reestablished by the random motion of ions (not the Na+/K+ pump).

b. Refractory Periods LO 4.6 Explain how the refractory period is responsible for two important characteristics of neural activity.

•

For one to two milliseconds after the generation of an action potential, another action potential cannot be generated no matter what kind of input the neuron receives; this time period is called the absolute refractory period. This period is followed by the relative refractory period, during which an action potential can only be elicited by high levels of stimulation.

c. Axonal Conduction of Action Potentials LO 4.7 Describe how action potentials are conducted along axons—both myelinated and unmyelinated.

• •

• • •

Once an AP is generated at the axon initial segment, it is transmitted along the axon; the purpose of axons is to transmit APs from the soma to the terminal buttons of the neuron.

Conduction of APs along an axon is not like the transmission of PSPs: Conduction of EPSPs and IPSPs is passive (like electricity through a cable); thus, it is instantaneous and decremental, whereas conduction of an AP along an axon is active, and therefore slower and nondecremental.

When voltage-gated Na+ channels on the hillock membrane open, Na+ ions rush in and a full-blown AP is generated.

The electrical disturbance that is created is transmitted passively to the next Na+ channels along the axon; in response, the voltage-gated Na+ channels there open and another fullblown potential is generated.

In reality, the sodium channels are so tightly packed that it is best to think of APs as waves of depolarization spreading down an axon; the AP is regenerated along the length of the axon.

– APs also spread from the hillock back through the cell body and dendrites. Little is currently known about the functions of these potentials.

– Transmission in the normal direction, from the hillock to the terminal buttons, is called orthodromic conduction; however, if the terminals are electrically stimulated, APs can be generated and actively transmitted back to the hillock. This is called antidromic conduction.

i. Conduction in Myelinated Axons • Many axons are myelinated by glia cells. Myelination insulates the semipermeable axon membrane, blocking the flow of ions through the axon at all but the nodes of Ranvier; paradoxically, this actually improves transmission.

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In myelinated axons, APs travel passively (decrementally and rapidly) between the nodes of Ranvier; but at each node, there is a “pause” while a full-blown AP is generated.

This is called saltatory conduction (“saltatory” means to skip or jump)—because much of the transmission of APs in myelinated axons is passive (from node to node), transmission in myelinated axons is faster and it requires less energy.

ii. The Velocity of Axonal Conduction • Larger axons conduct faster; myelinated axons conduct faster. iii. Conduction in Neurons Without Axons • Many interneurons do not have axons and their transmission is decremental. d. The Hodgkin-Huxley Model in Perspective LO 4.8 Explain the shortcomings of the Hodgkin-Huxley model when applied to neurons in the mammalian brain.

•

The traditional Hodgkin-Huxley model is too simplistic to fully represent neural conduction in the mammalian brain. The original model does not account for the following: o Many neurons fire APs in the absence of input or do not fire APs at all. o APs vary in terms of amplitude, duration, and frequency. o Dendritic function is more complex than previously believed; for example, dendrites appear to be able to actively conduct action potentials.

4. Synaptic Transmission: Chemical Transmission of Signals Among Neurons (see Figures 4.6–4.8 in Biopsychology) a. Structure of Synapses LO 4.9 Describe the structure of different types of synapses.

• • • • • •

Some synapses occur on little buds on dendrites; these buds are called dendritic spines.

Other dendritic synapses occur right on the dendrite shaft.

In addition to axosomatic and axodendritic synapses, there are: (1) axoaxonic synapses, (2) dendrodendritic synapses, (3) dendroaxonic synapses, (4) synapses between the main shafts of axons, and (5) nondirected synapses.

Some dendrodendritic synapses can transmit in either direction.

Axoaxonic synapses mediate presynaptic inhibition; postsynaptic inhibition is mediated by axodendritic and axosomatic synapses.

Most synapses that are discussed in textbooks are directed synapses (synapses where the site of release and the target site are in close apposition).

There are also nondirected synapses: for example, some presynaptic axons have a string-ofbeads appearance and the neurotransmitter is widely dispersed from each bead to many targets in the general area. This arrangement is common for monoamine neurotransmitters.

b. Synthesis, Packing, and Transport of Neurotransmitter Molecules LO 4.10 Describe how neurotransmitter molecules are synthesized and packaged in vesicles.

•

There are two main types of neurotransmitters: small-molecule transmitters, synthesized in the cytoplasm and packed into vesicles by the Golgi complex; and large-molecule

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transmitters, synthesized in the soma by ribosomes and then moved down to the terminals by microtubules.

There can be small- and large-molecule transmitters in the same terminal button; this is called coexistence.

c. Release of Neurotransmitter Molecules (see Figure 4.9 in Biopsychology) LO 4.11 Explain the process of neurotransmitter exocytosis.

• • • •

The arrival of an AP at a terminal button opens voltage-gated calcium channels in the button membrane and Ca++ ions enter the button.

The entry of the Ca++ ions causes the synaptic vesicles to fuse with the presynaptic membrane and empty their contents into the synaptic cleft—a process called exocytosis.

Small-molecule transmitters are usually released each time an action potential arrives at the terminal; by contrast, large-molecule transmitters are released gradually in response to multiple action potentials.

Most documented cases of coexistence have involved one small-molecule neurotransmitter and one neuropeptide, although coexistence of two small-molecule neurotransmitters has also been noted.

d. Activation of Receptors by Neurotransmitter Molecules (see Figure 4.10 in Biopsychology) LO 4.12 Describe the differences between ionotropic and metabotropic receptors.

• •

After its release, neurotransmitters diffuse across the synaptic cleft to the post-synaptic membrane; there it binds to receptors in the postsynaptic membrane. There are specific receptors for each neurotransmitter.

The binding of the neurotransmitter to its receptors can influence the postsynaptic neuron in one of two fundamentally different ways: – It can act at an ionotropic receptor directly associated with a channel in the postsynaptic membrane and induce brief EPSPs or IPSPs. – It can act at a metabotropic receptor associated with a signal protein that is attached to a G-protein inside the neuron. This G-protein can either move to a nearby ion channel, activate it and cause a change in the membrane potential, or it can lead to the production of chemicals, called second messengers, that can have more enduring and far-reaching effects on the sensitivity of the neuron.

– One type of metabotropic receptor is the autoreceptor. Found in the presynaptic membranes; these are stimulated by the neuron’s own neurotransmitter and are thought to mediate negative feedback.

e. Reuptake, Enzymatic Degradation, and Recycling (see Figure 4.11 in Biopsychology) LO 4.13 Explain how neurotransmitters are removed from a synapse.

Neurotransmitters are deactivated in the synapse by one of two mechanisms: • Some neurotransmitters are broken down in the synapse by enzymes.

• Other neurotransmitters are deactivated by reuptake into the presynaptic neuron, where they are recycled. f. Glia, Gap Junctions, and Synaptic Transmission (see Figure 4.12 in Biopsychology) LO 4.14 Describe the roles of glia and gap junctions in synaptic transmission.

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5.

Gap junctions are narrow spaces between adjacent neurons that are bridged by fine tubular channels that contain cytoplasm.

Therefore, the cytoplasm is continuous, allowing electrical signals and small molecules to pass from one neuron to the next (sometimes they are called electrical synapses).

These gap junctions allow direct communication between two or more neurons in the nervous system; these types of connections seem to be an integral feature of local inhibitory circuits.

Gap junctions can also form between glial cells, or between glia and neurons.

The existence of gap junctions between pre- and postsynaptic neurons and adjacent astrocytes can form tripartite synapses, allowing astrocytes to synchronize activity between groups of neurons.

Neurotransmitters (see Figures 4.14–4.16 in Biopsychology) a. Overview of the Neurotransmitter Classes LO 4.15 Name the classes of neurotransmitters.

•

There are three classes of conventional small-molecule neurotransmitters: the amino acids, the monoamines, and acetylcholine.

b. The Roles and Functions of Neurotransmitters LO 4.16 Name and compare different neurotransmitters.

Amino Acid Neurotransmitters • Amino acids are the individual building blocks of proteins; they also serve as the transmitters at fast-acting, point-to-point synapses.

• There is conclusive evidence that glutamate, aspartate, glycine, and gamma-aminobutyric acid (GABA) are neurotransmitters.

• Glutamate, aspartate, and glycine come from the proteins that we eat; GABA is synthesized from glutamate.

Monoamine Neurotransmitters • Monoamine neurotransmitters are formed by slight modifications to amino acid molecules; thus the name “monoamine” (one amine).

• They are often released from string-of-beads-type axons and they have slow, lingering, and diffuse effects; neurons that release monoamines typically have their cell bodies in the brain stem.

• There are four monoamine neurotransmitters and they belong to one of two subclasses: − catecholamine neurotransmitters: these include dopamine, norepinephrine, and epinephrine; all three are synthesized from the amino acid tyrosine and tyrosine is converted to L-DOPA, to dopamine, to norepinephrine, to epinephrine. − indolamine neurotransmitter: serotonin; synthesized from the amino acid tryptophan.

Acetylcholine • Acetylcholine (ACh) is a small molecule transmitter at neuromuscular junctions, many synapses in the ANS, and at some CNS synapses; it is created by the addition of an acetyl group to a choline molecule.

• Acetylcholine is the only neurotransmitter known to be deactivated in the synapse by enzymatic degradation rather than by reuptake; it is deactivated by acetylcholinesterase.

Unconventional Neurotransmitters • The soluble gas neurotransmitters include nitric oxide and carbon monoxide.

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The gasses are produced in the neural cytoplasm and diffuse immediately through the cell membrane into the extracellular fluid and into nearby cells to stimulate production of second messengers.

They are difficult to study as they act rapidly and are immediately broken down, existing for only a few seconds.

Anandamide is an inhibitory endocannabinoid (marijuana-like) neurotransmitter that is released from dendrites and cell bodies.

Neuropeptide Transmitters • Peptides are short chains of 10 or fewer amino acids. Over 50 peptides are putative neurotransmitters; they are the largest neurotransmitters.

• There are 5 categories of neuropeptides with widely varied functions.

• Endorphins are an example of a neuropeptide transmitter; they are opiate-like transmitters that are important for analgesia and in the reward systems of the brain.

6. Pharmacology of Synaptic Transmission and Behavior (see Figures 4.17–4.18 in Biopsychology) • Drugs that facilitate a transmitter’s effects are called agonists; drugs that reduce a transmitter’s effects are called antagonists. a. How Drugs Influence Synaptic Transmission LO 4.17 Provide a general overview of how drugs influence synaptic transmission.

• •

Drugs act upon one or more of the seven steps in neurotransmitter action; the exact mechanism varies from one drug to another.

Atropine and curare are ACh antagonists; atropine blocks muscarinic receptors, whereas curare paralyzes by blocking nicotinic receptors.

b. Behavioral Pharmacology: Three Influential Lines of Research LO 4.18 Describe three examples of how drugs have been used to influence neurotransmission.

Wrinkles and Darts: Discovery of Receptor Subtypes • Acetylcholine binds to two main types of receptors: nicotinic and muscarinic.

• The two receptor types have a different distribution in the nervous system and interact with different drugs.

• Atropine is a muscarinic antagonist. Curare and botox are nicotinic antagonists.

Pleasure and Pain: Discovery of Endogenous Opioids • The drug morphine binds to endogenous opioid receptors in the brain.

Tremors and Mental Illness: Discovery of antischizophrenic drugs • The first two drugs that effectively treated some symptoms of schizophrenia were later found to be dopamine D2 receptor antagonists. < Return to Table of Contents

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Chapter 4: Neural Conduction and Synaptic Transmission

LECTURE LAUNCHERS Lecture Launcher 4.1: Electrophysiology and Techniques for Cell Identification Use the virtual lab from the Howard Hughes Medical Institute to demonstrate the technique of intracellular recordings and the measurement of membrane potentials to your students. Go to http://www.hhmi.org and place “neurophysiology virtual lab” in the search box. Click on the link that shares that name. In a small class, ask one or more students to perform the activities in the virtual lab. In a bigger class, you can demonstrate, narrating while you go along. To save time, have your “leech” dissected before class starts; then you can demonstrate the intracellular recording, response testing, dye injection, and cell identification immediately.

Lecture Launcher 4.2: Passive and Active Transport across the Neural Membrane Students in an Introductory Biopsychology class often have problems recognizing the differences between passive and active transport of ions across the cell membrane. To access an excellent series of animations that illustrates the differences between passive and active transport across the neural membrane, go to http://www.hhmi.org/ and place “diffusion across membranes” in the search box. Click on the link that shares that name when it comes up from your search.

Using this animation, you can illustrate the differences in ATP utilization during active versus passive transport, facilitated diffusion, and the effects of equilibrium on movement of ions.

Lecture Launcher 4.3: Listening to Action Potentials “Hearing” an action potential can help students appreciate their temporal dynamics. Play the two auditory recordings of action potentials that can be found by going to http://www.faculty.washington.edu and place “sounds of neuroscience” in the search bar. Click on the link that states “Neuroscience for Kids-Sounds of Neuroscience.” < Return to Table of Contents

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Biopsychology, Tenth Edition

ACTIVITIES Activity 4.1: Modeling the Benefits of Saltatory Conduction To demonstrate the increased rate of conduction gained by axonal myelination and saltatory conduction of the action potential, ask 10 students to come to the front of the class and form two lines (five students in each line) that will represent the axons of two different neurons. Separate each student in a line by about 10 feet.

Give the first student in each line a ball; this ball represents the action potential (and the first student in line represents the axon hillock). The task of each line (axon) is to pass the ball to the next person in line, until it reaches the last person in line (i.e., to conduct the action potential the length of the axon to the “terminal button”). Students in Line A will represent an unmyelinated axon; they have to walk the ball to the next person in line before passing it to them. Students in Line B will represent a myelinated axon; they can throw the ball to one another (representing saltatory conduction between each node of Ranvier).

Unless it is full of butterfingers, the “action potential” should move much faster, and with less expenditure of energy, in Line B than in Line A—illustrating the two key benefits of saltatory conduction!

Activity 4.2: Modeling Electrical and Chemical Signaling in Neurons To demonstrate some of the characteristics of electrical and chemical signaling, ask two groups of five students each to come to the front of the classroom and form two lines, with each person separated by one arm length. One line should be on the left side of the classroom and the other on the right. Have the lines separated by 10 feet. The left-most person in each line represents the somatodendritic region of a neuron, the right-most person in each line represents the terminal buttons of a neuron, and the people in the middle represent the axon of that neuron. Have the “terminal button” person in each line hold several tennis balls, ping-pong balls, Nerf balls, or similar soft objects in their hands. These represent the neurotransmitter of the neuron.

Begin by having each person in line face the front of the class, holding their left arm up in the air. Each person will communicate with the next person (part of the neuron) by lowering the left arm and touching the next person on the shoulder. To start the demonstration, tell the “somatodendritic region” of the left neuron to lower their arm when you say “Go.” When they touch the next person in line, they will drop their arms and touch the person to their left. This will continue until the “terminal button” is touched. This person cannot pass an electrical signal to the somatodendritic “person-part” of the next neuron because of the large physical gap between them, so they will have to communicate “chemically” by rolling the tennis balls to that person. Some of the balls will not be retrieved and the ones that are must be put in the person’s pockets (or some other representation of a “receptor”), and then that person can touch the shoulder of the next person in their line, starting the electrical conduction of the signal in that “neuron.”

Using this kind of model, you can demonstrate things like the need for chemical signaling in the nervous system, the difference in speed between electrical and chemical signaling, and the fact that some “neurotransmitters” will not be received by the postsynaptic neuron (and will be inactivated by simply drifting away from the synapse).

Activity 4.3: Three Colossal Neurons To demonstrate how neurons work and how they network together, use the exercise available at the National Institutes of Health. Place “Three Colossal Neurons” in your search engine and click on the link associated with NIH.gov. Students who participate in this type of demonstration have been shown to learn more as measured by testing their knowledge. < Return to Table of Contents 13 ..

Chapter 4: Neural Conduction and Synaptic Transmission

WEB LINKS Web Link 4.1: Neurotransmitter Chemistry Go to http://www.benbest.com and click on the link titled “Articles About Science Topics.” Select the bottom link “The Anatomical Basis of Mind.” Once on that site, select “Chapter 10 Brain Neurotransmitters” to reach your final destination.

Looking for diagrams of neurotransmitter molecules. These aren’t pretty, but they are a nice collection.

Web Link 4.2: Endogenous Neuroactive Extracellular Signal Transducers Go to http://www.neurotransmitter.net/index.php and click on the link entitled “Endogenous Neuroactive Extracellular Signal Transducers.”

A detailed list that includes neurotransmitters, neuromodulators, neuropeptides, neurosteroids, and neuroactive hormones. The list does not include growth factors, cytokines, and intracellular second messengers. Links are provided to articles that provide reviews on the particular chemical.

Web Link 4.3: How Botox Works Go to http://www.howstuffworks.com/ and place “botox” in the search bar. Click on the first search result titled “Botox: What You Need to Know.” A simple description.

Web Link 4.4: Botox Go to http://www.rxlist.com/ and place “botox” in the search box. Select the first link labeled “botox.” A more medical view of the effects of “botox.”

Web Link 4.5: Nicotinic Receptors Go to http://www.psychiatrist.com/ and place “nicotinic receptors” in the search box. Select “Paying Attention to Your Acetylcholine, Part 1: Structural Organization of Nicotinic Receptors.” Nice diagram of action in nicotinic receptors.

Web Link 4.6: Nicotinic Receptors Go to https://www.psychiatrist.com/ and place “nicotinic receptors” in the search box. Select “Paying Attention to Your Acetylcholine, Part 2: The Function of Nicotinic Receptors,” by Stephen M. Stahl, M.D., Ph.D. Web Link 4.7: Molecules Place “psychedelic pharmacology” in your search browser. Click on the link associated with Psychedelic Information Theory. Models of molecules allow comparisons. The psilocin/serotonin comparison is quite interesting. < Return to Table of Contents

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5 The Research Methods of Biopsychology: Understanding What Biopsychologists Do TABLE OF CONTENTS Chapter-at-a-Glance

2

Learning Objectives

3

Brief Chapter Outline

4

Teaching Outline

6

Lecture Launchers

16

Activities

17

Demonstrations

18

Web Links

19

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Chapter 5: The Research Methods of Biopsychology

CHAPTER-AT-A-GLANCE

Brief Outline Chapter Introduction (p. 104) 5.1 Methods of Visualizing and Stimulating the Living Human Brain (pp. 104–109) 5.2 Recording Human Psychophysiological Activity (pp. 109–112) 5.3 Invasive Physiological Research Methods (pp. 112–115) 5.4 Pharmacological Research Methods (pp. 115–118) 5.5 Genetic Engineering (pp. 118–120) 5.6 Neuropsychological Testing (pp. 121–124) 5.7 Behavioral Methods of Cognitive Neuroscience (pp. 124–126) 5.8 Biopsychological Paradigms of Animal Behavior (pp. 126–129)

Instructor’s Manual Resources Lecture Launcher 5.1, Activity 5.1 Lecture Launcher 5.4, Activity 5.2 Activity 5.3, Demonstration 5.1

Lecture Launcher 5.2

Lecture Launcher 5.3, Activity 5.4

< Return to Table of Contents

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LEARNING OBJECTIVES After completion of this chapter, the student should be able to: LO 5.1 LO 5.2 LO 5.3 LO 5.4 LO 5.5 LO 5.6 LO 5.7 LO 5.8 LO 5.9

Describe two x-ray-based techniques for visualizing the living human brain.

Describe the positron emission tomography (PET) technique.

Describe three magnetic-field-based techniques for imaging the living human brain.

Describe two transcranial stimulation techniques.

Describe two psychophysiological measures of brain activity.

Describe two psychophysiological measures of somatic nervous system activity.

Describe two psychophysiological measures of autonomic nervous system activity.

Describe the process of stereotaxic surgery.

Describe four types of lesion methods, and explain why it is important to be cautious when interpreting the effects of lesions.

LO 5.10 Describe the technique of electrical brain stimulation.

LO 5.11 Describe four invasive electrophysiological recording methods.

LO 5.12 Describe the various methods of drug administration.

LO 5.13 Describe the method of selective neurotoxic lesions.

LO 5.14 Describe two techniques for measuring chemical activity in the brain.

LO 5.15 Describe two techniques for locating particular neurotransmitters or receptors in the brain.

LO 5.16 Describe gene knockout and gene replacement techniques, and explain what is meant by the term transgenic.

LO 5.17 Explain how green fluorescent protein has been used as a research tool in the neurosciences.

LO 5.18 Explain how opsins have been used as a research tool in the neurosciences.

LO 5.19 Describe three approaches to neuropsychological testing.

LO 5.20 Describe those tests that are often administered as part of an initial common neuropsychological test battery.

LO 5.21 Describe tests that might be used by a neuropsychologist to investigate in more depth general problems revealed by a common neuropsychological test battery.

LO 5.22 Describe the Wisconsin Card Sorting Test.

LO 5.23 Describe the paired-image subtraction technique.

LO 5.24 Understand the default mode network, and know the structures that are part of that network.

LO 5.25 Explain what a mean difference image is.

LO 5.26 Describe three behavioral paradigms used to study species-specific behaviors.

LO 5.27 Describe the Pavlovian conditioning paradigm and the operant conditioning paradigm.

LO 5.28 Describe four seminatural animal learning paradigms. < Return to Table of Contents

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Chapter 5: The Research Methods of Biopsychology

BRIEF CHAPTER OUTLINE Lecture Launcher 5.1: Observing the Activity of the Living Brain PART ONE Methods of Studying the Nervous System 1. Methods of Visualizing and Stimulating the Living Human Brain a. X-Ray-Based Techniques b. Radioactivity-Based Techniques c. Magnetic-Field-Based Techniques d. Transcranial Stimulation 2. Recording Human Psychophysiological Activity a. Psychophysiological Measures of Brain Activity b. Psychophysiological Measures of Somatic Nervous System Activity c. Psychophysiological Measures of Autonomic Nervous System Activity 3. Invasive Physiological Research Methods a. Stereotaxic Surgery b. Lesion Methods c. Electrical Stimulation d. Invasive Electrophysiological Recording Methods 4. Pharmacological Research Methods a. Routes of Drug Administration b. Selective Chemical Lesions c. Measuring Chemical Activity of the Brain d. Locating Neurotransmitters and Receptors in the Brain 5. Genetic Engineering a. Gene Knockout and Gene Replacement Techniques b. Fantastic Fluorescence and the Brainbow c. Optogenetics: A Neural Light Switch PART TWO Behavioral Research Methods of Biopsychology Lecture Launcher 5.2: Beating Neuropsychological Tests 6. Neuropsychological Testing a. Modern Approach to Neuropsychological Testing b. Tests of the Common Neuropsychological Test Battery c. Tests of Specific Neuropsychological Function d. Frontal Lobe Function 7. Behavioral Methods of Cognitive Neuroscience a. Paired-Image Subtraction Technique b. Default Mode Network c. Mean Difference Images

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Biopsychology, Tenth Edition 8. Biopsychological Paradigms of Animal Behavior a. Paradigms for Assessment of Species-Common Behaviors b. Traditional Conditioning Paradigms c. Seminatural Animal Learning Paradigms < Return to Table of Contents

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Chapter 5: The Research Methods of Biopsychology

TEACHING OUTLINE PART ONE Methods of Studying the Nervous System 1. Methods of Visualizing and Stimulating the Living Human Brain This section explains the methods used to explain how the nervous systems of living humans and animals can be studied. a. X-Ray-Based Techniques (see Figure 5.1 in Biopsychology) LO 5.1 Describe two x-ray-based techniques for visualizing the living human brain. i. Contrast X-rays • To take an X-ray photograph of an object, a beam of X-rays is passed through it onto a photographic plate; any part of the object that absorbs X-rays differently than the surrounding medium will be distinguishable.

• Standard X-rays can’t be used to study the brain because it is composed of many overlapping structures that all absorb X-rays to about the same degree.

• Contrast X-rays solve this problem in some cases; a radio-opaque material is introduced into the structure of interest to make it “stand out” from the others on an X-ray photograph.

• For example, in cerebral angiography a radio-opaque dye is injected into the carotid artery; it reveals the displacement or enlargement of blood vessels. ii. X-Ray Computed Tomography (see Figure 5.2 in Biopsychology) • Provides a 3-dimensional view of a structure.

• The X-ray gun and the X-ray detector rotate in apposition around the brain at one level, taking a series of measurements from which an image of one section is constructed; this is repeated at multiple levels.

• The CT-scan image of the brain is not high-resolution. b. Radioactivity-Based Techniques LO 5.2 Describe the positron emission tomography (PET) technique. i.

• • • • • •

Positron Emission Tomography (PET) (see Figure 5.3 in Biopsychology) This method highlights brain areas that are active, rather than showing a detailed map of all brain structures.

The patient is injected with radioactive 2-deoxyglucose because 2-DG is structurally similar to glucose; it is taken up by neurons as if it were glucose.

More active neurons need more energy and take up more 2-DG; unlike glucose, 2-DG cannot be metabolized by neurons and it accumulates in them.

The patient is injected with radioactive 2-DG and then engages in the activity under study (e.g., reading) while a PET scan of the brain is being taken.

The PET scan reveals on a series of images of horizontal sections where radioactivity has accumulated, thus indicating what areas were particularly active during the test.

Radioactive-labeled drugs or ligands can also be administered that bind to specific target molecules in the brain.

c. Magnetic-Field-Based Techniques (see Figures 5.4–5.6 in Biopsychology)

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Biopsychology, Tenth Edition LO 5.3 Describe three magnetic-field-based techniques for imaging the living human brain. i. Magnetic Resonance Imaging • MRI has higher resolution than CT. • Images are created from measurements of the waves emitted by hydrogen atoms after they are placed in a magnetic field; its high spatial resolution stems from the fact that neural structures differ considerably in their density of hydrogen atoms.

ii. Functional MRI (see Figure 5.7 in Biopsychology) • An fMRI allows brain activity to be measured by imaging the increase in oxygen (blood) flow to all active brain areas.

• The four advantages fMRI has over PET include: (1) nothing must be injected into the subject; (2) one image provides structural and functional formation; (3) the spatial resolution is better; and (4) changes can be measured in real time.

• A disadvantage of fMRI is that the images are not of neural activity, as many assume.

• The signal recorded from an fMRI is called the BOLD signal (blood-oxygen-level-dependent signal).

• The relation of the BOLD signal to neural activity is complex and variable.

• Also, fMRI scans are too slow (they take two to three seconds) compared to many neural responses (which occur in milliseconds). iii.

• • • • d.

Diffusion Tensor Imaging (see Figure 5.8 in Biopsychology) DTI provides a means of imaging axonal tracts rather than cell bodies.

The technique is based on the rapid diffusion of water molecules along tracts.

DTI is unique in that it allows investigation of interconnectivity among structures.

Some connectomes of simple organisms have been completed.

Transcranial Stimulation LO 5.4 Describe two transcranial stimulation techniques. i. Transcranial Magnetic Stimulation (TMS) allows researchers to noninvasively stimulate the brain, using a focused magnetic field to disrupt brain activity and produce a temporary “lesion.”

• The effects of disruption on cognition and behavior are assessed.

• TMS is often employed to circumvent the difficulties that brain imaging studies have in determining causation. ii. Transcranial Direct Current Stimulation (tDCS) can be used to temporarily stimulate an area of cortex while observing the effects on cognition and behavior.

2. Recording Human Psychophysiological Activity a. Psychophysiological Measures of Brain Activity LO 5.5 Describe two psychophysiological measures of brain activity. i. Scalp Electroencephalography (EEG): (see Figures 5.9–5.11 in Biopsychology) • An EEG signal is measured through an array of scalp electrodes.

• EEG waves reflect the sum total of all of the electrical events in the head (APs, EPSPs, IPSPs, eye movements, blood flow, etc.); thus, the EEG reveals little about the nature of the underlying neural activity.

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Chapter 5: The Research Methods of Biopsychology •

• •

Its value lies in the fact that particular EEG waveforms are associated with particular states of consciousness; generally low-amplitude, fast EEG activity is associated with an alert aroused state; and high-amplitude, slow EEG activity (alpha waves) is associated with a relaxed, but awake, state.

EEG can be used to study brain activity in real time, in response to specific events. These are called evoked potentials. Usually, many evoked potentials are used to generate an averaged evoked potential in order to reduce the noise of the background EEG activity.

EEG recordings are a valuable diagnostic tool: For example, the presence of high-amplitude spikes in the EEG (i.e., epileptic spikes) is the primary criterion for diagnosing epilepsy.

ii. Magnetoencephalography • Brain activity is measured in terms of changes in magnetic fields on the surface of the scalp. b. Psychophysiological Measures of Somatic Nervous System Activity LO 5.6 Describe two psychophysiological measures of somatic nervous system activity. i. Muscle Tension (see Figure 5.12 in Biopsychology) • An electromyogram (EMG) measures the changing difference in the voltage between two large electrodes placed on the skin above a large muscle; the amplitude of EMG signals indicates the combined level of tension in the underlying muscle.

• The raw signals are usually integrated so that the data are easier to work with; the height of the curve of integrated EMG activity indicates the number of spikes in the EMG signal per unit of time. ii. Eye Movement (see Figure 5.13 in Biopsychology) • In an electrooculogram (EOG), eye movements are recorded by placing four electrodes around the eye; the signal results from the fact that the front of eye is more positively charged than the back.

• The direction of movement can be inferred from the relation between the activity recorded on two channels: (1) above vs. below and (2) left vs. right. c. Psychophysiological Measures of Autonomic Nervous System Activity LO 5.7 Describe two psychophysiological measure of autonomic nervous system activity. i. Skin Conductance • Skin conductance level (SCL) is the general level of skin conductance associated with a particular situation.

• A skin conductance response (SCR) is a rapid change in skin conductance in response to a particular event; one application is the lie detector test. ii. Cardiovascular Activity • An electrocardiogram (ECG) shows changes in cardiac function, including heart rate, which reflects changes in emotion.

• Blood pressure is expressed as peak pressure during systoles over minimum pressure during diastoles; 130/70 mm/Hg is normal, greater than 150/90 is hypertension. The device commonly used to measure blood pressure is a sphygmomanometer.

• Plethysmography is the measurement of the volume of blood in a body structure (e.g., penis); this is done either with a strain gauge or by measuring the amount of light absorbed by the structure.

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Biopsychology, Tenth Edition 3. Invasive Physiological Research Methods In most cases, laboratory animals serve as the subjects when invasive procedures are required to directly manipulate or measure the brain. a. Stereotaxic Surgery (see Figure 5.14 in Biopsychology) LO 5.8 Describe the process of stereotaxic surgery.

• • •

The first step in many invasive biopsychology experiments is stereotaxic surgery; it allows accurate placement of lesions, probes, electrodes, and other devices into the brain.

The method employs a stereotaxic atlas and a stereotaxic instrument (head holder and electrode holder).

The reference point is often bregma (the point where two main plates of the rat skull naturally fuse together).

b. Lesion Methods (see Figure 5.15 in Biopsychology) LO 5.9 Describe four types of lesion methods, and explain why it is important to be cautious when interpreting the effects of lesions.

• • • • • •

The aspiration method is often used to remove cortical tissue.

The radio-frequency (high-frequency) electrolytic lesion is the most common subcortical lesion; the tissue is destroyed by the heat of the current.

Small knife cuts are often used for severing tracts.

Reversible lesions are useful because the same subjects can be repeatedly tested. Tissue can be anesthetized or cooled to the point that all neural activity temporarily stops.

Lesion studies must be interpreted with caution; a lesion inevitably damages structures other than the one that the surgeon targeted, and lesions seldom remove a targeted structure completely.

The behavioral effects of unilateral lesions are much milder than bilateral lesions.

c. Electrical Stimulation LO 5.10 Describe the technique of electrical brain stimulation.

• •

The effects of electrical stimulation are often opposite to those of a lesion to the same brain site.

Electrical stimulation research is done prior to any lesioning.

d. Invasive Electrical Recording Methods (see Figure 5.16 in Biopsychology) LO 5.11 Describe four invasive electrophysiological recording methods. i. Intracellular Unit Recording • This method measures changes in the membrane potential of a neuron over time; it requires a microelectrode positioned inside a neuron.

• It is next to impossible to record intracellularly in a freely moving animal because it is difficult to keep the microelectrode inside the neuron. ii. Extracellular Unit Recording • In this method, a microelectrode is positioned near a neuron.

• The signal is a series of spikes; each spike indicates an action potential from a nearby neuron.

Spikes of the same amplitude are assumed to come from the same neuron.

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Chapter 5: The Research Methods of Biopsychology iii. Multiple-Unit Recording • Multiple-unit recording provides an indication of the rate of firing of many neurons in the general vicinity of the electrode tip.

• An electrode larger than a microelectrode picks up the action potentials from many nearby neurons.

• The signal is integrated so that the height of the curve indicates the number of action potentials in the vicinity per unit of time. iv. Invasive EEG recording • Implanted electrodes are used to record EEG in laboratory animals because scalp electrodes do not allow as clear or finite position recording.

4. Pharmacological Research Methods (see Figures 5.17–5.19 in Biopsychology) a. Routes of Drug Administration LO 5.12 Describe the various methods of drug administration.

• •

These include IG, IP, IV, SC, and IM. These peripheral routes all suffer from the fact that many drugs cannot pass the blood-brain barrier; this problem can be overcome by administering drugs via intraventricular cannula or by microinjection of drugs directly into brain tissue.

b. Selective Chemical Lesions LO 5.13 Describe the method of selective neurotoxic lesions.

Sometimes, drugs can be injected into the brain that produce chemical lesions that are more selective than electrical lesions might be. For example, 6-hydroxydopamine (6-OHDA) is a neurotoxin that selectively destroys dopaminergic and noradrenergic neurons in the vicinity of the injection site. c. Measuring the Chemical Activity of the Brain LO 5.14 Describe the two techniques for measuring chemical activity in the brain.

• • • • • •

In 2-deoxyglucose autoradiography, radioactive 2-DG is injected; then the animal performs the behavior of interest.

The animal is immediately killed, its brain is removed and sliced, and the slices are coated with a photographic emulsion.

After a few days in the dark, the areas of the brain that were particularly active during the test activity show up as dark spots of radioactivity.

A technique that allows the measurement of specific neurotransmitters in behaving animals is called cerebral dialysis.

A fine U-shaped tube is inserted into the brain of an animal; its tip is made of a semipermeable dialysis membrane, a solution of artificial cerebrospinal fluid circulates through the tube.

Because the tip of the tube is semipermeable, chemicals can continuously move from the brain into the solution in the tube (down a concentration gradient), which can then be removed for later analysis using a chromatograph.

d. Locating Neurotransmitters and Receptors in the Brain LO 5.15 Describe two techniques for locating particular neurotransmitters or receptors in the brain.

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Biopsychology, Tenth Edition

• • •

Immunocytochemistry begins by injecting antigens (foreign proteins) into an animal so that the animal will create and bind antibodies to the antigen to remove or destroy it.

Antibodies for most of the brain’s peptide neurotransmitters and receptors have been created; these can be labeled with a dye or radioactive element and then used to identify specific neuroproteins in slices of brain tissue.

In situ hybridization allows peptides and proteins in the brain to be located; labeled hybrid RNA strands with a base sequence complementary to the mRNA for synthesizing the target neuroprotein. The hybrid RNA binds to the complementary mRNA in the target cells and allows the target neuroprotein’s location to be marked.

5. Genetic Engineering a. Gene Knockout and Replacement Techniques LO 5.16 Describe gene knockout and gene replacement techniques, and explain what is meant by the term transgenic.

• • • • • • • • •

These techniques involve the creation of organisms that lack a specific gene; any measurable neural or behavioral anomalies are then noted.

An example of genetic engineering is in Melanopsin Knockout Mice.

Melanopsin is a protein found in some neurons in the mammalian retina, which has been implicated in the control of circadian rhythms, since many of the neurons project to the hypothalamus.

It was discovered that the knockout of the gene reduced, but did not eliminate, the responses of the clock to changes in light. Melanopsin contributes to the control of circadian clock, but it is not the only factor.

PROBLEMS: 1) Most behaviors are determined by multiple genes; 2) eliminating one gene usually alters the expression of other genes; and 3) gene expression is dependent upon experience, which may be altered by the absence of the missing gene.

These techniques involve the replacement of one gene with another.

Sometimes, genetic information from a different species is implanted, creating a transgenic subject.

In some applications, pathological human genes are used to create transgenic mice, which are then used to study the neural basis of human disease.

In other applications, genes are manipulated so that researchers can turn them on or off with light or chemical signals.

b. Fantastic Fluorescence and the Brainbow (see Figures 5.20–5.21 in Biopsychology) LO 5.17 Explain how green fluorescent protein has been used as a research tool in the neurosciences.

• •

The GFP gene can be inserted into target cells that are later exposed to blue light. This produces bright green fluorescence for visualization.

The GFP gene can be altered to synthesize proteins the fluoresce in different colors.

c. Optogenetics LO 5.18 Explain how opsins have been used as a research tool in the neurosciences.

•

Opsin genes can be inserted into a particular type of neuron allowing the neuroscientist to use light to hyperpolarize or depolarize the neuron.

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PART TWO Behavioral Research Methods of Biopsychology 6. Neuropsychological Testing a. Modern Approach to Neuropsychological Testing LO 5.19 Describe three approaches to neuropsychological testing.

• •

Methods used to assess psychological deficits of human patients suspected of having brain damage.

Traditionally, a single neuropsychological test was administered to a patient. This approach changed in the 1960s to include a standard battery of neuropsychological tests; currently, it is most common for a customized-test-battery approach to be used.

b. Tests of the Common Neuropsychological Test Battery LO 5.20 Describe those tests that are often administered as part of an initial common neuropsychological test battery. i. Intelligence: The WAIS (see Table 5.1 in Biopsychology) • Most neuropsychological assessments begin with the Wechsler Adult Intelligence Scale (WAIS).

• It has 11 subtests; six comprise the verbal scale (e.g., digit span, information, similarities), five comprise the performance scale (e.g., block design, object assembly). ii. Memory The information subtest and the digit span test are memory tests that comprise part of the WAIS; however, these are notoriously bad measures of memory. iii. Language Lateralization • The WAIS verbal subtests reveal significant language impairments in a variety of ways; if the WAIS was not done, the token test is a good initial screening test for language-related deficits.

There are 20 tokens of two different shapes, two different sizes, and five different colors; the subject is asked to carry out various acts such as, “Touch the small blue circle and then the large green square.”

• If the token test identifies language deficits, it is followed by a battery of tests of language ability.

• A test for the lateralization of language skills is also often included when assessing language function.

• In the sodium amytal test, the anesthetic sodium amytal is injected first into one carotid artery and then, many minutes later, into the other; typically, the patient is mute following an injection ipsilateral to the dominant hemisphere for language, but makes only a few minor speech errors after an injection contralateral to the dominant hemisphere for language.

• In the dichotic listening test, three pairs of digits are presented to the subject through headphones. Each digit in the pair is presented simultaneously, one to each ear; the subjects are asked to report the six digits that they heard. They do slightly better through the ear contralateral to the hemisphere dominant for language. c. Tests of Specific Neuropsychological Function LO 5.21 Describe tests that might be used by a neuropsychologist to investigate in more depth general problems revealed by a common neuropsychological test battery.

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i. Memory If memory deficits are discovered, the neuropsychologist attempts to answer four key questions: • Is short-term or long-term memory affected? Or both?

• Are the deficits anterograde or retrograde? Or both?

• Do the deficits involve semantic or episodic memory? Or both?

• Do the deficits involve explicit memory or implicit memory? Or both? ii. Language • Patients with speech problems must be further tested for problems of phonology, syntax, or semantics.

• Patients with dyslexia must be tested for reading or pronunciation problems. d. Frontal-Lobe Function (see Figure 5.22 in Biopsychology) LO 5.22 Describe the Wisconsin Card Sorting Test.

• • • • •

The Wisconsin Card Sorting Test is often used to assess frontal lobe function.

Each card in the deck has one, two, three, or four triangles, circles, squares, or crosses that are all red, green, yellow, or blue.

The subject is told to sort the cards into four different piles, but is not told on what basis the sorting is to be accomplished. They are told after each card is placed in a pile whether or not it was correctly placed.

At first, the patient must learn to sort by color, but once she or he has learned this sorting principle, the correct principle changes without warning to form or number.

Patients with frontal-lobe lesions adapt poorly to rule changes; they perseverate (they continue to respond in a previously correct fashion long after it has become incorrect).

7. Behavioral Methods of Cognitive Neuroscience (see Figures 5.23 in Biopsychology) •

The premise is that complex cognitive processes are the combined activity of simple cognitive processes and that each constituent cognitive process is mediated by neural activity in a particular area of the brain.

a. Paired-Image Subtraction Technique LO 5.23 Describe the paired-image subtraction technique.

•

PET or fMRI images of tasks that differ in only one constituent cognitive process are compared; the difference between the two images is viewed as specific to the one constituent cognitive process that was different between the two images.

b. Default Mode Network LO 5.24 Understand the default mode network, and know the structures that are part of that network.]

• •

Interpretation of different images is complicated by the fact that there is substantial brain activity when the mind simply wanders. This activity is termed the brain’s default mode.

Brain structures that are active in the default mode are referred to as the default mode network, which comprises various regions of the brain.

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Chapter 5: The Research Methods of Biopsychology LO 5.25 Explain what a mean difference image is.

•

Mean Difference Image is often used to reduce the noise associated with random cerebral events and is a representation of activity that is common to many volunteers.

8. Biopsychological Paradigms of Animal Behavior a. Paradigms for Assessment of Species-Common Behaviors LO 5.26 Describe three behavioral paradigms used to study species-specific behaviors.

•

These behaviors are displayed in the same form by virtually all members of a species, of the same sex (e.g., grooming, swimming, nest building, copulating).

i. Open-Field Test • The open-field test provides three measures of emotionality: (1) degree of inactivity; (2) thigmotaxis; and (3) defecation. ii. Tests of Aggressive and Defensive Behaviors • Aggression and defense can be studied by recording encounters between a small male intruder and a colony’s dominant (alpha) male. Aggression involves a sideways approach, sideways pushing, piloerection, and biting directed at the back; defense involves boxing, rolling over onto the back, biting the face, freezing, and fleeing. iii. Tests of Sexual Behavior • Rats’ sexual behavior is another species-common behavior that is widely studied.

• Two common measures of female rat sexual receptivity are (1) lordosis quotient (proportion of mounts producing lordosis), and (2) degree of concavity of the back during lordosis.

• Male rat behaviors measured include number of mounts to intromission, number of intromissions to ejaculation, and time to reinitiate mounting after ejaculation (the postejaculatory interval). b. Traditional Conditioning Paradigms LO 5.27 Describe the Pavlovian conditioning paradigm and the operant conditioning paradigm.

•

•

Traditional conditioning paradigms play an important role in biopsychology for three reasons: – conditioning is a phenomenon of primary interest to psychologists; – conditioning procedures are often used to train laboratory animals to perform as required in behavioral experiments; and – researchers can infer much about the psychological state of an animal from its ability to learn and perform various responses.

There are two kinds of traditional conditioning paradigms: – Pavlovian conditioning: in which a neutral stimulus called a conditional stimulus (CS; e.g., tone) is paired with an unconditional stimulus (US; e.g., meat powder) that elicits an unconditional response (UR; e.g., salivation). As the CS becomes associated with the US, it begins to elicit a response on its own, which is referred to as a conditional response (CR). The CR is usually similar to the UR, but this is not always the case.

– Operant conditioning: in which the rate of a particular response is increased by reinforcement or decreased by punishment.

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Biopsychology, Tenth Edition c. Seminatural Animal Learning Paradigms (see Figures 5.24–5.25 in Biopsychology) LO 5.28 Describe four seminatural animal learning paradigms.

The following four examples are controlled laboratory paradigms for studying forms of learning that are assumed to occur in the rat’s natural environment: i. Conditioned Taste Aversion • This is the most influential ethoexperimental learning paradigm; rats and many other animals learn the relation between a new taste and subsequent gastrointestinal distress in one trial and subsequently avoid the novel taste.

• Taste aversion conditioning experiments in the 1960s challenged three widely held views of learning that had grown out of the study of the traditional conditioning paradigms: – the view that learning is a gradual step-by-step process by showing that it could occur reliably in one trial.

– the view that temporal contiguity is necessary for learning by showing that conditioning occurred even when the taste and distress were separated by several hours.

– the view that associations between any two stimuli are equally easy to learn (the principle of equipotentiality) by showing that rats could learn the relation between gastrointestinal distress and a taste, but not a light. ii. Radial-Arm Maze • Used to study foraging behavior in the laboratory.

• Foraging in the wild is complex; the rat must learn where food is likely to be, but not to immediately revisit a stripped site.

• In the radial-arm maze, rats quickly learn to go directly to the arms that are baited with food each day, but they rarely visit the same arm twice on a given trial. iii. Morris Water Maze • Another laboratory paradigm used to study rat spatial ability; the Morris water maze is a large tub of milky water. To get out of the water, rats must learn to swim to a slightly submerged (invisible) goal platform.

• Rats learn to do this very quickly, even when they are placed in the water at a different position on each trial; they use external room cues to guide them.

• It is interesting to look at their search strategies when the platform has been moved to a new location. iv. Conditioned Defensive Burying • Based on the observation that rats exposed to an inanimate object that has been the source of a single aversive stimulus (e.g., a shock, a bad odor, an air blast, or a flash) will often bury it.

• They bury it by facing it and spraying bedding or sand at it with their head and forelegs.

• It has been used to study anti-anxiety drug effects; anti-anxiety drugs reduce conditioned defensive burying at low doses. < Return to Table of Contents

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Chapter 5: The Research Methods of Biopsychology

LECTURE LAUNCHERS Lecture Launcher 5.1: Observing the Activity of the Living Brain In the last decade, advances in functional imaging techniques have permitted brain scientists to observe the function of the living brain in a way never before possible. Before lecturing on some of these techniques, introduce the class to the idea of watching brain activity with some of the latest technologies. Many videos from neuroscience laboratories are available on You Tube (ex: https://www.youtube.com/ and search “visualizing the activity of neurons in the brain”). Engage students in a conversation about how fast technology is advancing our understanding of the human brain.

Lecture Launcher 5.2: Beating Neuropsychological Tests In addition to being used for biopsychological and neuroscience research, neuropsychological tests are commonly employed as part of the legal process of determining whether an individual who has suffered a brain injury is eligible for disability and/or compensation. Injuries to the frontal lobe are particularly common. Briefly discuss the range of functions that are supported by the frontal lobe. Then, have the class discuss how an individual can be trained to beat the Wisconsin Card Sorting Test (e.g., see: Victor, T. L. and Abeles, N. (2004). Coaching Clients to Take Psychological and Neuropsychological Tests: A Clash of Ethical Obligations. Professional Psychology: Research and Practice 35: 373–379).

Lecture Launcher 5.3: The Mystery of the Jumping Frog Once there was a man who had trained a frog to jump every time he said “Jump!” He was curious about the connection between the senses and movement, so he decided to conduct an experiment. He cut off one of the frog’s legs and then said, “Jump!” and the frog jumped. So, he cut off another leg and said, “Jump!” again, and the frog jumped, though not as well as the last time. He cut off a third leg and said, “Jump!”

The frog made a rather feeble movement, but obviously attempted to jump. So, the man cut off the fourth leg and said, “Jump!” The frog just lay quietly on the ground. The man said, “Jump!” again, this time a little louder. The frog did not move. The man yelled “Jump!” as loud as he could and still the frog did not move. The man then concluded that frogs without legs could not hear!

Most students can see that the man in this story was not a very good researcher. His methods were a bit crude and cruel, but more importantly, he did not draw appropriate conclusions from his research and thus learned little from his experiment. This story can be used to begin a discussion of the role of planning in research or the difficulty in drawing conclusions from this type of data. Lack of behavior can frequently be related to many causes. Hypothesizing other causes for behavior in lesion studies can be interesting if you have a class ready for such thought processes.

Lecture Launcher 5.4: The History of Neuroscience Talking about methodology is a good place to examine the history of neuroscience. The increase in information made available, as different techniques are developed and the advances in other fields that lead to explorations about the brain, can make for a usable lecture structure. < Return to Table of Contents

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Biopsychology, Tenth Edition

ACTIVITIES Activity 5.1: Practical Aspects of Conducting MRI studies There are many practical aspects involved in using MRI on human subjects. Use the following game from the Nobelprize.org Web site to illustrate those practicalities and to test their knowledge of human imaging.

(Go to http://nobelprize.org/ and place “MRI the magnetic game” in the search bar. Select “MRI” from the results to move to the game page. One option is to play this game for the class: At each step in the game, you can interject a brief explanation of why you made the choice that you did. Another option is to allow one student to play each stage of the game. Then, each time a choice is made by a student, you can explain why or why not the choice they made was correct or incorrect.

Activity 5.2: Recording ECG An educational game located at the Nobelprize.org Web site provides an excellent illustration of the process of recording ECG and the interpretation of ECG results. (Go to http://nobelprize.org/ and place “Electrocardiogram game” in the search bar. Click on the link titled “electrocardiogram.” The game can be used in its entirety. However, if you just want to illustrate the process of ECG recording, then the game can be stopped just after the output section of the game. As with Activity 5.1, you can either play this game yourself as a means of illustrating the ECG process, or you can have one or several students play it for you as you speak about ECG recording.

Activity 5.3: Problems with the Interpretation of the Results of Brain Lesions and Other Invasive Procedures There are a number of problems associated with the interpretation of various brain lesioning and stimulation techniques. Choose one of the techniques presented in Chapter 5 and break the class into teams of three to four students. Have them write down as many potential problems with the technique you have chosen. After they are done, have one member from each team present their ideas to the rest of the class. After each presentation, discuss what is or is not wrong with the issues they have raised.

Activity 5.4: Pavlov’s Dog An educational game located at the Nobelprize.org Web site can be used to illustrate the process of Pavlovian conditioning (Go to http://nobelprize.org/ and place “Pavlov’s Dog” in the search bar. Click on the link with the same name.) The game allows you to control the timing and presentation of various stimuli to a dog in an attempt to make it salivate in response to a conditional stimulus. Play the game while the students watch and ask them for input as to what actions you should perform to make the dog salivate. < Return to Table of Contents

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Chapter 5: The Research Methods of Biopsychology

DEMONSTRATIONS Demonstration 5.1: Stereotaxic Atlas and Instrument In this demonstration, bring a small stereotaxic instrument and a stereotaxic atlas into the classroom.

Describe the major components of the instrument, including the head holder, the upper incisor bar, and the electrode holder. Describe how a stereotaxic atlas is used to provide coordinates to allow an investigator to manipulate a subcortical region in a rat brain. < Return to Table of Contents

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Biopsychology, Tenth Edition

WEB LINKS Web Link 5.1: Neuroscience and Psychophysiology Links Go to http://www.socialpsychology.org/ and page down to box on the left-hand side of the page that is titled “Other Psychology Pages.” Click on the link in that box titled “Links by Psychology Area.” Once you arrive on this page, page down until you reach a clickable link for the neuroscience and psychophysiology links.

Click on that link.

Links to neuroscience and psychophysiology websites and laboratories, teaching resources and online tutorials, professional organizations, and more.

Web Link 5.2:The Human Brain Project http://hendrix.ei.dtu.dk/home.html THOR Center for Neuroinformatics: Human Brain Project Repository This research site provides images and movies derived from functional imaging studies using PET and fMRI technologies. It is of use to faculty seeking images for lectures on neural imaging.

Web Link 5.3: 3D Brain Image Gallery Go to http://www.brainhq.com/ and page down to the bottom of the page. Click on the link for “Brain Resources” and page down to the “Image Gallery.” Click on the link for the image gallery and click on the link called “3D Brain Image Gallery” at the top of that page.

Web Link 5.4: Computerized Tomography (CT) – Head Go to http://www.radiologyinfo.org/ and place “Head CT” in the search bar. Click on the first link to reach the page on that contains CT images.

From the patient’s point of view. Some nice images that might be useful in class.

Web Link 5.5: How CAT Scans Work Go to http://health.howstuffworks.com/ and place “Cat Scan” in the search bar. Click on the link titled “How Cat Scans Work.”

A good basic explanation with useful images.

Web Link 5.6: How MRI Works http://electronics.howstuffworks.com/ and place “MRI” in the search bar. Click on the link titled “How MRIs work.”

A good basic explanation with useful images.

Web Link 5.7: The Basics of MRI Place “Hornak basics of mri” in your search engine. Click on the link associated Rochester Institute of Technology by looking for the link with “rit.edu” in the address.

Detailed explanation with lots of images.

Web Link 5.8: The Role of Neuroimaging in Diagnosis Go to https://www.ncbi.nlm.nih.gov/ in your navigation bar on your web browser and select “PMC” from the dropdown menu on the left-hand side of the website. Type “3181933” in the search bar. This will lead you to an easy-to-read article on using neuroimaging in diagnosis.

Web Link 5.9: Introduction to fMRI Go to http://www.radiologyinfo.org/ and place “fMRI” in the search bar. Click on the first link titled “Brain Imaging, Functional” to take you to the website on fMRI.

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Chapter 5: The Research Methods of Biopsychology Web Link 5.10: Fluorescence In Situ Hybridization (FISH) Go to https://www.ncbi.nlm.nih.gov/ in your navigation bar on your web browser and select “PMC” from the dropdown menu on the left hand side of the website. Type “3917523” in the search bar. This will lead you to an article on using fluorescence in situ hybridization as a brain imaging technique.

Web Link 5.11: Behavioral Techniques in Preclinical Neuropsychopharmacology Research Go to http://www.acnp.org/ and place “Behavioral Techniques in Preclinical Neuropsychopharmacology Research” in the search bar. Click on the first link with the same name.

By J. E. Barrett and K. A. Miczek, in Psychopharmacology – The Fourth Generation of Progress.

Web Link 5.12: Knockout Mice Go to https://www.genome.gov/ and place “knockout mice fact sheet” in the search bar. Click on the link with the same name.

What is a knockout mouse?

What are knockout mice used for?

What are the drawbacks of knockout mice?

How are knockout mice made?

Web Link 5.13: Optogenetics-Controlling the Brain With Lights Go to http://www.scientificamerican.com/ and place “Optogenetics-Controlling the Brain with Lights” in the search bar. Click on “How to Use Light to Control the Brain.”

< Return to Table of Contents

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6 The Visual System: How We See TABLE OF CONTENTS Chapter-at-a-Glance

2

Learning Objectives

3

Brief Chapter Outline

4

Teaching Outline

5

Lecture Launchers

14

Activities

18

Demonstrations

19

Assignments

20

Web Links

21

Handout List

23

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Chapter 6: The Visual System

CHAPTER-AT-A-GLANCE

Brief Outline Chapter Introduction (p. 134) 6.1 Light Enters the Eye and Reaches the Retina (pp. 135–138)

6.2 The Retina and Translation of Light into Neural Signals (pp. 138– 144)

6.3 From Retina to Primary Visual Cortex (pp. 144–146) 6.4 Seeing Edges (pp. 146–152) 6.5 Seeing Color (pp. 152–156) 6.6 Cortical Mechanisms of Vision and Conscious Awareness (pp. 156– 163)

Instructor’s Manual Resources Lecture Launchers 6.1, 6.6, Activity 6.3, Assignment 6.2 Lecture Launcher 6.2, Activities 6.1, 6.2, 6.4, Demonstrations 6.1, 6.2 Lecture Launcher 6.7, Assignment 6.1 Lecture Launchers 6.3, 6.8, 6.9 Lecture Launchers 6.4, 6.5, 6.10, Assignments 6.3, 6.4

< Return to Table of Contents

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Biopsychology, Tenth Edition

LEARNING OBJECTIVES After completion of this chapter, the student should be able to: LO 6.1 LO 6.2

LO 6.3 LO 6.4 LO 6.5 LO 6.6 LO 6.7 LO 6.8 LO 6.9 LO 6.10 LO 6.11 LO 6.12 LO 6.13 LO 6.14 LO 6.15 LO 6.16 LO 6.17 LO 6.18 LO 6.19 LO 6.20 LO 6.21 LO 6.22 LO 6.23 LO 6.24

Explain how the pupil and the lens can affect the image that falls on the retina.

Explain why some vertebrates have one eye on each side of their head wheras other vertebrates have their eyes mounted side by side on the front of their heads. Also, explain the importance of binocular disparity.

Describe the structure of the retina, and name the cell types that make up the retina.

Describe the duplexity theory of vision, and explain the differences between the photopic and scotopic systems.

Explain the difference between the photopic and scotopic spectral sensitivity curves, and explain how that difference can account for the Purkinje effect.

Describe the three types of involuntary fixational eye movements and explain what happens when all eye movements are blocked.

Describe the process of transduction.

Describe the components and layout of the retina-geniculate-striate system.

In the context of the retina-geniculate-striate system, explain what is meant by retinotopic.

Describe the M and P channels.

Explain the neural basis of contrast enhancement.

Describe the methods used by David Hubel and Torsten Wiesel to map the receptive fields of visual system neurons, and define the term receptive field.

Describe the characteristics of the receptive fields of retinal ganglion cells, lateral geniculate neurons, and striate neuron of lower layer IV. Describe the characteristics of the receptive fields of simple and complex cells.

Describe the organization of the primary visual cortex.

Describe the changing view of visual system receptive fields.

Describe the component and opponent-process theories of color vision.

Describe Land’s demonstration of color constancy, and explain his retinex theory.

Describe the three classes of visual cortex, and identify their locations in the brain.

Explain what happens when an area of primary visual cortex is damaged.

Describe the areas of secondary visual cortex and association cortex involved in vision.

Explain the difference between the dorsal and ventral streams and the functions that have been attributed to each stream by different theories.

Describe the phenomenon of prosopagnosia and discuss the associated theoretical issues.

Describe the phenomenon of akinetopsia and discuss the associated theoretical issues.

< Return to Table of Contents

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Chapter 6: The Visual System

BRIEF CHAPTER OUTLINE Lecture Launcher 6.1: The Snellen Eye Chart 1. Light Enters the Eye and Reaches the Retina a. Pupil and Lens b. Eye Position and Binocular Disparity Lecture Launcher 6.2: Transduction at Rods and Cones 2. The Retina and Translation of Light into Neural Signals a. Structure of the Retina b. Cone and Rod Vision c. Spectral Sensitivity d. Eye Movement e. Visual Transduction: The Conversion of Light to Neural Signals 3. From Retina to Primary Visual Cortex a. Retina-Geniculate-Striate System b. Retinotopic Organization c. The M and P Channels 4. Seeing Edges a. Lateral Inhibition and Contrast Enhancement b. Receptive Fields of Visual Neurons c. Receptive Fields: Neurons of the Retina-Geniculate-Striate System d. Receptive Fields e. Organization of Primary Visual Cortex f. Changing Concept of Visual Receptive Fields: Contextual Influences in Visual Processing Lecture Launcher 6.3: Negative After-Effects—Put the Fish in Its Bowl 5. Seeing Color a. Component and Opponent Processing b. Color Constancy and the Retinex Theory Lecture Launcher 6.4: A Veritable Melange of Illusions 6. Cortical Mechanisms of Vision and Conscious Awareness a. Three Different Classes of Visual Cortex b. Damage to Primary Visual Cortex: Scotomas and Completion c. Functional Areas of Secondary and Association Visual Cortex d. Dorsal and Ventral Streams e. Prosopagnosia f. Akinetopsia < Return to Table of Contents

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Biopsychology, Tenth Edition

TEACHING OUTLINE 1. Light Enters the Eye and Reaches the Retina (see Figures 6.3–6.4 in Biopsychology) • Vision is the most studied of the senses.

• Review the major structures of the eye (Figure 6.4). a. Pupil and Lens LO 6.1 Explain how the pupil and the lens can affect the image that falls on the retina.

• • • • • • •

The amount of light reaching the retina is regulated by donut-shaped bands of contractile tissue, the irises, which give eyes their color.

Light enters the eye through the pupil, a hole in the iris.

Note that the size of the pupil is a compromise between sensitivity (the ability to detect the presence of a dimly lit object) and acuity (the ability to see the details of the object).

Behind each pupil is a lens, which focuses incoming light on the retina.

Ciliary muscles adjust the lenses to focus visual images sharply on each retina, regardless of the distance of the image from the eyes; this focusing is called accommodation.

When we look at something near, the ciliary muscles contract, tension on the lenses is reduced, and they become more cylindrical.

When we look at a distant object, the muscles relax, tension on the lens is increased, and the lenses flatten.

b. Eye Position and Binocular Disparity LO 6.2 Explain why some vertebrates have one eye on each side of their head whereas other vertebrates have their eyes mounted side-by-side on the front of their heads. Also, Explain the importance of binocular disparity.

• •

Unlike most vertebrates, most mammals have two eyes on the front of their heads, rather than one on each side. This cuts down the field of view, but it ensures that most of what is seen is seen through both eyes.

Because each eye sees things from a slightly different perspective, there is a difference in the two retinal images; this binocular disparity is greater for closer things. The degree of binocular disparity associated with a particular visual stimulus helps the brain create a threedimensional perception from two two-dimensional retinal images, thus achieving depth perception.

2. The Retina and Translation of Light into Neural Signals (see Figures 6.5–6.10 in Biopsychology) a. Structure of the Retina LO 6.3 Describe the structure of the retina, and name the cell types that make up the retina.

• • • •

After light passes through the pupil and lens, it reaches the retina.

The retina has five layers: receptor layer, horizontal cell layer, bipolar layer, amacrine cell layer, and retinal ganglion cell layer.

The receptor layer is the farthest from light; therefore, incoming light is distorted by four layers of neurons before reaching the receptors.

The fovea is a pit about 330 M in diameter; it is the only part of the retina capable of mediating high-acuity vision. This is due, in part, to the fact that axons of the retinal ganglion cells are thinnest over the fovea and light is distorted less before reaching the layer of receptors. The

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Chapter 6: The Visual System

• • • •

fovea is roughly in the center of your field of vision, which is why you tend to hold tasks that require a high degree of acuity (e.g., threading a needle) in the center of your visual field.

The optic disk is where the axons of retinal ganglion cells penetrate the retina and exit the eye; the optic disk has no receptors, thus creating a blind spot.

We all have a blind spot at the optic disk, due to the exit of axons from the retinal ganglion cells.

We are normally unaware of our blind spots, even when looking through one stationary eye, because of completion; the visual system is able to use visual information gathered from receptors around the optic disk to “complete” the visual image.

Completion illustrates the creativity of the visual system.

b. Cone and Rod Vision LO 6.4 Describe the duplexity theory of vision, and explain the differences between the photopic and scotopic systems.

• • • • • •

In a sense, each of us has two visual systems: the photopic system functions in lighted conditions, and the scotopic system functions in dim light.

Cones mediate photopic vision and rods mediate scotopic vision; this is called the duplexity theory of vision.

The photopic system mediates high-acuity vision; the scotopic system mediates low-acuity vision.

The photopic system has low sensitivity with few receptors’ information combined at the next cell level (low convergence).

The scotopic system has high sensitivity with many receptors converging on ganglion cells (high convergence).

Only cones are in the fovea; rods predominate in the periphery.

c. Spectral Sensitivity LO 6.5 Explain the difference between the photopic and scotopic spectral sensitivity curves, and explain how that difference can account for the Purkinje effect.

• • • • •

Generally, more intense lights appear brighter.

However, wavelength also has a substantial effect on the perception of brightness.

Our visual systems are not equally sensitive to all wavelengths in the visible spectrum; lights of the same intensity, but of different wavelengths, can differ in brightness.

A graph of this is called a spectral sensitivity curve.

Humans having both rods and cones have two curves, photopic and scotopic (see Figure 6.10).

d. Eye Movement LO 6.6 Describe the three types of involuntary fixational eye movements, and explain what happens when all eye movements are blocked.

• • •

Our eyes are in continual motion; they make a series of fixations (about three per second) connected by saccades (rapid movements between fixations).

Eye movements keep the visual image in continual motion on the retina; the importance of this movement is illustrated by the fact that stabilized retinal images disappear. Most visual system neurons respond to change, not to steady input.

What we perceive at any instance is the sum of the input that has been received during the last few fixations; this temporal integration of retinal images explains why our visual images are

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Biopsychology, Tenth Edition detailed, colored, and wide-angled, despite the small size of the fovea. It also explains why things don’t disappear when we blink. e. Visual Transduction: The Conversion of Light to Neural Signals (see Figures 6.11–6.12 in Biopsychology) LO 6.7 Describe the process of visual transduction.

• • • • • • • • •

Transduction is the conversion of one form of energy to another; the first step in visual transduction is conversion of light to neural signals by the rods and cones.

Transduction by rods is well understood. There is a pink substance in rods called rhodopsin; light is absorbed by rhodopsin, and this bleaches it (removes its color). This bleaching occurs because retinal and opsin, the two components of rhodopsin, separate in light.

The bleaching reaction hyperpolarizes the rods, thus the bleaching reaction transduces light to a cascade of intracellular events, resulting in a neural signal.

When rhodopsin is totally bleached by intense light, rods lose their ability to absorb light and transduce; however, in the dark, retinal and opsin are reunited, and rhodopsin regains its color and its ability to absorb light and transduce.

Strong evidence that the absorption of light by rhodopsin is the first step in scotopic vision is the correspondence between rhodopsin’s absorption spectrum and the scotopic spectral sensitivity curve.

Rhodopsin is a G-protein-linked receptor that responds to light by initiating a cascade of intracellular chemical events.

Cyclic GMP is an intracellular chemical that keeps Na+ channels partly open when rods are in darkness; rods are thus slightly depolarized.

Bleaching rods via exposure to light results in an intracellular cascade of events that deactivates cyclic GMP, closing Na+ channels, which hyperpolarizes the rod and reduces the release of glutamate.

Rods thus transmit signals through the neural system via inhibition.

3. From Retina to Primary Visual Cortex (see Figure 6.13 in Biopsychology) a. Retina-Geniculate-Striate System LO 6.8 Describe the components of the retina-geniculate-striate system.

• • •

This is called the retina-geniculate-striate pathway.

The primary visual cortex is called striate cortex after the stripe seen in a Nissl-stained cross section of lower layer IV; the stripe is composed of the terminals of axons from the lateral geniculate nuclei.

The retinal ganglion cell axons from the nasal hemiretinas decussate via the optic chiasm (they are contralateral); those from the temporal hemiretinas remain ipsilateral, providing redundancy for the system.

b. Retinotopic Organization LO 6.9 In the context of the retina-geniculate-striate system, explain what is meant by retinotopic.

The most important feature of visual cortex organization is its retinotopic layout; the surface of the visual cortex is a map of the retina demonstrated when Dobelle et al. (1974) stimulated the visual cortex of patients, who were blind from peripheral damage, with an array of electrodes. The patients saw a pattern of light that corresponded to the pattern on the cortex of electrodes that were simultaneously activated.

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c. The M and P Channels LO 6.10 Describe the M and P channels.

The retina-geniculate-striate system includes two largely independent channels: the P pathway and the M pathway.

• Parvocellular layers (P layers) are found in the top four layers of each lateral geniculate nucleus (LGN) and are composed of small-body neurons (parvo means “small”); they are responsive to color, fine detail patterns, and react to slow or stationary objects.

• Magnocellular layers (M layers) are found in the bottom two layers of the LGN, are composed of large-body neurons (magno means “large”), and are responsive to rods and movement.

4. Seeing Edges (see Figures 6.14 and 6.15 in Biopsychology) • Edges are the most important stimuli in our visual world; they define the position and extent of things.

• Edge perception is the perception of a contrast between two adjacent areas of the visual field; this lecture will focus on how the visual system controls brightness contrast. a. Lateral Inhibition and Contrast Enhancement LO 6.11 Explain the neural basis of contrast enhancement.

• • • •

The perception of edges is so important that there is a mechanism in the visual system that enhances our perception of brightness contrast; this is called contrast enhancement, thus what we see is even better than the physical reality.

The Mach bands illusion is the result of contrast enhancement. In it, light areas that are near the border with a dark region appear lighter than they really are, and the area of the dark region that lies along this border looks darker than it really is.

The mechanisms of contrast enhancement were studied in the eye of the horseshoe crab because of its simplicity; it is a simple compound eye, with each of its individual receptors (ommatidia) connected by a lateral neural network (the lateral plexus).

When an ommatidium is activated, it inhibits its neighbors via the lateral plexus. Contrast enhancement occurs because receptors near an edge on the dimmer side receive more lateral inhibition than receptors on the dimmer side further away from the edge, while receptors near the edge on the brighter side receive less lateral inhibition than the receptors on the brighter further away from the edge.

b. Receptive Fields of Visual Neurons LO 6.12 Describe the methods used by David Hubel and Torsten Wiesel to map the receptive fields of visual system neurons, and define the term receptive field.

• • •

In the late 1950s, Hubel and Wiesel developed a method that became the standard method for studying visual system neurons.

Visual stimuli are presented on a screen in front of a curarized subject (usually a cat or a monkey); the image is artificially focused on the retina by an adjustable lens in front of the eye (because the ciliary muscles are curarized).

Once an extracellular electrode is positioned in the neural structure of interest, so that it is recording the action potentials of only one neuron, the neuron’s receptive field is mapped; the receptive field of a neuron is the area of the visual field within which appropriate visual stimuli can influence the firing of that neuron.

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Biopsychology, Tenth Edition •

Once the receptive field is defined, the task is to discover what particular stimuli presented within the field are most effective in changing the cell’s firing.

c. Receptive Fields: Neurons of the Retina-Geniculate-Striate System (see Figures 6.16–6.17 in Biopsychology) LO 6.13 Describe the characteristics of the receptive fields of retinal ganglion cells, lateral geniculate neurons, and striate neuron of lower layer IV. •

• •

•

Most retinal ganglion cells, lateral geniculate nucleus neurons, and neurons in lower layer IV of the striate cortex have similar receptive fields: They are smaller in the foveal area, circular, monocular, and they have both an excitatory and an inhibitory area separated by a circular boundary.

Neurons in these regions have two patterns of responding: (1) on firing or (2) inhibition followed by off firing.

The most effective way to influence the firing of these neurons is to fully illuminate only the “on area” or the “off area” of its receptive field. If one light is shone in the “on area” and one is simultaneously shone in the “off area,” their effects cancel one another out by lateral inhibition. These neurons respond little to diffuse light.

In effect, many neurons of the retina-geniculate-striate pathway respond to brightness contrast between the centers and peripheries of their visual fields.

d. Receptive Fields LO 6.14 Describe the characteristics of the receptive fields of simple and complex cells.

Simple Cortical Cells (see Figure 6.18 in Biopsychology) • Simple cortical cells in the striate cortex have receptive fields like those that were just described, except that the two areas of the receptive fields are divided by straight lines.

• These cells respond best to bars or edges of light in a particular location in the receptive field and in a particular orientation (e.g., 45º).

• All simple cells are monocular.

Complex Cortical Cells • Most of the cells in the striate cortex are complex cells; they are more numerous, but are like simple cells in that they respond best to straight SP-line stimuli in a particular orientation; they are not responsive to diffuse light.

• Complex cells are unlike simple cells in that the position of the stimulus within the receptive field does not matter; the cell responds to the appropriate stimulus no matter where it is in its large receptive field.

• Over half of the complex cells are binocular, and about half of those that are binocular display ocular dominance. e. Organization of Primary Visual Cortex LO 6.15 Describe the organization of the primary visual cortex.

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Hubel and Wiesel reached 3 important conclusions: – Neurons are organized into vertical “columns” where each neuron responds to stimuli from the same part of the retina.

– Related columns are “clustered” together. Half of a cluster receives input from the left eye, the other half from the right eye.

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Preferred stimuli in neurons becomes increasingly complex from retina to thalamus to primary visual cortex.

Changing Concept of Visual Receptive Fields: Contextual Influences in Visual Processing LO 6.16 Describe the changing view of visual system receptive fields.

• • •

Research based solely on the study of reactions to simple stimuli cannot provide a complete explanation of how the visual system works. Receptive field properties depend on the scene in which the stimuli to its field are embedded.

Each eye movement changes the scene or “contextual influences” that are outside of a neuron’s receptive field A visual neuron’s receptive field is not hardwired but a plastic property that is fine-tuned by context.

5. Seeing Color (see Figures 6.19–6.20 in Biopsychology) a. Component and Opponent Processing LO 6.17 Describe the component and opponent-process theories of color vision.

• •

This is also called trichromatic theory; first proposed in 1802 by Thomas Young and refined by von Helmholtz in 1852.

Component processing occurs at the receptor level.

Key Idea: One of three different photopigments coats each cone; each photopigment reacts optimally to a particular part of the spectrum of electromagnetic energy; the ratio of cones activated at a particular part of the color spectrum creates a summed stimulus and thus color differentiation.

• •

The opponent processing theory was first proposed by Hering in 1878.

Opponent processing occurs at all levels of the visual system beyond the receptors.

Key Idea: Three classes of cells: One that becomes more active to red and less active to green; one that becomes more active to blue and less active to yellow; and one that becomes more active to bright and less active to dark areas.

•

With regard to color vision, red-green and blue-yellow opponent cells fire in response to input from cones; when red cells are “on,” one cannot see green, and when yellow cells are “on,” one cannot see blue.

b. Color Constancy and the Retinex Theory LO 6.18 Describe Land’s demonstration of color constancy, and explain his retinex theory.

• • • •

This is the tendency for an object to be perceived as the same color despite major changes in wavelengths of light that it reflects.

Perception of color constancy allows objects to be distinguished in a memorable way.

Land demonstrated in his 1977 experiments that the color of objects is not a simple relationship with the wavelength being reflected, but depends partly on the light reflected by surfaces surrounding the objects.

Land’s retinex theory of color vision follows the premise that the color of an object is determined by its reflectance, and the visual system calculates the reflectance of surfaces by 10 ..

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comparing the ability of a surface to absorb light in the three bandwidths corresponding to the three classes of cones.

Dual-opponent cells provide the means to analyze contrast between wavelengths reflected by adjacent areas of their receptive fields.

6. Cortical Mechanisms of Vision and Conscious Awareness (see Figures 6.21–6.27 in Biopsychology) • The occipital cortex and large parts of parietal and temporal lobe cortex is visual cortex.

• Primary visual cortex is located in the occipital lobe, secondary visual cortex is located in the prestriate cortex (surrounds primary visual cortex), and the inferotemporal cortex, and most of visual association cortex, is posterior parietal cortex. a. Three Different Classes of Visual Cortex LO 6.19 Describe the three classes of visual cortex, and identify their locations in the brain.

• • •

The primary visual cortex receives most of its input from the visual relay nuclei of the thalamus.

The secondary visual cortex receives its input from the primary visual cortex.

The visual association cortex receive input from areas of secondary visual cortex and from secondary areas of other sensory systems.

b. Damage to Primary Visual Cortex: Scotomas and Completion LO 6.20 Explain what happens when an area of primary visual cortex is damaged.

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• • •

•

Individuals with damage to primary visual cortex have scotomas or areas of blindness in the corresponding areas of the visual field; scotomas are plotted by a perimetry test.

Many patients with large scotomas are unaware of them: For example, patients with the complete destruction of the left striate cortex cannot detect stimuli in their right visual fields (they are hemianopic), yet when they stare at a face, or even half a face, that falls entirely in their left visual field, they report seeing an entire face.

This phenomenon is called completion.

Amazingly, when forced to guess, some brain-damaged patients can respond to stimuli in their scotomas (e.g., can grab a moving object or guess the direction of its movement), all the while claiming to see nothing; this is called blindsight.

Blindsight is thought to be mediated by visual pathways that are not part of the retinageniculate-striate system; for example, one hypothesis is that the retina-geniculate-striate system mediates pattern and color perception, whereas a system involving the superior colliculus and the pulvinar nucleus of the thalamus mediates the detection and localization of objects in space.

This phenomenon emphasizes that parallel models (multiple-path models), rather than serial models (single-path models), are needed to explain many perceptual phenomena.

c. Functional Areas of Secondary and Association Visual Cortex LO 6.21 Describe the areas of secondary visual cortex and association cortex involved in vision.

• •

Secondary visual cortex and the portions of association cortex that are involved in visual analysis are both composed of different areas, each is specialized for a particular type of visual analysis.

Using PET, fMRI, and evoked potentials, researchers have delineated about a dozen different functional areas of the human visual cortex.

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d. Dorsal and Ventral Streams LO 6.22 Explain the difference between the dorsal and ventral streams, and the functions that have been attributed to each stream by different theories.

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• • • •

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Visual information is believed to flow along two anatomically and functionally distinct pathways: – A dorsal stream, with information flowing from primary visual cortex through the dorsal prestriate secondary visual cortex to association cortex in the posterior parietal region.

– A ventral stream, with information flowing from primary visual cortex through the ventral prestriate secondary visual cortex to association cortex in the posterior parietal region.

Traditionally, the dorsal stream was believed to be involved in the perception of where objects are (a where system) because neurons here appear to respond to spatial location or movement.

The ventral stream was believed to be involved in the recognition of that object (a what system) because neurons here respond to different classes of objects.

The “where” vs. “what” theory is supported by observations of patients who suffer damage to the posterior parietal cortex or inferotemporal cortex.

More recently, Milner and Goodale (1993) have proposed that the dorsal stream is actually involved in directing behavioral interactions with objects (which would include, but not be restricted to, analyses of where objects are, a behavioral control path), while the ventral stream is responsible for the conscious recognition of objects (a conscious perception path).

The “behavioral control” vs. “conscious perception” theory is supported clinical observations of patients who retain visual control of movement but lose conscious awareness or vice versa.

e. Prosopagnosia LO 6.23 Describe the phenomenon of prosopagnosia and discuss the associated theoretical issues.

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•

•

• •

Agnosia is a failure to recognize that is not attributable to a simple sensory deficit, or to motor, verbal, or intellectual impairment (gnosis means “to know”); the case of Dr. P., the man who mistook his wife for a hat, is a classic example of visual agnosia.

Prosopagnosia, the inability to recognize faces, is the most interesting and controversial form of visual agnosia; prosopagnosics can readily recognize objects (chairs, tables, hats), but they have extreme difficulty telling one face from another. A prosopagnosic may even fail to recognize her or his own face in a mirror.

The existence of prosopagnosia has led to the view that there is a special area in the brain for the recognition of faces and that it is damaged in prosopagnosics; the finding of neurons in the inferotemporal cortices of macaque monkeys that appear to respond only to conspecific faces supports this view.

However, reports that a farmer who suffered from prosopagnosia also lost his ability to recognize specific species of cows, suggesting that prosopagnosia may not be specific to faces; prosopagnosics may have difficulty distinguishing between visually similar members of complex classes of visual stimuli, of which faces are simply the most obvious class.

Prosopagnosia is associated with damage to the ventral stream, in an area between the occipital and temporal lobes called the fusiform face area.

Recall the hypothesis that the ventral stream is a region involved in conscious perception; this idea led Tranel and Damasio (1985) to search for evidence that prosopagnosics had lost the ability to consciously, but not unconsciously, recognize faces. Indeed, they found that prosopagnosics responded to familiar faces with a huge change in skin conductance, even though they claimed not to recognize the photographs.

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Researchers have subsequently discovered different areas in the ventral stream that respond to houses or cats. These areas appear to alternate with regions most activated by the sight of humans, perhaps accounting for reported difficulties in observing cases of agnosia specific to any one class of visual stimulus.

It seems likely that prosopagnosia is not a unitary disorder; it appears that only some patients have pattern recognition deficits restricted to facial recognition.

Akinetopsia LO 6.24 Describe the phenomenon of akinetopsia and discuss the associated theoretical issues.

• • • • •

Akinetopsia is a deficiency in the ability to see movement progress in a normal smooth fashion.

It can be triggered by high doses of certain antidepressants.

It is often associated with damage to the medial temporal area (MT), near the junction of the temporal, parietal, and occipital lobes.

Sometimes the MT is called V5, or MT/V5.

The following four lines of research have implicated the MT in the perception of movement: – Patients with damage akinetopsia tend to have unilateral or bilateral damage to movement.

– As measured by fMRI, activity in the MT increases when humans view movement.

– Blocking activity of the MT with TMS produces motion blindness.

– Electrical stimulation of the MT induces visual perception of motion.

< Return to Table of Contents

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Chapter 6: The Visual System

LECTURE LAUNCHERS Lecture Launcher 6.1: The Snellen Eye Chart All of your students will be familiar with the Snellen eye chart (a version can be downloaded and printed from http://www.i-see.org/. Once on the homepage, click “Eye Charts” and click on the “Snellen Eye Chart” link. Many students may not really know what “20/20 vision” means—a shortcoming you can use to open your discussion of the visual system. If you have 20/20 vision, you are able to read the line labeled “20” from a distance of 20 feet, and thus your vision is normal. If you can read lines with a lower number, you have better-than-normal vision. Alternatively, if you can only see the top line (labeled “200”) clearly from 20 feet away, you have 20/200 vision (you have to be 20 feet from the chart to see what most people see from 200 feet away), and you are legally blind.

Lecture Launcher 6.2: Transduction at Rods and Cones Students often have a hard time understanding the concept of transduction and how a photon can be transduced into a hyperpolarization of the rods. The animation can be found by going to http://sites.sinauer.com/ and placing “Neuroscience Purves” in the search bar. Select the Fifth Edition of the Purves Book by clicking on the picture of the book. Page down that webpage and click on the file folder labeled “resources” toward the bottom of the page. Once there, click on the link for the student companion site for the book. From that page select Chapter 11 and animations to get to the animation on transduction.

This animation will help you to walk students through the steps of transduction.

Lecture Launcher 6.3: Negative After-Effects—Put the Fish in Its Bowl Some of the best classroom visual illusions are based on negative after-effects and color vision. The site by Eric Chudler (http://faculty.washington.edu/) provides one such illustration. Once you arrive at the homepage for Washington faculty, place “Chudler Fish in a Bowl” in the search bar. Select the matching result. You can use this to introduce the idea of negative after-effects and tee up your discussion about component versus opponent process theories of color vision.

Lecture Launcher 6.4: A Veritable Melange of Illusions Lectures on sensation and perception always benefit from the fact that the brain often embellishes the physical world when it is interpreting the sensory information that it receives. You can illustrate this idea early by sharing some of the illusions available at PBS’s “Secret Life of the Brain” site. To find the site, place “Secret Life of the Brain” in your browser search bar and click on the result that identifies it as part of the PBS series. Once on the site, select “Mind Illusions” from the clickable links on the homepage. In particular, the illusion based upon Lincoln’s face works very well in a class.

Lecture Launcher 6.5: Biology versus Learning Vision is an excellent subject to use to discuss the difference between the biology of behavior and the role of learning or experience. Students are fascinated with the idea of recovered vision. You can describe the case study from Oliver Sacks’ book.

Reference Sacks, O. W. (1995). An Anthropologist on Mars: Seven Paradoxical Tales. Knopf Canada. Ch. 4: To See and Not See. Lecture Launcher 6.6: Visual Aids This course needs visual aids for students to master the physical relationships of structures. Use as many diagrams and models as you can for the course. With the eye, this is more essential as students may feel that they know more about the eye than the brain, but their real understanding may be very superficial.

(Some of my students do not think about the fact that the pupil is actually a hole!) While it is apparent that 14 ..

Biopsychology, Tenth Edition damage to the visual system can lead to blindness, the more subtle forms of visual impairment may not be as obvious to them.

One way to cover the structures of the eye is to follow the path of light through the various structures to the areas of cortex in the brain. At each point, after describing the structure and its function, ask the students: “How could this structure be damaged?” Then ask: “What would happen to your vision if this structure was damaged or missing?”

Lecture Launcher 6.7: The Experience of Macular Degeneration Tying the text content to human experience brings the content to life. Begin the lecture by asking students if they know anyone with some type of vision problem. You may even have students in the class who can relate to something more rare than near or far sightedness.

For many people without vision problems, either you can see (with or without correction) or you are blind.

They may not be aware of some of the more subtle differences in visual perception that can indicate a problem or pose difficulties for someone with a disorder such as macular degeneration.

Ask the students to imagine what macular degeneration might be like. Then compare their comments to some of the examples from people who experience this problem.

This list of descriptions points out some of these more subtle distortions. For example: “Visual Distortion: ‘I see wavy words, and the letters vary in size and look like they are distorted like in a funhouse mirror.’ Damage to the retina may result in distortion and wavy vision due to the stretching and distortion to the retinal layers. Imagine you are projecting slides onto a screen when someone wrinkles the screen.”

“Come and Go Vision: ‘Now I see it. Now I don’t.’ Macular degeneration patients develop small areas of vision loss or blindness. They may see an object when it falls on the peripheral retina. Then as they attempt to look straight at the object, the image falls inside the blind spot and it disappears. During reading, parts of the words may fall inside the blind spots, causing parts of the word to suddenly disappearing.”

“Photostress: ‘When I come in out of the sun, I don’t see well. Things look dark.’ Photostress is a term used to describe bleaching out of the chemicals in the rods and cones. These chemicals are created to react to light and thus create vision. Outside in bright sun, the light exposure uses up the chemicals.

Unfortunately, the damaged retina may be unable to rapidly produce new chemicals and vision may seem to decrease or dark spots may appear. This is the same process we all experience when someone takes a flash picture of us, and we see a dark afterimage for a short period. Unfortunately, in macular degeneration the spot or decrease in vision may last much longer.”

“Better Vision at Night: ‘I see much better at night!’ The majority of the rod cells are located in the peripheral retina and are thus unaffected by macular degeneration. Rod cells function in lower levels of light allowing the patient to have better vision.”

“The Paradox of Peripheral Vision Sensitivity: ‘I see a tiny speck of paper on the floor, but I can’t seem to recognize faces.’ The peripheral retina is very sensitive to small objects and relative motion. With the central retina damaged, the patient may not be able to see faces straight ahead while seeing stars, lint on a shoulder or speck of paper on the floor, because they are picked up in the peripheral retina or side vision. If they try to look straight at the object, it may disappear just as words or other objects do.

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Chapter 6: The Visual System Family members often mistake this ability as an indication that the patient can see better than he or she claims.”

At this point, the students will probably be asking questions about the disorder, how it is treated, and more importantly, how the brain might deal with this problem. This makes a good lead-in to the pathways responsible for central or cone vision.

Web Link 6.4 The Many Visual Problems of Macular Degeneration Lecture Launcher 6.8: Complementary Colors and Opponent Processing Theory To be able to make sense of opponent processing theory, a student needs to understand the concept of complementary colors and color illusions or after-images. While most of us have a few examples of simple images with reversed colors from other courses, it is often a good idea to help students to see that what they are learning could be used outside the classroom. How could the knowledge they are gaining be used to entertain? Do people who are not scientists actually use this information? A fun example is a children’s book called Hello, Red Fox where the illustrations are in complementary colors and white areas are left to view the resulting after-image. Where does opponent processing take place, in the retina or in the brain?

Ask the students to stare at a projected image or a book page to create an after-image. Count to 60 to be sure that the image has plenty of time to get established. Then have the student look at a white field. Can they see the after-image in the complementary colors? Now try this again only view with one eye and test the after-image with the other. Is opponent processing done in the retina or in the brain?

Reference Carle, E. (2001). Hello, Red Fox. Aladdin.

A children’s book called Hello, Red Fox by Eric Carle is a great way to begin the discussion of after-images. In it, the illustrations are in complementary colors and there are white pages designed for viewing the after-image colors.

Lecture Launcher 6.9: Colorblindness Another Book Chapter/Video that can be used effectively to begin a conversation is Sacks’ Island of the Colorblind.

“Knut Nordby and his two siblings were born without the ability to see color. Declared legally blind as a child and sent to a school to learn Braille, Knut rebelled. By developing mental compensations, he taught himself to lead a normal life and today is a researcher specializing in color vision at the University of Oslo. In this program, Knut travels with neurologist/author Oliver Sacks to the tiny coral atoll in Micronesia called Pingelap, where almost 10 percent of the population are congenitally colorblind. Together, they set up a clinic and interview residents to learn about life in a society of people where so many have never seen the world in color.”

You may wish to show the class how color blindness is tested and offer to test the class or refer them to an online version of a color blindness test. I have occasionally detected colorblind students who did not know that they were colorblind, though most know they have a problem, although they might not know the specific terms to describe it.

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Biopsychology, Tenth Edition Students may want to know why it is important to detect or know about color blindness since it cannot be treated with glasses or contact lenses, or even surgery. A current application comes when designing a Web site. The colored text and background may be quite attractive and visible to the creator, but impossible to read for a colorblind individual. This is illustrated well in a Web site that allows you to determine text and background colors and then select a type of color blindness to see the effects.

Reference Sacks, O. W. (1988). Island of the Colorblind. Vintage Books.

“An exploration of a society where total congenital colorblindness is the norm, this book is also a meditation on islands and the strange neurological malady on Guam which resembles Parkinson’s Disease and Alzheimer’s Disease and may provide a key to understanding these diseases. Drawn to the tiny Pacific atoll of Pingelap by intriguing reports of an isolated community of islanders born totally colorblind, Dr. Sacks finds himself setting up a clinic in a one-room island dispensary, where he listens to these achromatopic islanders describe their colorless world in rich terms of pattern and tone, luminance and shadow.”

Web Link 6.8 Color Blindness Illustration Lecture Launcher 6.10: The Visual Agnosias The agnosias related to vision are a little difficult for some people to accept. If someone can see, how could he not be able to recognize his own wife?

The use of case studies as supplemental material can help students to understand the fine differences in perception, but sometimes seeing a person with such a disorder has much more of an impact. YouTube has many excellent videos on this topic. You can also describe some of the cases from one of Oliver Sacks’ books.

References Sacks, O. W. (1995). An Anthropologist on Mars: Seven Paradoxical Tales. Knopf Canada. Ch. 4: To See and Not See. Sacks, O. W. (1985). The Man Who Mistook His Wife for a Hat and Other Clinical Tales. Summit Books. Ch. 8: Eyes Right! < Return to Table of Contents

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Chapter 6: The Visual System

ACTIVITIES Activity 6.1: Free Cocktail Sausage The “Check It Out” activity on page 137 of Biopsychology is a great example of binocular disparity. Walk the students through this visual illusion using the instructions presented in that activity.

Activity 6.2: Blind Spot Students are often fascinated by their first experience with their own blind spot. You can use the “Check It Out” activity on page 140 to illustrate this to them; however, this would necessitate having each student bring their textbook to class. Alternatively, you can draw your own blind-spot test stimulus on a chalkboard/whiteboard and have several students come up to the board and then slowly step backwards— asking them to state for the class when they have “seen” their own blind spot. As another alternative, you can download and print the blind spot testers (12 per page) available at http://faculty.washington.edu/ and place “Chudler Blind Spots” in the search bar. Print out the testers by selecting “Blind Spot Testers” from the search results and hand these out to the students.

Activity 6.3: Cow Eye Dissection Cow eyes can be ordered from most butcher shops and can be used for an in-class illustration of the anatomy of the eye. For safety reasons, you should probably do this dissection; ideally this dissection would be performed under a document projector system. Some very good instructions about how to perform such a dissection can be found at http://www.exploratorium.edu/. Once on that homepage, place “Cow’s Eye Dissection” in the search bar and select the matching link from the results.

Activity 6.4: Blindsight Demonstration The phenomenon of blindsight is one that intrigues many students, eliciting doubt from many of them. To convince the doubtful, use this demonstration from the folks at Serendip: http://serendip.brynmawr.edu/ Once on the homepage, place “blindsight” in the search bar. Click on the link for “Blindsight: Seeing What You Don’t See.” This is a great demonstration, even in a large class. Bring a student who is a good sport to the front to the class. Go over the instructions with them, let them do a practice round to make sure that they understand the instructions and to give you a chance to adjust the stimulus parameters, and then let them complete 20 to 25 trials before you plot the results. On each trial, have the student fixate on the X and move the mouse for each trial. However, you should code each trial as “z-definitely saw stimulus,” “xmaybe saw the stimulus,” or “c-did not see the stimulus,” based on their verbal responses; this makes it easier for them to keep their eyes fixated on the X. < Return to Table of Contents

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DEMONSTRATIONS Demonstration 6.1: Building a Retina Use sheets of colored paper or craft foam sheets to create a model of the retina. (Use different colored transparency film to use as overheads.) Cut out cells in different colors and in proportional sizes. Ask students to help you to create different areas of the retina with the cells, such as the fovea, peripheral retina, blind spot, or retina with disease characteristics.

Demonstration 6.2: Visual Perimeter Measure the visual perimeter of a student as a demonstration or allow students to work in pairs to measure each other’s perimeter. Students often do not believe that they can detect motion at a point where they are unable to determine the color of the object. They also enjoy seeing that the map that they get is similar to the visual field described in the text. This activity makes the separation of motion and color vision more apparent.

Equipment Stand Perimeter, Schweiger Type < Return to Table of Contents

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Chapter 6: The Visual System

ASSIGNMENTS Assignment 6.1: Predicting the Outcome of Lesions to the Visual System A diagram of the pathways in the visual system can be marked with lesion locations. Students can use their understanding of the transmission of the signal from the retina to the cortex to determine the behavioral or perceptual effects of the lesions.

Handout 6.1 Lesions in the Visual System Assignment 6.2: What If Our Vision Were Tuned to a Different Frequency?

Human vision is in a range of frequencies that are adaptive to our survival. What might we be aware of or what might we miss if: • our vision were only in the infrared range?

• our vision were only in the ultra-violet range?

Assignment 6.3: Analysis of the Visual Environment Describe a visual experience. For example: Looking at a Monet painting or watching the cars drive past your house.

Point out the aspects of the experience that are dependent on the functioning of each part of the visual system.

Assignment 6.4: Connecting Vision Loss to CNS Damage Use the internet to find materials written by and about people with different types of vision loss.

Write a brief report indicating the things that he or she is most uncomfortable with in terms of their vision loss.

• What aspect of vision has he or she lost?

• What types of vision remain?

• How helpful is this residual vision?

• How does this personal experience compare with the descriptions in your text?

• What type of damage is the likely cause of the vision loss? < Return to Table of Contents

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WEB LINKS Web Link 6.1: Netter Medical Images http://www.netterimages.com I learned anatomy with Frank Netter’s drawings, and I still think they’re some of the best available.

Web Link 6.2: Visionary: A Dictionary of Vision Terminology From your web browser, type “Liden Visionary Dictionary” in the search bar. Select the link titled “Visionary-A Dictionary of Terminology in Vision.”

Students seeking definitions of terminology used in vision research will find this site of use. The dictionary entries also include line drawings that explain and reinforce vision concepts.

Web Link 6.3: The Joy of Visual Perception Go to http://www.yorku.ca/ and place “The Joy of Visual Perception” in the search bar. Click on the matching link from the search results.

A Web-based book on vision authored by Dr. Peter K. Kaiser. The book is a mixture of topics on perception and visual neurophysiology. The figures in each section would make excellent additions to any lecture. The section on Master Diagram of the Eye, for example, has a nice line drawing illustrating the various structures of the eye. Other sections include figures on retinal receptors and receptive fields. This site is a resource for faculty looking for figures and artwork and for students who would like a different approach to visual perception.

Web Link 6.4: The Many Visual Problems of Macular Degeneration Go to https://www.macular.org/ and click on the link in the upper left-hand corner that is called “About Macular Degeneration.”

Web Link 6.5: Retina Reference http://www.retinareference.com/ The anatomy of the retina and diseases of the retina are the focus of this site. The site contains some marvelous images of the retina and visual system that would be useful in lectures on vision.

Web Link 6.6: The Neural Organization of the Vertebrate Retina http://webvision.med.utah.edu/ This site contains a comprehensive treatment of the retina. Each segment provides text description, full color images, and QuickTime movies. This site can be used as a faculty reference for vision and as a faculty resource for figures to supplement lecture. The site is appropriate for advanced seminar classes.

Web Link 6.7: Color Blind Homepage http://www.colorvisiontesting.com Multiple resources including testing for color blindness and images of the world from the colorblind eye.

Web Link 6.8: Color Blindness Illustration To find the website you need, place “color vision by Cal Henderson” in your browser’s search bar. Click on the matching link that comes up from your search.

This site uses text and background to demonstrate the effects of color blindness on people’s ability read text.

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Chapter 6: The Visual System Web Link 6.9: Blindsight Demonstration The phenomenon of blindsight is one that intrigues many students, eliciting doubt from many of them. To convince the doubtful, use this demonstration from the folks at Serendip: http://serendip.brynmawr.edu/.

Once on the homepage, place “blindsight” in the search bar. Click on the link for “Blindsight: Seeing What You Don’t See. This site provides an online demonstration of the phenomenon known as blindsight.

Web Link 6.10: Receptive Fields Animation Go to http://www.sumanasinc.com/ and click on “Animation Gallery” from the tabs available at the top of the page. From the Animation Gallery, select “Biopsychology/Neuroscience” from the available links. Once there, select “Receptive Fields of the Retina” from the available animation links.

This site provides an animation of the receptive fields of the retina.

Web Link 6.11: Prosopagnosia: Test My Brain To find the website you need, place “Seven Signs and Symptoms of Face Blindness” in your browser’s search bar. Select the link that is associated with “Test My Brain.”

A website that helps identify classic symptoms of face blindness.

Web Link 6.12: Retinal Implants Go to https://www.technologyreview.com/ and place “vision restoring implants that fit inside the eye” in the search box. Click on the link that matches that name.

An article that describes retinal implants. < Return to Table of Contents

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HANDOUT LIST Handout 6.1 Lesions in the Visual System < Return to Table of Contents

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Chapter 6: The Visual System

Handout 6.1: Lesions in the Visual System Name: ________________________________________ Section: ___________ Date: ___________

The diagram represents the pathways followed by the visual information as it moves from the retina to the striate cortex.1 Identify and describe the effect of a lesion at points: A. B. C. D. E. F.

< Return to Table of Contents 1

Image revised from Gray’s Anatomy: http://www.bartleby.com/107/illus763.html

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7 Mechanisms of Perception: Hearing, Touch, Smell, Taste, and Attention: How You Know the World TABLE OF CONTENTS Chapter-at-a-Glance

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Learning Objectives

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Brief Chapter Outline

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Teaching Outline

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Lecture Launchers

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Activities

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Assignments

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Chapter 7: Mechanisms of Perception

CHAPTER-AT-A-GLANCE

Brief Outline Chapter Introduction (p. 166) 7.1 Principles of Sensory System Organization (pp. 167-169) 7.2 Auditory System (pp. 169–176)

7.3 Somatosensory System: Touch and Pain (pp. 176-184) 7.4 Chemical Senses: Smell and Taste (pp. 184-189) 7.5 Selective Attention (pp. 189–192)

Instructor’s Manual Resources Lecture Launchers 7.1, 7.4, Activity 7.2 Lecture Launcher 7.2, Activity 7.1, Demonstration 7.1, Assignment 7.1 Activity 7.3 Activity 7.4, Demonstration 7.2, 7.3 Lecture Launcher 7.3

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LEARNING OBJECTIVES After completion of this chapter, the student should be able to: LO 7.1 LO 7.2

LO 7.3 LO 7.4 LO 7.5 LO 7.6 LO 7.7 LO 7.8 LO 7.9 LO 7.10 LO 7.11 LO 7.12 LO 7.13 LO 7.14 LO 7.15 LO 7.16 LO 7.17 LO 7.18 LO 7.19 LO 7.20 LO 7.21 LO 7.22 LO 7.23 LO 7.24 LO 7.25

Name and define the three types of sensory cortex.

In the context of sensory system organization, explain what is meant by each of the following terms: Hierarchical organization, functional segregation, and parallel processing. Summarize the current model of sensory system organization.

Explain the relationship between the physical and perceptual dimensions of sound.

Describe the components of the human ear, and explain how sound is processed within its various structures.

Describe the major pathways that lead from the ear to the primary auditory cortex.

Describe the neural mechanisms underlying sound localization.

Describe the organization of auditory cortex.

Describe the effects of damage to the auditory system.

Name some of the cutaneous receptors, and explain the functional significance of fast versus slow receptor adaptation.

Describe the two major somatosensory pathways.

Describe the cortical somatosensory areas and their somatotopic layout.

Name the areas of association cortex that somatosensory signals are sent to, and describe the functional properties of one of those areas.

Describe the two major types of somatosensory agnosia.

Describe the rubber-hand illusion and its neural mechanisms.

Explain why the perception of pain is said to be paradoxical.

Define neuropathic pain and describe some of its putative neural mechanisms.

Describe two adaptive roles for the chemical senses.

Describe the olfactory system.

Describe the gustatory system.

In the context of the gustatory system, explain what is meant by broad versus narrow tuning.

Explain the potential effects of brain damage on the chemical senses.

Describe the two characteristics of selective attention, and explain what is meant by exogenous versus endogenous attention.

Describe the phenomenon of change blindness.

Describe the neural mechanisms of attention.

Describe the disorder of attention known as simultanagnosia.

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Chapter 7: Mechanisms of Perception

BRIEF CHAPTER OUTLINE Lecture Launcher 7.1: A Veritable Melange of Illusions 1. Principles of Sensory System Organization a. Types of Sensory Areas of Cortex b. Features of Sensory System Organization Lecture Launcher 7.2: Auditory Illusions: Rising Tones or Falling Tones…and Random Tunes?

2. Auditory System a. Physical and Perceptual Dimensions of Sound b. The Ear c. From the Ear to the Primary Auditory Cortex d. Subcortical Mechanisms of Sound Localization e. Auditory Cortex f. Effects of Damage to Auditory System 3. Somatosensory System: Touch and Pain a. Cutaneous Receptors b. Two Major Somatosensory Pathways c. Cortical Areas of Somatosensation d. Somatosensory System and Association Cortex e. Somatosensory Agnosias f. Rubber-hand Illusion g. Perception of Pain h. Neuropathic Pain 4. Chemical Senses: Smell and Taste a. Adaptive Roles of the Chemical Senses b. Olfactory System c. Gustatory System d. Broad Tuning vs. Narrow Tuning e. Brain Damage and the Chemical Senses

5. Selective Attention a. Characteristics of Selective Attention b. Change Blindness c. Neural Mechanisms of Attention d. Simultanagnosia < Return to Table of Contents

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TEACHING OUTLINE 1. Principles of Sensory System Organization (see Figures 7.1 in Biopsychology) • We have discussed the visual system from the eye to the striate (primary visual) cortex.

• This lecture will focus on cortical mechanisms involved in the processing of visual and auditory information. a. Types of Sensory Area of Cortex LO 7.1 Name and define the three types of sensory cortex.

• •

Traditionally, sensory-system organization has been viewed according to the following model: input flows from receptors to thalamus, to primary sensory cortex, to secondary sensory cortex, and finally to association cortex.

Primary sensory cortex is the cortex that receives input directly from thalamic sensory relay nuclei; the secondary sensory cortex of a sensory system receives input primarily from the primary sensory cortex of that system; association cortex is cortex that receives input from more than one sensory system.

b. Features of Sensory System Organization LO 7.2 In the context of sensory system organization, explain what is meant by each of the following terms: hierarchical organization, function segregation, and parallel processing.

Summarize the current model of sensory system organization. i. Hierarchical Organization • The major feature of the traditional sensory-system model is its serial and hierarchical organization. Sensory systems are thought to be hierarchical in two ways: (1) sensory information is thought to flow through brain structures in order of their increasing neuroanatomical complexity, and (2) sensation is thought to be less complex than perception.

• The neuroanatomical hierarchy is thought to be related to the functional hierarchy; perception is often assumed to be a function of cortical structures.

• Sensation refers to the simple process of detecting the presence of a stimulus; perception refers to the complex process of integrating, recognizing, and interpreting complex patterns of sensations. The need for this distinction is illustrated by the case of Dr. P., the man who mistook his wife for a hat; he had severe visual perception problems in the absence of disturbances in visual sensation. ii. Functional Segregation • Each of the three levels of the cerebral cortex (primary, secondary, and association) is organized so that different parts of the various structures specialize in different kinds of analysis. iii. Parallel Processing • Sensory systems are organized so that information flows between different structures simultaneously along multiple pathways. iv. Summary Model of Sensory System Organization • It is now clear that sensory systems are characterized by a parallel, functionally segregated, hierarchical organization.

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The question arises: If different types of information are processed in different specialized zones that are found in different structures connected by multiple pathways, how are complex stimuli perceived as an integrated whole? This is known as the binding problem.

2. Auditory System (see Figures 7.2–7.8 in Biopsychology) a. Physical and Perceptual Dimensions in Sound LO 7.3 Explain the relationship between the physical and perceptual dimensions of sound.

• • •

The amplitude, frequency, and complexity of the molecular vibrations of sound are linked to loudness, pitch and timbre.

Fourier analysis is the mathematical procedure for breaking down complex waves into their component sine waves.

Pitch perception is related to fundamental frequencies.

b. The Ear LO 7.4 Describe the components of the human ear, and explain how sound is processed within its various structures.

• • • •

Vibrations in the air are transmitted through the tympanic membrane (ear drum), ossicles (three small bones), and oval window into the fluid of the cochlea.

The vibrations bend the organ of Corti and excite hair cells in the basilar membrane.

The tectorial membrane rests on the hair cells.

The organization of the organ of Corti is tonotopic; higher frequencies excite receptors closer to the oval window, thus with exposure to noise, as well as decrements due to age, damage to the high frequency receptors occurs first.

c. From the Ear to the Primary Auditory Cortex LO 7.5 Describe the major pathways that lead from the ear to the primary auditory cortex.

• • • • •

Unlike the visual system, there is no one major auditory projection from ear to cortex.

Hair cells synapse on neurons whose axons enter the metencephalon and synapse in the ipsilateral cochlear nucleus.

From the cochlear nucleus, some fibers project to the nearby superior olives, which projects to the inferior colliculus via the lateral lemniscus.

From the inferior colliculus, fibers ascend to the medial geniculate nucleus of the thalamus; and from there, fibers ascend to the primary auditory cortex in the lateral fissure.

The projections from each ear are bilateral.

d. Subcortical Mechanisms of Sound Localization LO 7.6 Describe the neural mechanisms underlying sound localization.

•

• •

The superior olives play a role in sound localization; the medial superior olives contain neurons that are sensitive to differences in the time of arrival of a sound at the two ears; the lateral superior olives contain neurons that are sensitive to differences in the amplitude of a sound at the two ears.

The layers of the superior colliculus that receive input from the superior olives are topographically organized.

Much of the research on sound localization has focused on the barn owl because of its amazing ability to localize sounds (it hunts mice by their rustling sounds as they move in the dark).

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e. Auditory Cortex LO 7.7 Describe the organization of auditory cortex.

• • • • •

The primary auditory cortex receives the majority of its input from the medial geniculate nucleus.

Adjacent to the primary auditory area are two other areas. Together these three areas are referred to as the core region.

Surrounding the core region is a band—often called the belt.

Areas of secondary auditory cortex outside of the belt are called the parabelt areas.

Secondary auditory cortex neurons respond best to complex tones.

Organization of Primate Auditory Cortex • The auditory cortex is tonotopically organized.

• In addition, it is organized into functional columns such that neurons in a given column all respond maximally to tones in the same frequency range.

• The primary auditory cortex is poorly understood in comparison to the primary visual cortex.

– Electrophysiology researchers have yet to discover what sort of stimuli will maximally activate neurons in the primary auditory cortex.

What Sounds Should Be Used to Study Auditory Cortex?

• Natural sounds have been shown to elicit the best responses in neurons.

Two Streams of Auditory Cortex • Auditory signals are processed by two large areas of association cortex: prefrontal cortex and posterior parietal cortex.

• The anterior auditory pathway is more involved in identifying sounds whereas the posterior auditory pathway is more involved in locating sounds.

Auditory-Visual Interactions • Sensory system interaction is not merely tagged on after unimodal analysis are complete; sensory system interaction seems to be an early and integral part of sensory processing. It occurs early in the pathway.

Where Does the Perception of Pitch Occur?

• Bendor and Wang suggest that a small area just anterior to primary auditory cortex responds to pitch rather than frequency. Therefore, these cells correctly code pitch when a fundamental frequency is absent. f.

Effects of Damage to the Auditory System LO 7.8 Describe the effects of damage to the auditory system.

Auditory Cortex Damage • Bilateral lesions of auditory cortex do not cause deafness, even if the lesions include secondary auditory cortex.

• Humans with extensive auditory cortex damage often have difficulty localizing brief stimuli or recognizing rapid complex sequences of sounds.

• Subcortical circuits serve a more complex and important auditory function than once assumed.

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Total deafness is rare, occurring in only 1% of hearing-impaired individuals due to the fact that auditory pathways are diffuse and parallel.

Two types exist: those associated with damage to the ossicles (conductive deafness) and those associated with damage to the cochlea or auditory nerve (nerve deafness).

Age-related hearing loss (part of the cochlea is damaged) results in a deficit in perceiving high frequencies. Frequently it is helped by a cochlear implant.

There is hearing loss also associated with tinnitus (ringing of the ears).

3. Somatosensory System: Touch and Pain (see Figures 7.9–7.13 in Biopsychology) • •

The somatosensory system comprises three subsystems: (1) an exteroceptive cutaneous system, (2) a proprioception system (monitors body position), and (3) an interoceptive system (monitors conditions within the body such as blood pressure).

We are going to focus on the exteroceptive cutaneous subsystem, which in turn comprises three somewhat distinct subsystems, which respond to: (1) mechanical stimulation of the skin (that is, to touch), (2) thermal stimulation (temperature), and (3) nociceptive stimuli (surface pain).

a. Cutaneous Receptors LO 7.9 Name some of the cutaneous receptors, and explain the functional significance of fast versus slow receptor adaptation.

•

• • •

There are seven kinds of cutaneous receptors; for example, there are (1) free nerve endings, which provide signals about pain and temperature; (2) Pacinian corpuscles, which are deep fast-adapting touch receptors; (3) Merkel receptors, and (4) Ruffini corpuscles, which are slow-adapting touch receptors.

In general, all cutaneous receptors respond to physical stimuli with altered patterns of ion flow across the neuronal membrane.

Both fast- and slow-adapting receptors contribute to “stereognosis,” the identification of objects by touch.

Tactile sensations are not specific to individual receptors but are produced by multiple receptor mechanisms.

Dermatomes The area of the body that is innervated by the left and right dorsal roots of a given segment of the spinal cord is called a dermatome (“skin slice”); the overlap between adjacent dermatomes means that destruction of a single dorsal root does not produce complete somatosensory loss. b. Two Major Somatosensory Pathways LO 7.10 Describe the two major somatosensory pathways.

The Dorsal-Column Medial-Lemniscus System • The dorsal-column medial-lemniscus system carries information about touch and proprioception to the cortex. The axons of receptors in the skin enter the spinal cord and ascend in the ipsilateral dorsal columns to the dorsal column nuclei, the axons of dorsalcolumn-nuclei cells decussate and ascend in the medial lemniscus to the ventral posterior nucleus (VPN). The axons of VPN cells ascend to the somatosensory cortex.

• Axons from the toes that ascend in the dorsal columns are the longest in the body.

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The other ascending somatosensory pathway.

The anterolateral system carries some crude information about touch, but its primary function is to mediate the perception of pain and temperature.

Axons in the anterolateral system synapse as soon as they enter the cord. The second-order axons decussate immediately and ascend in one of three different anterolateral pathways: 1) the spinothalamic tract, which projects to the ventral posterior nucleus of the thalamus; 2) the spinoreticular tract, which projects to the reticular formation and then to the parafascicular and intralaminar nuclei of the thalamus; and 3) the spinotectal tract, which projects to the mesencephalic tectum.

Mark and his colleagues found that lesions to the VP thalamus produce a loss of somatosensation and sharp pain perception, while lesions to the parafascicular and intralaminar nuclei of the thalamus reduced perception of chronic pain without disrupting cutaneous sensitivity.

c. Cortical Areas of Somatosensation LO 7.11 Describe the cortical somatosensory areas and their somatotopic layout.

• •

The various thalamic nuclei receiving somatosensory information project to: (1) primary somatosensory cortex (SI) in the postcentral gyrus; (2) secondary somatosensory cortex (SII), which is ventral to SI; and (3) to the posterior parietal cortex.

The primary somatosensory cortex is organized somatotopically; it is known as the somatosensory homunculus. Studies by Kaas and others have shown that instead of one homunculus (as indicated by the classic early studies of Penfield), primary somatosensory cortex comprises four parallel somatotopically organized strips, each sensitive to a different kind of somatosensory input.

Effects of Damage to the Primary Somatosensory Cortex • Cortical lesions to the primary somatosensory cortex have only minor effects on tactual sensitivity—mainly on the sensitivity of the hands. This is due primarily to the numerous parallel pathways. d. Somatosensory System and Association Cortex LO 7.12 Name the areas of association cortex that somatosensory signals are sent to, and describe the functional properties of one of those areas.

• •

Somatosensory signals are conducted to the areas of association cortex in prefrontal and the posterior parietal cortex.

Posterior parietal cortex contains bimodal neurons that respond to both somatosensory and visual stimuli.

e. Somatosensory Agnosias LO 7.13 Describe the two major types of somatosensory agnosia.

Large lesions to parietal cortex occasionally produce somatosensory agnosias; for example, astereognosia is the loss of the ability to recognize objects by touch in the absence of defects in somatosensation, and asomatognosia is a loss of the ability to recognize parts of one’s own body (e.g., the case of Aunt Betty; described in Chapter 7 of Biopsychology). f.

Rubber-hand Illusion (see Figure 7.14 in Biopsychology) LO 7.14 Describe the rubber-hand illusion and its neural mechanisms 9 ..

Chapter 7: Mechanisms of Perception

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This illusion can be produced by screening a healthy volunteer’s hand while stroking both the hidden hand and a rubber hand that is placed in clear sight.

Volunteers quickly perceive that the rubber hand is part of their body.

This illusion might be mediated by bimodal neurons (visual and somatosensory) in the posterior parietal and frontal cortices.

g. Perception of Pain LO 7.15 Explain whey the perception of pain is said to be paradoxical.

Lack of Clear Cortical Representation of Pain • Although most people think of pain as bad, it is very adaptive; cases of congenital pain insensitivity rarely survive their teens (e.g., they suffer many burns, lacerations, and joint problems, and any internal disorder such as appendicitis is lethal (see the case of Miss C. in Chapter 7 of Biopsychology)).

• The cortical representation of pain is very complex; SI and SII are both activated by painful stimuli, but removal of both areas does not change the perception of pain.

• Using PET, researchers have found that the anterior cingulate cortex has been consistently implicated in cortical perception of pain; however it appears that this activation is more related to emotional responses to pain rather than the perception of pain.

• Melzack and Wall (1965) were impressed by the ability of emotional and cognitive factors to block pain; they concluded that there must be a circuit descending from the forebrain that can block incoming pain signals (gate-control theory).

• The first direct evidence of such a descending analgesia circuit came from the discovery that stimulation of the periaqueductal gray (PAG) produced analgesia in rats; surgery could be performed under PAG-stimulation-produced analgesia.

• Next, it was discovered that there were receptors for opiate analgesics (e.g., morphine) in the PAG and several other sites; this suggested that the body produced its own opiates (called endogenous opiates or endorphins), and several were subsequently isolated.

• Several lines of evidence led Basbaum and Fields to propose a descending analgesia circuit; the circuit goes from the PAG to the raphé nucleus and then descends via the dorsal columns to the dorsal horns of the spinal cord.

• The absence of pain has been linked with a gene that influences the synthesis of the sodium ion channels. This discovery could lead to the creation of a new generation of analgesics. h. Neuropathic Pain LO 7.16 Define neuropathic pain and describe some of its putative neural mechanisms.

• • •

Neuropathic pain is severe and chronic pain in the absence of a recognizable pain stimulus.

It typically develops after the injury.

Glial cells are thought to trigger hyperactivity in neural pain pathways.

4. Chemical Senses: Smell and Taste (see Figures 7.18–7.20 in Biopsychology) a. Adaptive Roles of the Chemical Senses LO 7.17 Describe two adaptive roles for the chemical senses.

• •

In humans, the main adaptive role of the chemical senses is the evaluation of potential foods.

In other species, pheromones (chemicals that influence members of the same species) may regulate social interactions.

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b. Olfactory System LO 7.18 Describe the olfactory system.

• • •

Smell is an olfactory system response to airborne chemicals; in humans there are about 350 different olfactory receptors, each having its own special receptor protein.

Although there appears to be no organization of receptors at the level of the olfactory mucosa, all receptors having the same receptor protein seem to project to the same area of olfactory bulb (chemotopic mapping).

Olfactory receptor cells are unusual in comparison to receptor cells in one important way: They are created across the lifespan and are constantly being replaced.

Olfactory Pathways from Receptors to Cortex • Transduction of olfactory stimuli occurs in olfactory receptors located in the olfactory mucosa of the upper nasal cavity.

• These cells send their axons through the cribriform plate to synapse on cells in the olfactory bulbs.

• Olfactory receptor axons terminate in discrete clusters of neurons called olfactory glomeruli.

– Each glomerulus receives input from several thousand olfactory receptor cells, all with the same receptor protein.

– There are two glomeruli in each olfactory bulb for each receptor protein.

– Like the other senses, there is evidence of a systematic layout: 1) There is mirror symmetry between left and right bulbs; 2) the glomeruli are sensitive to particular odors and are arranged on the bulbs in the same way in different members of the same species and; 3) the layout is similar in related species.

• Neurons from the olfactory bulb then send axons directly to the piriform cortex (primary olfactory cortex) and amygdala of the temporal lobes (making olfaction the one sensory modality that gains access to the telencephalon without passing through the thalamus).

• These areas project to various parts of the limbic system (which is responsible for the emotional perception of odorants) and to the medial dorsal nucleus of the thalamus.

• The dorsomedial nucleus of the thalamus eventually passes the olfactory information on to the orbitofrontal cortex, where the odor is consciously perceived. c. Gustatory System LO 7.19 Describe the gustatory system.

• •

• • • •

Taste operates in tandem with smell; gustatory receptors are arranged in clusters called taste buds.

The traditional view is that there are five primary tastes and each is associated with a unique receptor: sweet, sour, bitter, salty and umami (meaty). However, many flavors cannot be recreated by combinations of the primary flavors and there are many receptor types and subtypes.

Thirty-three gustatory receptor proteins have been identified: one umami, two sweet, and 30 bitter proteins. These are g-protein-linked receptors.

Salty flavors seem to activate taste neurons by altering neural activity by acting on ion channels directly, rather than through a receptor.

There are taste receptors in the throat, esophagus, and lungs in addition to the mouth.

Gustatory Pathways: – gustatory stimuli are transduced by taste buds on the tongue and oral cavity;

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• •

in each taste bud a single presynaptic cell synapses with the efferent neuron leaving the taste bud—the presynaptic cell integrates the signals from all receptors in the taste bud; – these axons project via the facial nerves (CN VII), the glossopharyngeal nerves (CN IX), and the vagus nerves (CN X) to the solitary nucleus of the medulla; – the solitary nucleus projects to (4) the ventral posterior nucleus of the thalamus; – neurons there relay the gustatory information to (5) primary gustatory cortex (near the facial region of SI) and secondary gustatory cortex (found deep in the lateral fissure).

The projections of the gustatory system appear to be largely ipsilateral, unlike the other sensory systems examined.

Coding in the gustatory cortex is complex and broadly tuned because neurons there respond to odor, texture, temperature, and satiation in addition to taste.

d. Broad Tuning Versus Narrow Tuning LO 7.20 In the context of the gustatory system, explain what is meant by broad versus narrow tuning.

• • • • •

The archaic five-primary component processing theory of taste implied that each gustatory receptor and neuron was broadly tuned (responds to many tastes).

More recent research actually suggest they are narrowly tuned (respond to only one stimulus).

Presynaptic cells seem to integrate the signals from all the receptive cells in its taste buds leaving presynaptic cells broadly tuned.

Primary cortex is broadly tuned and responds to odor, texture, and temperature.

Secondary cortex signals the pleasantness of food and satiety.

e. Brain Damage and the Chemical Senses LO 7.21 Explain the potential effects of brain damage on the chemical senses.

• •

Anosmia is an inability to smell, commonly caused by damage to the olfactory nerves passing through the cribriform plate—also linked to epilepsy, Down Syndrome, Parkinson’s disease, multiple sclerosis, and other neurodegenerative disorders.

Ageusia is an inability to taste; it is rare, but may be caused by damage to the facial nerve.

5. Selective Attention a. Characteristics of Selective Attention LO 7.22 Describe the two characteristics of selective attention, and explain what is meant by exogenous versus endogenous attention.

• • •

Selective attention allows us to consciously perceive just a fraction of what we unconsciously sense.

May be top-down or bottom-up.

May be focused by internal cognitive processes (endogenous attention; believed to be topdown) or by external events (exogenous attention; believed to be bottom-up).

b. Change Blindness (see Figure 7.21 in Biopsychology) LO 7.23 Describe the phenomenon of change blindness.

Change blindness is a classic example of the effects of selective attention; it can be demonstrated by alternately showing subjects two pictures that are identical in every aspect but one. If there is a brief delay between each picture, subjects often take a long time to spot what becomes an obvious difference between the pictures once they are attending to the right location.

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c. Neural Mechanisms of Attention LO 7.24 Describe the neural mechanisms of attention.

• • • •

Work in both human and nonhuman primates has revealed that different parts of the brain mediate attention to different types of stimuli; for example, faces activate the ventral visual pathway, while the position of that face activates the dorsal visual pathway.

Top-down processing may originate in the prefrontal lobe and the posterior parietal cortex.

Selective attention is believed to work by strengthening the representation of attended-to stimuli and weakening the representations of the remaining stimuli.

Spatial attention can induce plastic changes to the visual fields of neurons, shifting them toward objects of current focus.

d. Simultanagnosia LO 7.25 Describe the disorder of attention known as simultanagnosia.

• •

Visual simultanagnosia is a difficulty in attending visually to more than one object at a time.

This is due to damage to the posterior parietal cortex.

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LECTURE LAUNCHERS Lecture Launcher 7.1: A Veritable Melange of Illusions Lectures on sensation and perception always benefit from the fact that the brain often embellishes the physical world when it is interpreting the sensory information that it receives. You can illustrate this idea early by sharing some of the illusions available on PBS’s “Secret Life of the Brain” site. To reach the site, place “Secret Life of the Brain” in your web browser and click on the matching link that comes up from your search. In particular, the illusion based upon Lincoln’s face works very well in a class. To reach the Lincoln face demonstration, click on “Mind Illusions” on the homepage. On the bottom right-hand corner, there will be a picture of Lincoln’s face that you can click to lead you to the demonstration.

Lecture Launcher 7.2: Auditory Illusions: Rising Tones or Falling Tones…and Random Tunes?

It is easy to find scads of good visual illusions, but much harder to get auditory ones that work (at least to my ear). Here are some that work just fine in a class setting, from a Web site maintained by Dr. Diana Deutsch at UCSD (Go to http://philomel.com/ and click on the link for “musical illusions and paradoxes.”

In particular, try the Tritone Paradox and the Mysterious Melody Illusion. The only potential glitch is trying to explain the music theory to your students beyond what the Web site provides, unless you are musically inclined. (I usually rely on having at least one student who can tell the class what an octave and a chromatic scale are.)

Lecture Launcher 7.3: Find the Difference The phenomenon of change blindness makes for some fantastic in-class demonstrations. Those demonstrations can also be made into a game by asking two students to compete in spotting the difference.

Go to http://www.cogsci.uci.edu/ and place “change blindness” in the search bar on the homepage. Click on the link with the matching name.

Lecture Launcher 7.4: Covering the Senses In the limited class time available to cover a single chapter, there is not enough time to cover all of the detail in the chapter or even address a single sense in detail. Since vision is covered in more detail in the last chapter, building on it by making comparisons to what was learned there can be useful. It may also be appropriate to use activities to reinforce the concepts that you would like to emphasize. < Return to Table of Contents

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ACTIVITIES Activity 7.1: Building An Ear Sometimes even college students need an opportunity to act a little silly. Assign students to play the roles of various structures in the ear, such as the pinna, eardrum, ossicles, hair cells, etc. Have them stand together to construct a working ear. You can then stand near the pinna and introduce sound stimuli that are soft or loud and high or low pitch and have the students respond, conducting the sound through the structures. Ask students who are not part of the ear to provide “coaching,” correcting improper conduction sequence or making suggestions about how a structure might be best represented.

Pull students out of the model or “incapacitate them” to represent damage to the auditory system.

Warning: The students can get very loud and the class may become a bit chaotic while constructing the “ear” and acting out the responses.

Activity 7.2: Pathways The conduction pathways for the various senses are relatively similar and therefore easily confused. Give students blank diagrams of the brain and brainstem and have them work together in small groups to map the various senses on a single diagram with each pathway marked in a different color.

Activity 7.3: Test for Receptor Density in Different Locations on the Skin The distribution of receptors on the skin is an interesting way to introduce the complexity of body structures and a discussion of the functional relationship between sense receptors and function. Many of the senses are located close to the brain, which facilitates transmission of information to the brain and then out to the motor system to control behavior. The skin receives information for the entire length of the body, but the different receptors transmit information to the brain at different rates, as well as encoding different types of information.

Each student should have a printout of a dermatome map and two toothpicks and a ruler or other measuring device with fine gradations.

Have the students work in pairs, testing different locations on the skin for the two-point threshold for touch/pressure. The experimenter should hold the toothpicks a small distance apart and touch the skin of the subject with either one or both toothpick points. The subject should report when the toothpicks are experienced at one or two locations. When the subject reliably reports two points in a region of skin, the distance is measured and recorded on the dermatome map.

Minimally, the students should check the palm and back of the hand, the fingertip, the cheek, the lower arm, the ankle. They can also choose other areas that they are comfortable testing.

Combine the results on a table posted in front of the class and/or handed out to students.

• • • •

What does this data tell you about the density of touch receptors on the skin?

What might you experience differently because of their distribution?

What areas of the skin would be helpful in sensing fine distinctions in textures?

What skin areas would be best for tolerating painful stimuli?

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Chapter 7: Mechanisms of Perception Activity 7.4: Research on Taste Experience the type of research used to collect information about preferences. Describe the type of controls necessary to prevent expectations from influencing taste. < Return to Table of Contents

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DEMONSTRATIONS Demonstration 7.1: Air vs. Bone Conduction Students sometimes do not believe that sound is conducted through their bones as well as through the ear canal. A simple demonstration can point out the role of bone conduction and help to explain why we do not sound like ourselves when we hear a recording.

You will need a metal coat hanger, string, and a hard object such as a pen or fork. Cut off a length of string about one yard long. Tie the center of the string to the hook of the hanger. Wrap each end of the string around the index finger of your hands and hold your hands up so that the hanger hangs free. Have someone tap the hanger with the pen. It should make a tinny clank. Insert the ends of your index fingers into the respective ear canals, blocking external sound. Stand and bend slightly forward so the hanger is suspended from your fingers. Have someone tap the hanger with the pen. The sound is now deeper and more resonant, like church bells.

Demonstration 7.2: Taste vs. Flavor To illustrate the critical role of olfaction to flavor, have the students try to identify a flavor while holding their nose. Flavored jelly beans are perfect for a mass demonstration. They are relatively inexpensive and everyone can participate. Alternatively, you can have a student place a small (emphasis on small!) amount of powdered cinnamon on their tongue while they hold their nose. They will be unable to identify the flavor until they let go of their nose.

Demonstration 7.3: Smell Relatively cheap smell kits are available through resources like Carolina Biological company and can be used to give students experience with identifying different smells. < Return to Table of Contents

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Chapter 7: Mechanisms of Perception

ASSIGNMENTS Assignment 7.1: Auditory Damage This activity can be used in class or as an assignment. Some types of hearing loss are due to damage to accessory structures in the ear. Describe how hearing might be affected if the damage occurred to the structures listed: pinna, tympanic membrane, ossicles, cochlea, auditory nerve, and eustachian tube. < Return to Table of Contents

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Biopsychology, Tenth Edition

WEB LINKS Web Link 7.1: Exploratorium Exhibits http://www.exploratorium.edu/ This site is a digital version of the popular science museum in San Francisco. In addition to several interesting visual illusions, the site has two modules that are relevant to auditory processing including: Ladle Rat Rotten Hut: This demonstration shows how intonation can radically alter perception of the meaning of a popular childhood fairy tale.

Go to http://www.exploratorium.edu/ and place “Ladle Rat Rotten Hut” in the search bar. Click on the link with the matching name.

Vocal Vowels:This interactive module allows students to select various models that, in turn, create unique sounds.

Go to http://www.exploratorium.edu/ and place “vocal vowels” in the search bar. Click on the link with the matching name.

Web Link 7.2: The Bionic Ear Go to http://www.cardiff.ac.uk/ and place “bionic ear” in the search bar. Click on the link with the matching name.

Compiled by Tim Jacob.

Web Link 7.3: Organ of Corti Go to http://hyperphysics.phy-astr.gsu.edu/ and click on the link to take you to the hyperphysics page. Once there, click on the “index” link on the upper right side of the webpage. A full index will appear on the far right of the page. Scroll down the index until you reach “Organ of Corti” and click on the link. Clear, simple diagrams and links to explanations of the physics of sound.

Web Link 7.4: Promenade ’Round the Cochlea Place “promenade ‘round the cochlea” in your search engine and select the link that shares that name.

Excellent diagrams. Good basic information on sound.

Web Link 7.5: Lumen Learn ’em Go to http://www.medscape.com and place “somatosensory system anatomy” in the search bar. Select the link that shares that name.

An excellent site that features both gross and detailed anatomy of the somatosensory system.

Web Link 7.6: Taste and Smell Go to http://www.nobaproject.com and click on the “browse” link. Then, place “taste and smell” in the search bar on that page to find the webpage dedicated to taste and smell. Select the link that shares that name.

Web Link 7.7: Seeing, Hearing, and Smelling the World Go to http://www.alchemical.org/ and click on the “optics” link. Once you have arrived at that page, page down to link entitled “The Senses” from the Howard Hughes Medical Institute.

An interesting overview of the senses with imbedded glossary for new terms.

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Chapter 7: Mechanisms of Perception Web Link 7.8: The Sense of Taste Place “Kimball Sense of Taste” in your browser’s search bar. Click on the link that is entitled “The Sense of Taste-RCN.” Web Link 7.9: Taste—A Brief Tutorial Place “The Physiology of Taste Jacob” in your browser’s search bar. Click on the link for the article by Tim Jacob.

Web Link 7.10: Olfaction—A Review Go to http://www.leffingwell.com/ and click on the “F&F Reviews” link. At the top of the page is another link called “Olfaction-A Review.”

John C. Leffingwell, Ph.D. Leffingwell & Associates. Current understanding of the physiological basis for olfaction.

Web Link 7.11: Olfaction—A Tutorial on the Sense of Smell Go to http://www.getbodysmart.com/ and click on the “Nervous System” link. Once there, click on the link titled “Sensory System.” From there, click on the link called “Olfactory System.”

A tutorial on the sense of smell.

Web Link 7.12: Rubber Hand Illusion Go to http://science.howstuffworks.com/ and place “Rubber Hand Illusion” in the search bar. Click on the link titled “How could you confuse a rubber hand for your own hand?”

Describes how the rubber hand illusion works. < Return to Table of Contents

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HANDOUT LIST Handout 7.1: Audition: Did You Hear That?

Demonstration to illustrate the difference between sound transmitted through air and sound transmitted through bone.

Handout 7.2: Auditory Damage This worksheet requires the student to figure out how damage to several components of the auditory system would affect hearing.

Handout 7.3: Lesions in Auditory Pathways This worksheet requires the student to predict how damage to the auditory pathways would affect hearing.

Handout 7.4: Skin Senses: Two-Point Thresholds This activity allows the student to compare the density of touch and pressure receptors at different locations on the body.

Handout 7.5: Taste This activity allows students to determine how well we can discriminate similar flavors. < Return to Table of Contents

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Chapter 7: Mechanisms of Perception Handout 7.1: Audition: Did You Hear That?

Objective: Differentiate between sound transmitted through air and sound transmitted through bone.

Materials: String A metal coat hanger A metal fork Instructions: Loop the center of a three-foot piece of string around the handle of the coat hanger. Wrap each end of the string snuggly around one index finger. Suspend the coat hanger from the strings. Have someone sharply hit the coat hanger with the metal fork or other hard object.

Now listen while someone else holds the hanger and you block your ears by inserting your index finger snuggly into the ear canal. Then, holding the hanger again, insert an index finger into each ear. Have someone hit the coat hanger again.

Discussion: The sound produced by the coat hanger is different under the three conditions. When the coat hanger is swinging freely, the sound is carried through the ear through the air. Some sound is also transmitted through the bones of the head.

With your index fingers in your ears, the sound traveling through the ear cannot reach the eardrum. This eliminates air conduction of sound. If someone else is holding the hanger, the sound waves bouncing off of your head can carry sound to the inner ear through the bones of the head.

When you suspend the coat hanger from your own fingers and insert your fingers into your ears, the sound is transmitted both through the bones from the air and also through the bones in your body.

Explorations: Ever wonder why your voice sounds funny in a tape recording? The tape recording allows the air and bone conduction from external sounds, just as when you listen to someone else speaking. When you speak, you also hear the sound of your voice carried through the bones of your head. Your voice probably sounds thinner and less resonant on the tape recording, but this is what others hear.

Try holding the fork low on the handle and striking the end of the fork against a hard surface. Can you hear the tone created? Hold it close to your ear. Then hold the handle of the fork against a tooth or against the bone just in back of your ear. This is another comparison of the difference between bone and air conduction.

Some hearing aids work by magnifying the sounds and creating vibration on this bone. This works if the hearing problem is due to damage in the middle ear and the inner ear is functioning. < Return to Table of Contents

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Biopsychology, Tenth Edition Handout 7.2: Auditory Damage Some types of hearing loss are due to damage to accessory structures in the ear.

Describe how hearing might be affected if the damage occurred to the structures listed: Pinna

Tympanic Membrane

Ossicles

Cochlea

Auditory Nerve

Eustachian Tube

< Return to Table of Contents

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Chapter 7: Mechanisms of Perception Handout 7.3: Lesions in Auditory Pathways It is possible for the nervous system to be injured somewhere in the auditory pathways.

What changes in the ability to hear would you expect to see in someone who has damage as indicated by the black marks labeled on the diagram?

A

B

C

D

E

< Return to Table of Contents

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Biopsychology, Tenth Edition Handout 7.4: Skin Senses: Two-Point Thresholds Objective: Determine the density of touch/pressure receptors on the skin at different locations on the body.

Materials: Two toothpicks Dermatome map Instructions: You will need another student to assist you in this activity.

You will be testing different locations on the skin to determine the two-point threshold for touch/pressure.

The student acting as the experimenter should hold the toothpicks in one hand with the points a small distance apart.

The student subject closes his or her eyes. The experimenter should touch the skin of the student subject with either one or both toothpick points. The subject should report when the toothpicks are experienced at one or two locations. Test each skin area several times.

When the subject reliably reports two points in a region of skin, the distance is measured and recorded on the dermatome map.

Minimally, you should check: • The palm • The back of the hand • The fingertip • The cheek • The lower arm • The ankle You may also choose other areas that you are comfortable testing.

Discussion: What does this data tell you about the density of touch receptors on the skin?

What might you experience differently because of their distribution?

Explorations: What areas of the skin would be helpful in sensing fine distinctions in textures?

What skin areas would be best for tolerating painful stimuli? < Return to Table of Contents 25 ..

Chapter 7: Mechanisms of Perception Handout 7.5: Taste Objective: Experience the type of research used to collect information about preferences.

Describe the type of controls necessary to prevent expectations from influencing taste.

Materials: At least three different brands of the same type of beverage (colas, lemonades, milks, etc.)

Lots of cups, at least one for each beverage per person Information: Most of us have a favorite beverage, french fry, or other food. Can we really tell the difference between this item and other similar products? Marketers try to encourage us to choose a brand and remain loyal to it. They sometimes provide evidence that their product is best by asking individuals to taste their product and a similar product and identify their favorite brand or state a preference. How much do we really know when we have seen a taste test?

Instructions: Cover or remove the labels from several different brands of a product. Label the containers for later identification (e.g., A, B, C).

Give each person taking the taste test twice as many labeled cups as there are products (a, b, c, d, e, f,...).

Put each product in two cups and record the labels for the product and cup.

Prepare a random order for tasting the products by rolling a die or drawing paper slips.

Have each individual taste each product and set the cups on the table with the most preferred product to the left and the least preferred product to the right.

Enter the data on a data sheet similar to the one attached to this description. Calculate the average ranking for each product by adding all of the rankings for the product (A1, A2, A3...) and dividing by the number of rankings.

Discussion: Could people discriminate between the different brands?

Could they identify their “favorite”?

When manufacturers develop a new version of a familiar product, how different do they have to be to compete?

Explorations: Design a study that would allow you to determine whether people can discriminate between different brands of the same type of product.

Could someone be trained to discriminate more accurately? Try to teach someone to discriminate by giving accurate feedback. Then test their discrimination abilities. Did he or she improve?

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PRODUCT

OBSERVER RANKING

AVG

A

B

1 2 3 4 5 6 7 8 9 10

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C

D

E

F

8 The Sensorimotor System: How You Move TABLE OF CONTENTS Chapter-at-a-Glance

2

Learning Objectives

3

Brief Chapter Outline

4

Teaching Outline

5

Lecture Launchers

13

Activities

14

Demonstrations

15

Assignments

16

Web Links

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Chapter 8: The Sensorimotor System

CHAPTER-AT-A-GLANCE

Brief Outline Chapter Introduction (p. 195) 8.1 Three Principles of Sensorimotor Function (pp. 196–198) 8.2 Sensorimotor Association Cortex (pp. 198–201) 8.3 Secondary Motor Cortex (pp. 201–203) 8.4 Primary Motor Cortex (pp. 203–205) 8.5 Cerebellum and Basal Ganglia (pp. 205–206) 8.6 Descending Motor Pathways (pp. 207–210)

8.7 Sensorimotor Spinal Circuits (pp. 210–216) 8.8 Central Sensorimotor Programs and Learning (pp. 216–219)

Instructor’s Manual Resources Lecture Launcher 8.1

Lecture Launcher 8.2 Lecture Launcher 8.3

Lecture Launchers 8.4, 8.5, 8.6, Demonstration 8.1, Assignment 8.1 Activities 8.1, 8.2, Assignment 8.3 Lecture Launcher 8.7, Assignment 8.2

< Return to Table of Contents

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LEARNING OBJECTIVES After completion of this chapter, the student should be able to:

LO 8.1 In the context of the sensorimotor system, explain what hierarchically organized means.

LO 8.2 Explain the important role of sensory input for motor output.

LO 8.3 Describe how learning changes the nature and locus of sensorimotor control.

LO 8.4 Describe and/or draw the general model of sensorimotor Function LO 8.5 Explain the role of the posterior parietal cortex in sensorimotor function, and describe what happens when it is damaged or stimulated.

LO 8.6 Explain the role of the dorsolateral prefrontal association cortex in sensorimotor function, and describe the response properties of neurons in this region of cortex.

LO 8.7 Explain the general role of areas of secondary motor cortex.

LO 8.8 Describe the major features of mirror neurons and explain why they have received so much attention from neuroscientists.

LO 8.9 Describe the conventional view of primary motor cortex function and the evidence upon which it was based.

LO 8.10 Describe the current view of primary motor cortex function and the evidence upon which it is based.

LO 8.11 Describe the structure and connectivity of the cerebellum, and explain the current view of cerebellar function.

LO 8.12 Describe the anatomy of the basal ganglia, and explain the current view of their function.

LO 8.13 Describe the two descending dorsolateral motor pathways of the spinal cord.

LO 8.14 Describe the two descending ventromedial motor pathways of the spinal cord.

LO 8.15 Compare and contrast the two dorsolateral motor pathways and the two ventromedial motor pathways.

LO 8.16 Describe the components of a motor unit, and distinguish between the different types of muscles.

LO 8.17 Describe the receptor organs of tendons and muscles.

LO 8.18 Describe the stretch reflex, and explain its mechanisms.

LO 8.19 Describe the withdrawal reflex, and explain its mechanisms.

LO 8.20 Explain what is meant by reciprocal innervation.

LO 8.21 Explain recurrent collateral inhibition.

LO 8.22 Describe the phenomenon of walking and the degree to which it is controlled by spinal circuits.

LO 8.23 Explain what is meant by a hierarchy of central sensorimotor programs, and explain the importance of this arrangement or sensorimotor functioning.

LO 8.24 Describe the various characteristics of central sensorimotor programs.

LO 8.25 Explain how the classic Jenkins and colleagues PET study of simple motor learning summarizes the main points of this chapter. < Return to Table of Contents

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Chapter 8: The Sensorimotor System

BRIEF CHAPTER OUTLINE Lecture Launcher 8.1: Shooting Sheep 1. Three Principles of Sensorimotor Function a. The Sensorimotor System Is Hierarchically Organized b. Motor Output Is Guided by Sensory Input c. Learning Changes the Nature and Locus of Sensorimotor Control d. General Model of Sensorimotor System Function 2. Sensorimotor Association Cortex a. Posterior Parietal Association Cortex b. Dorsolateral Prefrontal Association Cortex Lecture Launcher 8.2: Remote Control of Mind Over Matter 3. Secondary Motor Cortex a. Identifying the Areas of Secondary Motor Cortex b. Mirror Neurons Lecture Launcher 8.3: Playing Penfield: Stimulating the Motor Homunculus 4. Primary Motor Cortex a. Conventional View of Primary Motor Cortex Function b. Current View of Primary Motor Cortex Function 5. Cerebellum and Basal Ganglia a. Cerebellum b. Basal Ganglia Lecture Launcher 8.4: Reflexive Behavior—Whole Class Participation 6. Descending Motor Pathways a. Dorsolateral Corticospinal Tract and Dorsolateral Corticorubrospinal Tract b. Ventromedial Corticospinal Tract and Cortico-brainstem-spinal Tract c. Comparison of the Two Dorsolateral Motor Pathways and the Two Ventromedial Motor Pathways 7. Sensorimotor Spinal Circuits a. Muscles b. Receptor Organs of the Tendons and Muscles c. Stretch Reflex d. Withdrawal Reflex e. Reciprocal Innervation f. Recurrent Collateral Inhibition g. Walking: A Complex Sensorimotor Reflex 8. Central Sensorimotor Programs and Learning a. A Hierarchy of Central Sensorimotor Programs b. Characteristics of Central Sensorimotor Programs c. Functional Brain Imaging of Sensorimotor Learning < Return to Table of Contents 4 ..

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TEACHING OUTLINE 1. Three Principles of Sensorimotor Function (see Figure 8.1 in Biopsychology) a. The Sensorimotor System Is Hierarchically Organized LO 8.1 In the context of the sensorimotor system, explain what hierarchically organized means.

The sensorimotor system is organized like a large, but effective company; the president (association cortex) issues general commands and lower levels (motor neurons and muscles) take care of the details. The advantage of this hierarchical arrangement is that higher levels are left free to focus on complex functions. b. Motor Output Is Guided by Sensory Input LO 8.2 Explain the important role of sensory input for motor output.

• •

Like a large company, the sensorimotor system carefully monitors the external world and the consequences of its own actions, and it acts accordingly; only ballistic movements (brief, allor-none, high speed movements) are not guided by sensory feedback.

Note the case of G.O., a former darts champion who suffered an infection that destroyed the somatosensory nerves of his arms. Even though he still had visual feedback, he had difficulty picking up buttons or coins, adjusting to unanticipated external forces, and maintaining a constant force (e.g., holding a pen, cup, or suitcase).

c. Learning Changes the Nature and Locus of Sensorimotor Control LO 8.3 Describe how learning changes the nature and locus of sensorimotor control.

• •

As a new company develops, more and more tasks become part of the routine and are taken over by lower levels of the organization; the same thing happens in the sensorimotor system.

After much practice, lower levels perform well-learned tasks with little higher involvement.

Why is the sensorimotor system like a large company in these three important respects? Is it mere coincidence? No, they are both complex behavioral systems that have evolved under the pressure to survive in competitive environments, thus it is not surprising that efficient companies and sensorimotor systems have a lot in common.

d. General Model of Sensorimotor System Function LO 8.4 Describe and/or draw the general model of sensorimotor function.

This chapter focuses on neural structures that play a role in voluntary behavior.

2. Sensorimotor Association Cortex a. Posterior Parietal Association Cortex (see Figure 8.2 in Biopsychology) LO 8.5 Explain the role of the posterior parietal cortex in sensorimotor function, and describe what happens when it is damaged or stimulated.

•

Before an effective response can be initiated, the sensorimotor system must know the positions of various parts of the body and of objects in the external world; current thinking is that the posterior parietal cortex performs these functions.

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•

•

The posterior parietal cortex receives input from visual, auditory, and somatosensory systems (that is why it is considered to be association cortex); most of its output goes to secondary motor cortices.

Electrical stimulation applied to inferior portions of the posterior parietal association cortex of conscious, nonsurgical patients at low currents had patients experiencing an intention to perform a particular action. At high currents, patients felt they actually performed the action.

However, in neither case did the action actually happen.

In addition to disrupting the accuracy of movements, large lesions of the posterior parietal cortex can produce apraxia.

– Apraxia is the inability to perform movements when requested to do so (in the absence of simple sensory or motor deficits, motivational deficits, or intellectual deficits). For example, an apraxic patient may have difficulty demonstrating hammering movements when asked to do so (even when they are demonstrated to him or her), but be perfectly capable of spontaneously hammering a nail.

– Apraxia is almost always associated with left hemisphere damage, but its symptoms are always bilateral.

Patients with contralateral neglect fail to respond to visual, auditory, or somatosensory stimuli from the contralateral half of the body.

– Contralateral neglect is usually produced by very large right parietal lesions.

– Patients with contralateral neglect may shave only the right half of their face, eat food from only the right half of their plate, or put only their right leg in their pants (for example, the case of Mrs. S.).

– Patients with contralateral neglect seem to ignore the left sides of their own body (egocentric left), as well as the left halves of objects regardless of where they are in space.

– However, there is evidence that these patients are capable of unconsciously perceiving objects in the left side of space.

b. Dorsolateral Prefrontal Association Cortex (see Figure 8.3 in Biopsychology) LO 8.6 Explain the role of the dorsolateral prefrontal association cortex in sensorimotor function, and describe the response properties of neurons in this region of cortex.

• • •

Projections to this area are from the posterior parietal cortex; this area projects to parts of the secondary motor cortex, the primary cortex, and to the frontal eye field.

Research suggests that the prefrontal association cortex is involved in assessments of external stimuli; neurons here may be activated by the characteristics of an object, its location, or by the response that the object elicits.

Further research shows that the motor neurons firing the earliest (prior to a motor task) are located in the dorsolateral prefrontal cortex, indicating that this area may work with posterior parietal cortex in decisions regarding voluntary response initiation.

3. Secondary Motor Cortex (see Figure 8.4 in Biopsychology) a. Identifying the Areas of Secondary Motor Cortex LO 8.7 Explain the general role of areas of secondary motor cortex.

•

It has become clear that there are at least eight areas of secondary motor cortex in each hemisphere of the primate brain: two distinct areas of premotor cortex, three distinct areas of supplementary motor area, and three smaller cingulate motor areas. They all send information to primary motor cortex, all receive input from primary motor cortex, all are interconnected with one another, and all send axons to the motor circuits of the brainstem.

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Functionally, each of these areas produces complex movements when stimulated and are activated both before and during voluntary movements. They are active when either side of the body is involved in a movement.

The exact role of each area of secondary motor cortex is not clear.

Premotor cortex neurons often respond to both visual and touch stimuli; thus, premotor areas of secondary motor cortex appear to encode spatial relations of external cues and program movements guided by these cues.

b. Mirror Neurons (see Figure 8.5 in Biopsychology) LO 8.8 Describe the major features of mirror neurons and explain why they have received so much attention from neuroscientists.

• • • •

Mirror neurons are neurons that fire when an individual performs a particular goal-directed hand movement toward a target object or when he/she observes the same goal-directed movement performed by another individual.

This discovery made in the 1990s is so exciting because it might provide a possible mechanism for social cognition (knowledge of the perceptions, ideas, and intentions of others).

At this time, individual mirror neuron recordings have been made only in the macaque monkey.

Functional brain imaging studies in humans have found areas of motor cortex that may contain mirror neurons.

4. Primary Motor Cortex (see Figure 8.6 in Biopsychology) a. Conventional View of Primary Motor Cortex Function LO 8.9 Describe the conventional view of primary motor cortex function and the evidence upon which it was based.

• • • • • •

•

Primary motor cortex is in the precentral gyrus of the frontal lobe. It is somatotopically organized; its organization was discovered by Penfield, who stimulated the cortices of conscious patients during brain surgery.

Recent evidence suggests that there is not a 1:1 relationship between a location on the body and its representation on the motor homunculus; instead, the body is diffusely represented on the homunculus and these representations can sometimes overlap.

The motor homunculus has a disproportionate representation of hands and mouth; in fact, two different areas of each primary motor cortex control the contralateral hand.

Each area of primary motor cortex receives feedback from the muscles and joints that it influences; one of the hand areas receives input from the skin rather than the joints and muscles of the digits; this feedback is presumably important for stereognosis.

Neurons in primary motor cortex seem to code for a preferred direction of movement. They fire most just before and during the movement; they fire most when the movement is in the preferred direction and less as the direction deviates from the preferred one.

Nicolesis and Chapin (2002) trained a monkey named Belle to move a robotic arm (located hundreds of miles away) in accordance with the activity of motor neurons in her primary motor cortex; this feat opens the door for further research on neurally-controlled prosthetic devices.

Effects of Primary Motor Cortex Lesions Lesions of the primary motor cortex produce contralateral astereognosia; they reduce the speed and force of contralateral movements, and they make it difficult to move one body part (e.g., a finger) independently of others. They do not produce paralysis.

5. Cerebellum and Basal Ganglia (see Figures 3.19 and 3.27 in Biopsychology) 7 ..

Chapter 8: The Sensorimotor System • •

The cerebellum and basal ganglia are both important subcortical sensorimotor structures, but neither participates directly in the transmission of signals to the spinal cord.

Their role seems to be to integrate and coordinate the activity of structures at various levels of the sensorimotor system.

a. Cerebellum (see also Chapter 3) LO 8.11 Describe the structure and connectivity of the cerebellum, and explain the current view of cerebellar function.

• • • • •

The cerebellum (means little brain) constitutes only 10% of the brain’s mass, but it contains over half the brain’s neurons; it is organized systematically in lobes.

It receives inputs from primary and secondary motor cortex, from brainstem motor nuclei, and from somatosensory and vestibular systems.

It is thought to correct deviations from intended movements.

Effects of diffuse cerebellar damage include loss of the ability to precisely control movement, adjust motor output to changing conditions, maintain steady postures, exhibit good locomotion, to maintain balance, speak clearly, and control eye movements.

Long-recognized role in motor learning, and more recently appreciated for diverse sensory, cognitive, and emotional responses.

b. Basal Ganglia (see also Chapter 3) LO 8.12 Describe the anatomy of the basal ganglia, and explain the current view of their function.

• •

The basal ganglia are part of a loop that receives information from various parts of the cortex and transmits it back to motor cortices via the thalamus.

Basal ganglia are involved in sequencing of movements; like the cerebellum, its role has recently been expanded to include a variety of nonmotor cognitive tasks.

6. Descending Motor Pathways (see Figures 8.7 and 8.8 in Biopsychology) There are four descending motor pathways on each side of the spinal cord—two descend in the dorsolateral areas of the spinal cord: (1) the dorsolateral corticospinal tract and (2) the dorsolateral corticorubrospinal tract; two descend in the ventromedial areas of the spinal cord: (3) the ventromedial corticospinal tract and (4) the ventromedial cortico-brainstem-spinal tract. a. Dorsolateral Corticospinal Tract and Dorsolateral Corticorubrospinal Tract LO 8.13 Describe the two descending dorsolateral motor pathways of the spinal cord.

• •

• •

Many axons from primary motor cortex descend through the medullary pyramids, decussates, and then continue to descend in the contralateral dorsolateral white matter of the spinal cord.

This is the dorsolateral corticospinal tract.

A second group of axons from primary motor cortex descends to the red nucleus of the midbrain. Axons from the red nucleus then decussate and descend through the medulla; some terminate in the nuclei of the cranial nerves, while others continue to descend in the dorsolateral spinal cord. This is the dorsolateral corticorubrospinal tract.

Most axons in the dorsolateral corticospinal tract and all of those in the dorsolateral corticorubrospinal tract synapse on interneuron pools in the contralateral spinal gray matter that control motor neurons of distal limb muscles.

Betz cells in the primary motor cortex descend contralaterally in the dorsolateral corticospinal tract and synapse on motor neurons that control the large weight-bearing muscles of the legs.

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Primates and a few other mammals capable of individual digit movement have dorsolateral corticospinal tract neurons that synapse directly on motor neurons.

b. Ventromedial Corticospinal Tract and Ventromedial Cortico-brainstem-spinal Tract LO 8.14 Describe the two descending ventromedial motor pathways of the spinal cord.

•

•

•

The axons of the ventromedial corticospinal tract descend ipsilaterally and terminate bilaterally in several segments of the spinal cord on the interneuron pools that control the motor neurons of trunk and proximal limb muscles on both sides of the body; the information delivery is more diffuse and goes to more levels than via dorsolateral paths.

The axons of the ventromedial cortico-brainstem-spinal tract also descend and terminate diffusely in the brainstem on interneurons in the tectum, vestibular nucleus, reticular formation, and the nuclei for the cranial nerves that innervate the face. From here, axons descend in the ventromedial portion of the spinal cord to influence trunk and proximal limb muscles on both sides of the body.

The different functions of these four tracts are demonstrated by the experiment of Lawrence and Kuypers (1968) on monkeys: – First, they cut the dorsolateral corticospinal tracts at the medullary pyramids; the monkeys lost their ability to move individual fingers and to release objects in their grasp (revealing the role of the dorsolateral corticospinal pathway in individual or fine movements of the digits); however, they had no difficulty releasing bars and branches when they were climbing.

– Next all of the monkeys received a second operation: o Half of the monkeys received a dorsolateral corticorubrospinal tract transaction.

These monkeys could stand, walk, and climb normally, but when they sat, their arms hung limply by their sides, and they were used like rubber-handled rakes. Thus, the corticorubrospinal tract seems to control the reaching movements of the limbs. o The other half of the monkeys received a transection of both ventromedial tracts (only their dorsolateral corticorubrospinal tract remained intact). These monkeys had great difficulty walking or even sitting (a noise would make them fall over); when they fed, they did so with elbow and whole-hand movements. Thus, the ventromedial paths seem to be involved with whole-body movements and postural control.

c. Comparison of the Two Dorsolateral Motor Pathways and the Two Ventromedial Motor Pathways LO 8.15 Compare and contrast the two dorsolateral motor pathways and the two ventromedial motor pathways.

• •

•

The similarities between the two are that each is composed of two tracts, one whose axons descend directly to the spinal cord and another whose axons synapse in the brainstem.

The differences between the two are as follows: the ventromedial pathways are more diffuse.

Many axons innervate interneurons on both sides of the spinal cord in several different segments. In contrast, the dorsolateral pathways terminate in the contralateral half of one spinal cord segment.

Another difference is that motor neurons activated by the ventromedial pathways project to proximal muscles of the trunk and limbs, whereas the motor neurons of the dorsolateral pathways project to distal muscles.

7. Sensorimotor Spinal Circuits (see Figures 8.9–8.16 in Biopsychology) 9 ..

Chapter 8: The Sensorimotor System

a. Muscles LO 8.16 Describe the components of a motor unit, and also distinguish between the different types of muscles.

• • • • • •

Review the anatomy of the motor end-plate, the neuromuscular junction, and the role of acetylcholine.

Motor units include a single motor neuron and all of the muscle fibers that it innervates; motor unit size is dependent on the movement accuracy required.

Motor pools include all motor neurons that innervate fibers of a single muscle.

Flexors (bend or flex a joint) vs. extensors (straighten or extend a limb) Synergistic (muscles that produce the same type of movement, either flexion or extension, at a joint) vs. antagonistic (muscles whose actions oppose one another at a joint) Dynamic contraction (one where muscles shorten to produce action at a joint) vs. isometric contraction (one where muscle tension increases, but muscle does not shorten and there is not action at joint).

b. Receptor Organs of Tendons and Muscles LO 8.17 Describe the receptor organs of tendons and muscles.

• •

Golgi tendon organs are embedded in tendons; muscle spindles are embedded in muscles.

Because Golgi tendon organs are connected in series with muscles, they are sensitive to muscle tension. In contrast, muscle spindles are connected in parallel with the muscle fibers and they are sensitive to muscle length.

c. Stretch Reflex LO 8.18 Describe the stretch reflex, and explain its mechanisms.

•

• • • •

You have all had your patellar tendon reflex tested by a doctor. The doctor raps the tendon of your relaxed thigh muscle; this stretches your thigh muscle and elicits an immediate compensatory contraction that makes your foot swing up. The patellar tendon reflex is a stretch reflex.

Notice that this reflex is monosynaptic.

The intrafusal motor neuron adjusts the length of the intrafusal muscle in relation to extrafusal muscle length to maintain the muscle spindle’s sensitivity to changes in extrafusal muscle length.

The function of the muscle-spindle feedback circuit is to make automatic adjustments in muscle tension in response to external forces.

The brain sends general instructions to the motor neurons (e.g., hold the glass of water), and the muscle spindle feedback circuit automatically adjusts the activity in the motor neurons to make sure that this instruction is carried out, even if there are unanticipated external influences (e.g., somebody brushing against the arm).

d. Withdrawal Reflex LO 8.19 Describe the withdrawal reflex, and explain its mechanisms.

•

Sensory neurons carrying signals evoked by a painful stimulus to a hand or foot synapse on interneurons that synapse on flexors of the same limb.

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Thus, about 1.6 milliseconds (the time for a signal to be transmitted across a two synapses) after the painful stimulus, a burst of action potentials can be recorded in the flexor motor nerves of the same limb, and the limb is withdrawn.

The limb is withdrawn before information about the painful event reaches the brain.

e. Reciprocal Innervation LO 8.20 Explain what is meant by reciprocal innervation.

• •

f.

When a muscle contracts, antagonist muscles automatically relax; this is mediated by inhibitory interneurons.

However, there is always some degree of co-contraction, for smoother, more precise movement.

Recurrent Collateral Inhibition LO 8.21 Explain recurrent collateral inhibition.

When a motor neuron fires, an axon collateral feeds onto an inhibitory interneuron in the ventral horn (i.e., onto a Renshaw cell), which synapses on the cell body of the motor neuron that activated it. Thus, motor neurons take an enforced rest after firing; this distributes the workload among the muscle’s motor pool.

g. Walking: A Complex Sensorimotor Reflex LO 8.22 Describe the phenomenon of walking and the degree to which it is controlled by spinal circuits.

• •

Walking is a very complex behavior integrating visual information; somatosensory information from the feet, knees, hips, arms, and so on; and information about balance from the semicircular canals of the inner ear.

This program of complex reflexes must be very plastic; it must adjust its output immediately to changes in the environment.

8. Central Sensorimotor Programs and Learning (see Figures 8.17 and 8.18 in Biopsychology) a. A Hierarchy of Central Sensorimotor Programs LO 8.23 Explain what is meant by a hierarchy of central sensorimotor programs, and explain the importance of this arrangement for sensorimotor functioning.

•

The central sensorimotor program theory suggests that all but the highest levels of the senorimotor system have certain activities programmed into them; complex movements are produced by activating the appropriate combinations of these programs, which are then executed without the need for control from higher levels in the system.

b. Characteristics of Central Sensorimotor Programs LO 8.24 Describe the various characteristics of central sensorimotor programs.

Central Sensorimotor Programs Are Capable of Motor Equivalence • Central sensorimotor programs are capable of motor equivalence; the same task can be solved in different ways. Control of this equivalence appears to be high in the system. For example, you can sign your name using your hand or your foot—in either case, the signatures are very

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•

similar and the secondary motor cortex for the preferred hand is activated (even when the foot signs).

Grillner (1985) showed that coordinated walking movements occurred in cats whose brains had been separated from their spinal cord if the cats were held over a treadmill. This suggests that the programs for some complex motor activities are wired into the spinal cord; these central sensorimotor programs are analogous to the protocols for a procedural automation.

Sensory Information that Controls the Central Sensorimotor Programs Is Not Necessarily Conscious • The sensory information that controls central sensorimotor programs does not have to be consciously perceived.

Central Sensorimotor Programs Can Develop Without Practice • Many complex species-typical behaviors do not have to be practiced for the central sensorimotor programs to develop; however, for many other behaviors practice is essential.

Practice Can Create Central Sensorimotor Programs • This sensorimotor learning “chunks” central sensorimotor programs and transfers control to lower levels of the CNS. c. Functional Brain Imaging of Sensorimotor Learning LO 8.25 Explain how the classic Jenkins and colleagues PET study of simple motor learning summarizes the main points of this chapter.

Functional brain-imaging (PET) during sensorimotor learning has revealed that: • Dorsolateral prefrontal cortex may be most involved when motor sequences are largely under conscious control.

• Premotor cortex is more important when a behavior is guided by sensory stimuli, whereas the supplementary motor cortex may be more important when a behavior can be performed automatically, with little sensory feedback necessary.

• Structures active during both new and well-practiced motor sequences: primary somatosensory cortex and primary motor cortex • Structures active primarily during new motor sequences: dorsolateral prefrontal cortex, premotor cortex, posterior parietal cortex, cerebellum • Structure active primarily during well-practiced motor sequences: supplementary motor area < Return to Table of Contents

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LECTURE LAUNCHERS Lecture Launcher 8.1: Sheep Shooting There is a good reaction-time game. Go to http://www.gamemeteor.com/ and search for “sheep dash.” Click on the result with the same name. This is a fun game to play with several students, as they will be competing with each other to get better reaction time scores. And it leads nicely into a discussion of how motor output is largely guided by sensory information.

Lecture Launcher 8.2: Remote Control of Mind over Matter Researchers have recently been successful in setting up a brain-to-brain interface between two humans. One person was able to direct the movement of the second person from miles away. These advancements have implications on cognitive neuroscience and the advancement of prosthetics for paralyzed individuals. Have students read the details of the experiment online. To find the experiment, go to http://www.youtube.com.

Place “Direct Brain to Brain Communication” in the search bar. Select the video called “Direct Brain to Brain Communication in Humans: A Pilot Study.”

Lecture Launcher 8.3: Playing Penfield: Stimulating the Motor Homunculus In the 1930s, Wilder Penfield and his colleagues used electrical brain stimulation techniques to map the motor homunculus in the human brain. To open your lectures on the sensorimotor system, use the “virtual brain stimulator” available from the PBS Web site. Place “Nova Mind Probe” in the search bar of your browser. Select the link that leads you to the PBS website for Nova.

Lecture Launcher 8.4: Reflexive Behavior—Whole Class Participation Here’s a fun way to demonstrate the role of reflexive behavior and get the attention of your class. As you are talking to your class, suddenly scream out as loudly and as violently as you can. There will be shrieks and people jumping in their seats; maybe even the odd profanity if you are really good. When the class settles back down, ask the students about their reflexive response to your sudden scariness. Count the number of students who vocalized, jumped out of their seats, jerked their heads, put their hands to their face or chest, etc. Note that reflexes are automatic behaviors that typically protect the body from harm.

Lecture Launcher 8.5: Muscle Function The point of muscles is to make movement possible. The most appropriate way to examine muscle function is through moving stimuli such as animations. Be sure to bring animations of the muscle cell actions to class or make them available to students for later study.

Lecture Launcher 8.6: Cross-Country Skiing Activities can be analyzed and the muscles needed for particular movements determined. Choosing an activity that students are familiar with, such as Olympic Cross Country skiing, can make the structure of the interaction between extensors and flexors much more interesting.

Lecture Launcher 8.7: Injury to the Motor System Injury can often clarify the normal function of a system and disruption of movement is particularly dramatic.

Videos of people with motor disorders is often key to providing students with the true impact of the problem. < Return to Table of Contents

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ACTIVITIES Activity 8.1: Grab the Disk You can use the Ebbinghaus illusion to illustrate the fact that the sensory information that controls central sensorimotor programs is not necessarily conscious. The best way to do this is with the use of an overhead projector. Create a transparency with the Ebbinghaus figure on it (there is one available at http://upload.wikimedia.org/). Once on the main website, place “Mond-vergleich.svg” into the search bar.

Select the file called “Mond-vergleich.svg” to create your transparency. Place the transparency under the overhead projector and ask the students which disk is bigger. Then, ask one or two students to come up and grab each of the two disks. The spread of their fingers will nicely illustrate this point to the rest of the class.

Activity 8.2: The Reflex Arc Concept When one touches a hot stove, pain receptors in the skin are stimulated. An impulse travels to the spinal cord via an afferent (sensory) neuron. This impulse is transmitted to an association neuron and then to a motor neuron. The hand is then quickly removed from the hot stove.

Characters Sensory neuron-first-order neuron Association neuron Motorneuron-lower motorneuron Second-order neuron of spinothalamic tract Third-order neuron of spinothalamic tract Upper motorneuron Scene With chalk, outline the cerebrum with its motor and sensory strips, the thalamus, and the spinal cord on the floor. Students then stand on the appropriate spot. For example, the first-order neuron has its cell body right outside the spinal cord, one hand extends toward the “hot stove,” the other extends into the spinal cord where it barely touches the association neuron. The association neuron is totally within the spinal cord, bridging the first-order sensory neuron to both the motorneuron and the second-order neuron.

The second-order neuron extends to the thalamus where it synapses with the first-order neuron, whose cell body is located in the sensory strip. Candy may be used to demonstrate the release of neurotransmitters. Each succeeding neuron can only transmit the impulse if the previous neuron has passed on a piece of candy.

Reference Chan, V., Pisegna, J. M., Rosian, R.L., & DiCarlo, S. E. (1996). Construction of a Model Demonstrating Neural Pathways and Reflex Arcs. Advances in Physiology Education 16, SI4-S42.

(Available online at http://advan.physiology.org/ and place “construction of a model of neural pathways and reflex arcs” in the search bar. Select the article with that same title. < Return to Table of Contents

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DEMONSTRATIONS Demonstration 8.1: Electrophysiology of the Undergraduate Neuroscience Student If you just happen to have an EMG lying around, you might like to consider this activity.

Students can use surface electrodes to record the electromyogram (EMG). The students then study the nature of the EMG (changes with tension and the temporal relationship with limb movement) and the concepts of flexion and extension, reaction time, and patellar (“knee jerk”) reflex.

Reference Lennartz, R. C. (1999). Electrophysiology of the undergraduate neuroscience student: A laboratory exercise in human electromyography, American Journal of Physiology. 277, S42–S50. < Return to Table of Contents

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ASSIGNMENTS Assignment 8.1: Following Pathways In learning about behaviors that involve multiple parts of the nervous system, it is helpful to follow the pathway of the information and to think about each step. One way to make this more interesting and helpful is to imagine damage at each step in the pathway and consider the effect that it would have on behavior.

Assignment 8.2: Development of Motor Control Using a diagram of the path that information takes in the control of movement, indicate the behavioral problem you would expect if there were damage to that area.

Human infants are at first limited to gross movements of the trunk, arms, and legs. The ability to move one finger independently of the other matures over time. What hypothesis would you suggest about which brain areas controlling movement mature early and which mature later?

Assignment 8.3: Discussion: Mike the Headless Chicken Why can a chicken continue to walk with its head cut off and a human being cannot?

Web Link 8.7 Mike the Headless Chicken < Return to Table of Contents

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WEB LINKS Web Link 8.1: Useful Diagrams on the Motor System Go to http://www.utdallas.edu/ and place “integrative neuroscience” in the search bar. Select the link for “Integrative Neuroscience/Systems Neuroscience” from the results.

Web Link 8.2: Neuromuscular Home Page http://neuromuscular.wustl.edu/ This site provides LOTS of diagnostic information on neuromuscular disorders.

Web Link 8.3: Spinal Cord Injury: Emerging Concepts Go to http://www.ninds.nih.gov/and place “Spinal Cord Injury: Emerging Concepts” in the search bar.

Select the matching result.

Web Link 8.4: Spinal Cord Injury Resources http://www.spinalcord.org/ This reference site provides links to pages devoted to spinal cord injury adjustment and common questions.

Web Link 8.5: Spinal Cord Injury Facts Go to http://www.rexdonald.com/ and click on the tab titled “SCI” at the top of the page.

Covers topics of incidence, prevalence, age, sex, ethnic groups, causes, costs, life expectancy, employment rates, etc. Finishes with explanation of a spinal cord injury.

Web Link 8.6: The Dana Foundation http://www.dana.org/ The Dana Web site features sites that offer responsible information about the brain.

Web Link 8.7: Mike the Headless Chicken Go to http://www.bbc.com/and place “headless chicken” in the search bar. elect the result titled “The chicken who lived for 18 months without a head.”

Yes, that is really what this link is about! < Return to Table of Contents

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9 Development of the Nervous System: From Fertilized Egg to You TABLE OF CONTENTS Chapter-at-a-Glance

2

Learning Objectives

3

Brief Chapter Outline

4

Teaching Outline

5

Lecture Launchers

12

Activities

13

Web Links

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CHAPTER-AT-A-GLANCE

Brief Outline

Instructor’s Manual Resources

Chapter Introduction (p. 222) 9.1 Five Phases of Neurodevelopment (pp. 223–230) 9.2 Postnatal Cerebral Development in Human Infants (pp. 230–232) 9.3 Effects of Experience on Postnatal Development of Neural Circuits (pp. 232–234) 9.4 Neuroplasticity in Adults (pp. 234– 237) 9.5 Disorders of Neurodevelopment: Autism and Williams Syndrome (pp. 237–240)

Lecture Launchers 9.1, 9.2, 9.3

Lecture Launcher 9.4

< Return to Table of Contents

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LEARNING OBJECTIVES After completion of this chapter, the student should be able to: LO 9.1 LO 9.2 LO 9.3 LO 9.4 LO 9.5 LO 9.6 LO 9.7 LO 9.8 LO 9.9 LO 9.10 LO 9.11 LO 9.12 LO 9.13 LO 9.14 LO 9.15 LO 9.16

Describe the development of the neural plate into the neural tube, and explain the term stem cell.

Describe the process of neural proliferation, and identify the two organizer areas.

Describe the process of migration and aggregation.

Describe the processes of axon growth and synapse formation. Also, Explain the chemoaffinity hypothesis and the topographic gradient hypothesis.

Describe the processes of neuron death and synapse rearrangement. Why is apoptosis safer than necrosis?

Describe the postnatal growth of the human brain. What sorts of growth account for the substantial increase in volume?

Describe the functions of the prefrontal cortex and what sorts of behaviors infants display prior to its development.

Explain the difference between a “critical period” and a “sensitive period” of development.

Explain the different effects of deprivation vs. enrichment on neurodevelopment.

Describe the effects of monocular deprivation on the development of ocular dominance columns.

Describe three examples of the effects of experience on topographic sensory maps.

Explain the role of spontaneous neural firing on neural development.

Describe the evolution in our thinking about the birth of new neurons in the adult mammalian brain. Also, explain the possible function(s) of adult-born hippocampal neurons.

Describe four examples of experience affecting the organization of the adult cortex.

Describe autism spectrum disorder and attempts to identify its neural mechanisms.

Describe Williams syndrome and attempts to identify its neural mechanisms.

< Return to Table of Contents

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BRIEF CHAPTER OUTLINE Lecture Launcher 9.1: Neurulation Animation 1. Five Phases of Neurodevelopment a. Induction of the Neural Plate b. Neural Proliferation Lecture Launcher 9.2: Video Microscopy of Neuronal Migration c. Migration and Aggregation Lecture Launcher 9.3: Growth Cone Migration in Cultured Neurons d. Axon Growth and Synapse Formation e. Neuron Death and Synapse Rearrangement 2. Postnatal Cerebral Development in Humans a. Postnatal Growth of the Human Brain b. Development of Prefrontal Cortex 3. Effects of Experience on Postnatal Development of Neural Circuits a. Critical Periods vs. Sensitive Periods b. Early Studies of Experience and Neurodevelopment: Deprivation and Enrichment c. Competitive Nature of Experience and Neurodevelopment: Ocular Dominance Columns d. Effects of Experience on Topographic Sensory Cortex Maps e. Experience Fine-Tunes Neurodevelopment Lecture Launcher 9.4: Neurogenesis 4. Neuroplasticity in Adults a. Neurogenesis in Adult Mammals b. Effects of Experience on the Reorganization of the Adult Cortex 5. Disorders of Neurodevelopment: Autism and Williams Syndrome a. Autism Spectrum Disorder b. Williams Syndrome < Return to Table of Contents

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TEACHING OUTLINE 1. Phases of Neurodevelopment a. Induction of the Neural Plate (see Figure 9.1 and 9.2 in Biopsychology) LO 9.1 Describe the development of the neural plate into the neural tube, and explain the term stem cell.

• • • • • •

About three weeks after conception, a patch of ectoderm on the dorsal surface of the embryo becomes distinguishable from the rest of the ectoderm. This patch is the neural plate, and it eventually develops into the nervous system.

The development of the neural plate seems to be induced by the underlying mesoderm.

Prior to induction of the neural plate, the cells of the dorsal ectoderm are totipotential (that is, if they are transplanted to a new site in the embryo, they develop in the same way as cells at the new site).

After neural plate induction, the cells there lose some of their totipotentiality; they can develop into any kind of neuron, but not any other kind of cell. These cells are said to be multipotent; they are called stem cells.

Stem cells have an almost unlimited capacity for self-renewal. When they divide, they create a cell for the body as well as another stem cell.

The neural plate develops into the neural groove and then into the neural tube, which subsequently develops into the CNS. By 40 days, the anterior end of the neural tube develops three swellings that become the forebrain, midbrain, and hindbrain.

b. Neural Proliferation LO 9.2 Describe the process of neural proliferation, and identify the two organizer areas.

• • •

After the neural tube is formed, the developing nervous system cells rapidly increase in number.

Cell division occurs in the ventricular zone of the neural tube (the zone next to the ventricle); when they leave the cell division cycle, cells migrate into other layers.

The complex pattern of proliferation is in part controlled by chemical signals from the two organizer areas, the floor plate and the roof plate.

c. Migration and Aggregation (see Figures 9.3 and 9.4 in Biopsychology) LO 9.3 Describe the processes of migration and aggregation.

• • • • • •

Cell migration can be radial migration or tangential migration; cells in the CNS usually do both as they move towards their final destination.

In somal translocation, a cell extends a process away from its soma that seeks attractive or repellant cues in its immediate vicinity; the cell follows attractive cues, and is repelled by repellant cues.

In glial-mediated migration; cells migrate away from the ventricular zone along a temporary network of radial glial cells, which are present in only the developing neural tube.

Many of these cells eventually develop into neurons.

The cells of the neocortex migrate in an inside-out pattern; the deepest layers form first so that the cells of the superficial layers must migrate through them.

Migration of the cells of the neural crest is of particular interest because these cells ultimately form the PNS, and thus many have a long way to migrate.

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Neural crest cells transplanted to a new part of the neural crest migrate to the destination that is appropriate for cells in the new location; thus, the migration routes must be encoded in the medium through which they travel, rather than in the cells themselves.

Many different types of chemical signals have been found that guide the migration of the axons of future PNS neurons; some of these are released by glial cells.

Once migration is complete, cells must aggregate correctly to form various neural structures.

This is hypothesized to be mediated by specialized neural cell adhesion molecules in the cell membranes (NCAMs).

Gap junctions between adjacent cells have been found to be particularly prevalent during brain development (see Chapter 4 for further description).

Gap junctions are not as wide as synapses, and the gaps are bridged by narrow tubes called connexins, through which cells can exchange cytoplasm.

There is increasing evidence that gap junctions play a role in migration and aggregation.

d. Axon Growth and Synapse Formation (see Figures 9.5–9.7 in Biopsychology) LO 9.4 Describe the processes of axon growth and synapse formation. Also, Explain the chemoaffinity hypothesis and the topographic gradient hypothesis.

Axon Growth • Once the aggregation of developing neurons is complete, axons and dendrites grow out from the neurons; growing to the correct target is particularly difficult for axons that have a long way to grow.

• Studies in which the same recognizable developing neuron has been labeled in different subjects demonstrate that the axons of some particular neurons grow to the same destination by the same route in every member of a species.

• This accurate axon growth seems to be directed by a growth cone at the growing axon tip, which extends and retracts finger-like filopodia, as if searching for the correct route by touch.

• Two hypotheses have been proposed to explain how growth cones make their way to their correct destination: the chemoaffinity hypothesis and the topographic-gradient hypothesis.

• Sperry’s classic eye-rotation regeneration experiments remain the classic example of data supporting the chemoaffinity hypothesis.

• Sperry cut the optic nerves of frogs, rotated their eyes, and waited for regeneration; after regeneration, it was clear from their misdirected feeding responses that the visual world of the frogs was rotated by the same degree as the eye rotation. The axons seemed to have regenerated back to their original targets.

• On the basis of this series of studies, Sperry proposed the chemoaffinity hypothesis; the hypothesis that the target of each growing axon has a specific chemical that draws the correct growing axon to it.

• The chemoaffinity hypothesis can’t explain how some developing axons follow the same indirect route in every member of a species.

• Currently, researchers believe that accurate axon growth is based on a variety of chemical signals; some attract the migrating axon, others repel it.

• These guidance molecules are often released by glial cells.

• In addition, axon migration can also be guided by other axons. In this situation, only the first axon (bearing a pioneer growth cone) that grows into an area has the ability to reach its correct target, following a variety of guidance molecules.

• The others appear to follow the pioneer growth cone’s route by a process called fasciculation; if a pioneer axon growth cone is destroyed by a laser, few of the other neurons in the nerve reach their correct destination.

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The topographic-gradient hypothesis has developed to account for axonal migration from one topographically organized structure to another.

According to this model, axon growth from one topographic array (such as a retina) to another (the optic tectum) is guided by the relative position of the cell bodies and terminals on two intersecting gradients (up-down and left-right) of chemicals on the originating tissue (the retina, in this case).

Synapse Formation • Once an axon reaches its target, synaptogenesis must occur.

• Glial cells, particularly astrocytes, are critically important; they increase the survival of developing synaptic connections.

• Synaptogenesis depends on a variety of signals, released by both the presynaptic and postsynaptic cells.

• Some of the chemical signals that play a role in the location and formation of synapses have been identified.

Summary: All of the evidence on axon growth and regeneration suggests that a variety of mechanisms can guide axon growth; the growth of different axons appears to be guided by different combinations of these mechanisms. e. Neuron Death and Synapse Rearrangement (See Figure 9.8 in Biopsychology) LO 9.5 Describe the processes of neuron death and synapse rearrangement. Why is apoptosis safer than necrosis?

Neural Death • Up to 50% of neurons that develop die during the course of normal development; the fact that neurons that make incorrect connections are more likely to die suggests that cell death increases the overall accuracy of synaptic connections.

• Most of this cell death is due to apoptosis; preprogrammed cell death that is believed to result from the lack of an appropriate trophic factor.

• Apoptosis is safer than necrosis, because in necrosis the cell breaks apart and may cause inflammation.

• There appear to be two types of triggers for apoptosis: 1) some developing neurons appear to be genetically programmed for an early death—once their functions are fulfilled, groups of neurons die together in the absence of any obvious physical stimulus; 2) some die because they fail to obtain life-preserving chemicals that are supplied by their targets.

• Three lines of evidence suggest that neurons die because they fail to compete successfully for some life-preserving factor (neurotrophins, such as nerve growth factor) supplied by their target: – Implantation of an extra target site decreases neuron death (e.g., an implanted extra limb decreases motor neuron loss); – Destroying some neurons before the period of neuron death increases the survival rate of the remainder; and – Increasing the number of axons that initially synapse on a target decreases survival rate of the remainder.

Synapse Rearrangement • As neurons die, the spaces they leave vacant on postsynaptic membranes are filled by sprouting axon terminals of surrounding neurons.

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Cell death results in synapse rearrangement; its effect is to focus the output of each neuron on fewer postsynaptic neurons.

2. Postnatal Cerebral Development in Humans a. Postnatal Growth of the Human Brain LO 9.6 Describe the postnatal growth of the human brain. What sorts of growth account for the substantial increase in volume?

• • • •

Brain volume quadruples between birth and adulthood; most of this increase in volume comes from increased numbers of synapses (synaptogenesis); myelination of axons; and increased dendritic branching.

Synaptogenesis is assumed to indicate increased analytic ability in a brain region; synaptogenesis in the visual cortex peaks at about four months postnatal, whereas in prefrontal cortex, maximal density is reached in the second year.

Myelination increases the speed of axonal conduction; again, sensory and motor areas are myelinated in the first few months of life, while the prefrontal cortex is not fully myelinated until adolescence.

Many synapses that form early in development are eventually lost; overproduction of synapses in the young brain may contribute to its greater plasticity.

b. Development of Prefrontal Cortex LO 9.7 Describe the functions of the prefrontal cortex and what sorts of behaviors infants display prior to its development.

• • • • •

The human brain develops more slowly than other species, not maturing until late adolescence.

In particular, the prefrontal cortex is the last part of the brain to reach maturity, and it is thought to mediate many higher cognitive abilities.

The development of prefrontal cortex parallels the course of human cognitive development.

It is linked to four main types of cognitive function: working memory, or the ability to keep information accessible for short periods of time; planning and completing sequences of actions; inhibiting inappropriate responses; and following rules for social behavior.

Diamond (1991) found that damage to the prefrontal cortex leads to perseverative errors in adults, so that their behavior looks more like an infant’s.

3. Effects of Experience on Postnatal Development of Neural Circuits (see Figure 9.9 in Biopsychology) • This section focuses on how external environmental events (experience) can influence the development and maintenance of neural circuits. Neurodevelopment results from an interaction between neurons and their environment.

• Key Rule: Neurons and synapses that are not activated by experience do not usually survive.

• One question asked about experience is whether the effects are permissive or instructive.

• Permissive experiences are those that are necessary for information in genetic programs to be manifested. Instructive are those that contribute to the direction of development. a. Critical periods vs. Sensitive periods LO 9.8 Explain the difference between a “critical period” and a “sensitive period” of development.

•

One important feature that affects experience is timing.

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If it is absolutely essential for an experience to occur within a particular time interval, it is called a critical period. If experience can have an effect outside of this interval, it is called a sensitive period.

The majority of experiential effects occur in a sensitive period.

One major advantage of the slowness of the developing brain is that it provides opportunities for experience to fine-tune development.

b. Early Studies of Experience and Neurodevelopment: Deprivation and Enrichment LO 9.9 Explain the different effects of deprivation vs. enrichment on neurodevelopment.

• • • • • •

Most research focuses on the sensory and motor systems.

There are two general manipulations of experience: sensory deprivation and enrichment.

The first studies on sensory deprivation involved rats reared in a dark environment.

Researchers found the rats to have fewer synapses and fewer dendritic spines in their visual cortex, and as adults they had deficits in depth and pattern perception.

Rats raised in enriched environment (complex) group cages, rather than alone in barren cages, had thicker cortexes with more dendritic spines and synapses per neuron.

The effects of sensory restriction can be seen in human infants born with cataracts.

c. Competitive Nature of Experience and Neurodevelopment: Ocular Dominance Columns LO 9.10 Describe the effects of monocular deprivation on the development ocular dominance columns.

• •

•

A competitive aspect to the effects of experience on neurodevelopment is illustrated by the disruptive effects of early monocular deprivation on the development of ocular dominance columns in the primary visual cortex.

Researchers have found that depriving one eye of input for just a few days early in life blocks the development of vision in that eye and the normal development of ocular dominance columns; this is due, in part, to a decrease in axonal sprouting of thalamic neurons terminating in visual cortex.

If the eye is blindfolded for several days, the columns of input from the deprived eye are decreased while the columns of input from the nondeprived eye are increased.

d. Effects of Experience on Topographic Sensory Cortex Maps LO 9.11 Describe three examples of the effects of experience on topographic sensory maps.

•

• •

Experience can play a key role on the development of topographic sensory maps: For example, Roe and colleagues found that surgically altering retinal ganglion output so that it connected with the medial geniculate (instead of lateral geniculate) caused auditory cortex to develop a retinotopic organization.

Knudsen and Brainard demonstrated that barn owls raised with vision-displacing prisms over their eyes showed a corresponding change in their auditory cortex to accommodate for the change in vision.

Similarly, there is some evidence that early musical training influences the organization of human auditory cortex; using fMRI, researchers have found that such training expands the part of auditory cortex that responds to complex musical tones.

e. Experience Fine-Tunes Neurodevelopment LO 9.12 Explain the role of spontaneous neural firing on neurodevelopment.

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Clearly, experience fine-tunes neurodevelopment in innumerable ways.

Experience alters development by influencing gene expression.

Early neurotransmitter activity alters development.

4. Neuroplasticity in Adults (see Figure 9.10 in Biopsychology) • It has only recently been appreciated that the adult brain is capable of considerable neuroplasticity.

• This principle has fundamentally changed the field’s view of neuroplasticity. a. Neurogenesis in Adult Mammals LO 9.13 Describe the evolution in our thinking about the birth of new neurons in the adult mammalian brain. Also, explain the possible function(s) of adult-born hippocampal neurons.

• • • • • • •

Evidence exists that neurogenesis occurs in the adult brain; for example, Nottebohm and his colleagues demonstrated an annual increase in neurons in song-production centers in the brains of adult male birds.

Neurogenesis has since been convincingly demonstrated in the hippocampus and the olfactory bulbs.

This neurogenesis can be substantial in the hippocampus. New cells are created near their final location in the dentate gyrus.

Neurogenesis in the olfactory bulb and striatal neurons come from adult neural stem cells near the lateral ventricle and then they migrate out to their final location.

Simply placing an adult animal in an enriched environment can increase neurogenesis in brain regions, such as the hippocampus.

Adult generated olfactory bulb and striatal neurons become interneurons while adult-generated hippocampal cells become granule cells in the dentate gyrus.

The function of these cells is unclear. Some believe they are integrated into memory function while others believe they are important in pattern separation (ability to separate distinct percepts into individual memories for storage). Still others believe these cells serve a role in mood and anxiety regulation and Freund and others believe they allow us to adapt to complex environments.

b. Effects of Experience on the Reorganization of the Adult Cortex LO 9.14 Describe four examples of experience affecting the organization of the adult cortex.

• • • •

Researchers have found that environmental enrichment, and the increase in activity that accompanies it, is a potent promoter of neurogenesis in the CNS. Experience in adulthood can lead to reorganization of sensory and motor cortical maps.

Plasticity research shows that one the brain has adapted to abnormal environmental conditions, it acquires the ability to adapt more effectively if it encounters those conditions again.

Neuroplasticity leads to hope for people suffering from brain damage.

5. Disorders of Neurodevelopment: Autism and Williams Syndrome (see Figure 9.12 in Biopsychology) During the course of development, even a small perturbation in the normal course of events can have dire consequences. a. Autism Spectrum Disorder (ASD) LO 9.15 Describe autism spectrum disorder and attempts to identify its neural mechanisms.

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Biopsychology, Tenth Edition • • • • • • • • • • • • • • •

ASD is a complex neurodevelopmental disorder.

Some commonalities are: 1) it emerges by the age of three and, 2) it does not increase in severity after this.

There exist two core symptoms: 1) a reduced capacity for social interaction, and 2) restricted and repetitive patterns of behavior.

75% of autistic individuals are males; many suffer from intellectual or learning disabilities and they are more likely to suffer from epilepsy.

Older parents are more likely to give birth to a child with autistic spectrum disorder.

The early warning sign of ASD is a delay in the development of social interaction.

ASD’s are the most prevalent childhood neurodevelopmental disorder.

ASD is difficult to treat. Some behavioral therapies can improve the lives of some individuals.

ASD is a heterogeneous disorder which means that some individuals may be severely impaired in some respects, but may be normal or superior in others.

Autistic savants are autistic patients who display amazing and specific cognitive abilities— such as feats of memory, drawing, or playing musical instruments.

Savants’ abilities remain a mystery; somehow the damage in certain brain areas has led to compensatory overdevelopment in others.

Genetic factors play a role in autism; there is a 20% chance of autism in the siblings of an autistic person, and a 60% chance if that sibling is a monozygotic twin. This suggests that many genes are involved interacting with the environment.

Neural mechanisms of autism are difficult to study.

Postmortem studies and MRI studies reveal brain damage in the cerebellum, amygydala, and frontal cortex.

Research shows that individuals with ASD have an abnormal reaction to faces (autistic individuals spend less time looking at faces, especially the eyes) implicates the fusiform area

b. Williams Syndrome LO 9.16 Describe Williams syndrome and attempts to identify its neural mechanisms.

• • • • • • • •

Williams syndrome is a neurodevelopmental disorder with intellectual disability and with a heterogeneous patter of abilities and disabilities.

Those with Williams syndrome are social, empathetic, and talkative.

Occurs in 1 in 7500 births.

Language abilities are remarkable for their characteristically low IQ’s.

Other cognitive strengths include near perfect pitch, a sense of rhythm and a remarkable ability to recognize faces.

Patients with Williams syndrome have severe attentional problems, poor spatial abilities, and they have great difficulty drawing objects.

Chromosome 7 appears to control the synthesis of elastin, a protein that imparts elasticity to organs and tissues.

Brain differences include decreased basal ganglia volume, general thinning of the cortex (greatest in the boundary of the parietal and occipital lobes and in the orbitofrontal cortex.

< Return to Table of Contents

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Chapter 9: Development of the Nervous System

LECTURE LAUNCHERS Lecture Launcher 9.1: Neurulation Animation The animation located at the following URL provides a simple, easy-to-control animation of embryonic development—focusing on the process of neurulation: Go to http://www.wesleyan.edu and place “learning objects studio” in the search bar. Click on the “Learning Objects Studio.” Once there, click on the link to go to the archives link embedded in the bottom paragraph. Once you are in the archives, click on the link to the “projects” page. Once you reach the “projects” page, scroll down until you reach the “neurulation” link on the left-hand side of the page. Once you enter the neurulation homepage, click on the link titled “neurulation animation.”

Lecture Launcher 9.2: Video Microscopy of Neuronal Migration Some of the most stunning images that have come out of the neurosciences in the past decade are those resulting from video microscopy. The following URL contains a large number of particularly compelling examples: http://www.rockefeller.edu/ and place “hatten movies” in the search bar. Once your search results are displayed, page down to the link titled “The Rockefeller University – Videos” and click on that link. That will take you to a page that has several videos of neuronal migration.

Lecture Launcher 9.3: Growth Cone Migration in Cultured Neurons The idea of a cellular process like a growth cone moving from the soma to the target destination of the neuron is one that many students have a hard time visualizing. To help them, and to get this part of your lecture rolling, use the video provided by Paul Letourneau. This video shows a growth cone responding to nerve growth factor in the environment. Go to http://www.youtube.com and place “Growth Cone Migration” in the search bar. Select the result titled “Growth cone guidance by an attractive surface (NGF).”

Lecture Launcher 9.4: Neurogenesis This is an excellent article on neurogenesis in the mammalian brain. Go to http://www.the-scientist.com/ and place “Neurogenesis in the Mammalian Brain” in the search bar. Select the matching link. < Return to Table of Contents

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Biopsychology, Tenth Edition

ACTIVITIES Activity 9.1: Autism on the Rise?

There is a rise in the diagnosis of autism. That trend has been receiving an increasing amount of press coverage over last past decade. There are also many hypotheses about the reasons for the increase in cases of autism. The videos and news articles located at the following URL on the MSNBC Web site contain a wealth of examples on this growing dialogue: Go to http://www.msnbc.msn.com/ and choose the link to MSNBC. Once on that site place “Autism Spectrum Disorder” in the search bar. Choose a recent video or news article from this page and have the students view it or read it. Then break the students into groups of four to five students and ask them to write down what they feel is wrong with the particular piece of media coverage they were just exposed to (there might be nothing wrong with it). Then ask each group to present the results of their brainstorm to the rest of the class. Use the resulting discussion as a lead-in to your autism lecture. < Return to Table of Contents

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Chapter 9: Development of the Nervous System

WEB LINKS Web Link 9.1 – Neural System Development Go to https://embryology.med.unsw.edu.au/. Select the tab titles “Systems Development” and drop down to the link for the neural system titled “Neural.”

This Web site produced by Dr. Mark Hill thoroughly covers embryonic neural development. Numerous explanations and videos are available to support student learning.

Web Link 9.2 – Evolution of the Mammalian Neocortex Go to http://www.sciencechannel.com/ and place “mammalian neocortex development” in the search bar.

Select the video that shares that same name.

A video available on the Science Channel. Discusses the evolution of the mammalian neocortex and how it has become specialized to help mammals survive.

Web Link 9.3 – Kaplan Review of Development of the Nervous System Go to https://www.youtube.com/ and place “Neuroscience Development of CNS” in the search bar.

Select the link titled “USMLE Step 1: Neuroscience Development of CNS Animation.”

This is the Kaplan review of Development of the Nervous System used by medical students to prepare for their qualifying exams. < Return to Table of Contents

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10 Brain Damage and Neuroplasticity: Can the Brain Recover from Damage?

TABLE OF CONTENTS Chapter-at-a-Glance

2

Learning Objectives

3

Brief Chapter Outline

4

Teaching Outline

5

Lecture Launchers

14

Web Links

17

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Chapter 10: Brain Damage and Neuroplasticity

CHAPTER-AT-A-GLANCE

Brief Outline Chapter Introduction (p. 243) 10.1 Causes of Brain Damage (pp. 244– 250) 10.2 Neurological Diseases (pp. 250– 257) 10.3 Animal Models of Human Neurological Diseases (pp. 257–259) 10.4 Responses to Nervous System Damage: Degeneration, Regeneration, Reorganization and Recovery (pp. 259– 264) 10.5 Neuroplasticity and the Treatment of CNS Damage (pp. 264–269)

Instructor’s Manual Resources Lecture Launchers 10.1, 10.2, 10.5, 10.6 Lecture Launchers 10.3, 10.7, 10.8

Lecture Launcher 10.4

< Return to Table of Contents

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Biopsychology, Tenth Edition

LEARNING OBJECTIVES After completion of this chapter, the student should be able to: LO 10.1 LO 10.2 LO 10.3 LO 10.4 LO 10.5 LO 10.6 LO 10.7 LO 10.8 LO 10.9 LO 10.10 LO 10.11 LO 10.12 LO 10.13 LO 10.14 LO 10.15 LO 10.16 LO 10.17 LO 10.18 LO 10.19 LO 10.20 LO 10.21 LO 10.22

Describe different types of brain tumors, and explain the difference between an encapsulated and an infiltrating tumor.

Describe differences between the two types of stroke: cerebral hemorrhage and cerebral ischemia.

Explain the difference between a contusion and a concussion, and define a countrecoup injury.

Describe two different types of infections of the brain.

Describe three different types of neurotoxins.

Discuss the symptoms of Down syndrome and what causes this disorder.

Define the difference between apoptosis and necrosis.

Define epilepsy. Also, describe four categories of epileptic disorders and some treatments for epilepsy.

Describe the symptoms of Parkinson’s disease and some treatments for this disorder.

Describe the symptoms of Huntington’s disease, and explain its genetic basis.

Describe the symptoms of multiple sclerosis and its risk factors.

Describe the symptoms of Alzheimer’s disease, and evaluate the amyloid hypothesis.

Describe the kindling model of epilepsy, and explain the ways in which it models human epilepsy.

Describe the transgenic mouse models of Alzheimer’s disease, and evaluate their efficacy.

Describe the events that led to the discovery of the MPTP model of Parkinson’s disease, and evaluate the utility of this animal model.

Explain the various types of neural degeneration that ensure following axotomy.

Compare neural regeneration within the CNS vs. the PNS. Describe three examples of cortical reorganization following damage to the brain, and discuss the mechanisms that might underlie such reorganization.

Describe the concept of “cognitive reserve,” and discuss the potential role of adult neurogenesis in recovery following CNS damage.

Discuss early work on neurotransplantation for the treatment of CNS damage.

Discuss the methods and findings of modern research on neurotransplantation.

Discuss methods of promoting recovery from CNS damage through rehabilitative treatment.

< Return to Table of Contents

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Chapter 10: Brain Damage and Neuroplasticity

BRIEF CHAPTER OUTLINE Lecture Launcher 10.1: Visualizing a Brain Tumor Lecture Launcher 10.2: Identification and Treatment of Cerebral Aneurysms 1. Causes of Brain Damage a. Brain Tumors b. Cerebrovascular Disorders: Stroke c. Closed-Head Injuries d. Infections of the Brain e. Neurotoxins f. Genetic Factors g. Programmed Cell Death Lecture Launcher 10.3: Apoptosis and Necrosis 2. Neurological Diseases a. Epilepsy b. Parkinson’s Disease c. Huntington’s Disease d. Multiple Sclerosis e. Alzheimer’s Disease 3. Animal Models of Human Neurological Diseases a. Kindling Model of Epilepsy b. Transgenic Mouse Models of Alzheimer’s Disease c. MPTP Model of Parkinson’s Disease 4. Responses to Nervous System Damage: Degeneration, Regeneration, Reorganization, and Recovery a. Neural Degeneration b. Neural Regeneration c. Neural Reorganization d. Recovery of Function After CNS Damage Lecture Launcher 10.4: Thinking Yourself Strong?

5. Neuroplasticity and the Treatment of CNS Damage a. Neurotransplantation As a Treatment for CNS Damage: Early Research b. Modern Research on Neurotransplantation c. Promoting Recovery from CNS Damage by Rehabilitative Training < Return to Table of Contents

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TEACHING OUTLINE 1. Causes of Brain Damage (see Figures 10.1–10.7 in Biopsychology) Much can be learned about the brain’s normal functioning by examining deficits after brain damage. a. Brain Tumors (see Figures 10.1–10.3 in Biopsychology) LO 10.1 Describe different types of brain tumors, and explain the difference between an encapsulated and an infiltrating brain tumor.

• • • •

A tumor (neoplasm) is a group of cells growing independently of the rest of the body; a tumor can be encapsulated or infiltrating; it can be benign or malignant.

20% of brain tumors are meningiomas that grow in the meninges; they are encapsulated and benign.

Gliomas are a more common infiltrating tumor.

Metastatic tumors are tumors that originate in one organ and spread to another; the symptoms of multiple cerebral tumors are often the first signs of lung cancer.

b. Cerebrovascular Disorders: Stroke (see Figures 10.4–10.5 in Biopsychology) LO 10.2 Describe differences between the two types of stroke: cerebral hemorrhage and cerebral ischemia.

• • • •

• • • •

•

“Stroke” is commonly used to refer to any cerebrovascular disorder of sudden onset.

An “infarct” is an area of dead or dying tissue that is surrounded by a penumbra (an area of dysfunctional tissue).

A stroke may be due to cerebral hemorrhage; the bursting of aneurysms (balloon-like dilations of weak areas of blood vessels) is a major cause of intracerebral bleeding. Aneurysms can be congenital or the result of infection, toxins, etc.

Cerebral ischemia is a disruption of blood supply to an area of the brain: – In thrombosis, a plug (a thrombus) becomes lodged at its site of formation; the plug may be due to a blood clot, fat, oil, cancerous cells, air bubbles, etc.; – In embolism, a plug (an embolus) travels from its site of formation and becomes lodged in a smaller blood vessel; and – In arteriosclerosis, the blood vessel walls thicken and the space inside narrows; usually from the accumulation of fat.

Ischemic brain damage takes a while to develop, does not occur equally in all regions of the brain, and the exact physiological mechanism for such damage varies from region to region.

One mechanism of ischemic brain damage is believed to be an excessive release of excitatory amino acids.

Glutamate, the brain’s most prevalent excitatory amino acid neurotransmitter, is released in excessive quantities when blood vessels are blocked.

The excessive glutamate over-activates glutamate receptors on postsynaptic membrane sites, thus too many Na+ and Ca++ ions are allowed to enter the postsynaptic neuron, which triggers either (a) an excessive release of glutamate, causing a cascade of this toxic effect or, (b) triggers a sequence of reactions that kills the postsynaptic neuron.

Researchers are currently studying the ability of NMDA receptor blockers administered directly after a stroke to reduce subsequent brain damage.

c. Closed-Head Injuries (see Figure 10.6 in Biopsychology)

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Chapter 10: Brain Damage and Neuroplasticity LO 10.3 Explain the difference between a contusion and a concussion, and define a contrecoup injury.

•

• • •

A brain contusion is an injury in which there is bleeding from the brain in the absence of a laceration. The bleeding results in a hematoma (a bruise or collection of clotted blood), contusions are caused by the brain hitting the skull, and they are often contrecoup (on other side of brain from blow).

Concussion is the diagnosis when a blow to the head disrupts consciousness, and there is no evidence of a contusion or other structural damage.

There is now substantial evidence that cognitive, motor, and neurological effects can last many years.

Chronic traumatic encephalopathy is the brain damage seen in boxers and football players who have suffered many concussions over time.

d. Infections of the Brain LO 10.4 Describe two different types of infections of the brain.

• • • •

Encephalitis is the general term for inflammation of the brain resulting from infection.

Bacterial infections can be treated with antibiotics, but if left untreated they can cause meningitis (inflammation of meninges), brain abscesses (pockets of pus), and general paresis (a syndrome of insanity and dementia).

Viral infections include infections that preferentially attack the nervous system (e.g., rabies virus) and infections that show no preference for the nervous system, but they sometimes attack it (e.g., mumps and herpes viruses).

Viruses may play a key role in the etiology of many neuropsychological disorders; their role is often hard to study because they may lie dormant and not produce symptoms until years after they invade the nervous system.

e. Neurotoxins LO 10.5 Describe three different types of neurotoxins.

• • • • f.

Brain damage can be produced by a variety of toxins in the environment: “mad hatters” were the result of mercury poisoning, “crackpots” were originally those who drank tea from cracked ceramic pots with lead cores—the result was poisoning.

A toxic psychosis is a mental illness produced by a neurotoxin.

Sometimes drugs used to treat a disease can have neurotoxic effects; for example, tardive dyskinesia is a disorder produced by prolonged exposure to certain antipsychotic medications.

Endogenous neurotoxins occur when the patient’s own body attacks itself.

Genetic Factors LO 10.6 Discuss the symptoms of Down syndrome and what causes this disorder.

• • •

Some genetic disorders are accidents of cell division (e.g., in Down syndrome, an extra chromosome in pair 21 is present in all cells). This extra chromosome produces characteristic physical alterations and intellectual impairment.

Other genetic disorders are products of abnormal recessive genes, as dominant genes that disturb neuropsychological function tend to be eliminated from the gene pool.

However, most diseases are associated with numerous loci in sections of chromosomes that do not contain protein-coding genes.

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Biopsychology, Tenth Edition g. Programmed Cell Death LO 10.7 Explain the different between apoptosis and necrosis.

• •

•

Dysfunctional neurons and other cells are often eliminated by activating genes that kill them; this programmed cell death is called apoptosis.

This is more adaptive than necrosis, in which neurons die passively as a result of injury and can itself cause inflammation. Apoptosis begins at the nucleus of the neuron and takes days; necrosis does not alter the nucleus until late in the process, which generally takes only a few hours.

Some cells die by a combination of necrosis and apoptosis.

2. Neurological Diseases a. Epilepsy (see Figures 10.8–10.10 in Biopsychology) LO 10.8 Define epilepsy. Also, describe four categories of epileptic disorders and some treatments for epilepsy.

• • • • • • •

Epilepsy is any disorder in which epileptic seizures recur spontaneously.

When convulsions (motor seizures) are present, epilepsy is easy to diagnose; convulsions often involve clonus (tremor), tonus (rigidity), loss of balance, and/or loss of consciousness.

However, many seizures involve subtle changes in thought, mood, and/or behavior with no convulsive symptoms whatsoever.

The observation of epileptic spikes in the EEG is incontrovertible evidence of epilepsy; however, failure to observe them does not prove that the person is not epileptic.

Epileptic auras sometimes precede an epileptic seizure.

Epilepsy has many causes; many types seem to be associated with impaired function at inhibitory synapses.

There are two main classes of seizures: focal seizures and generalized seizures.

Focal Seizures • Focal seizures are those that do not involve the entire brain.

• There is not usually accompanied by a loss of consciousness.

• Simple partial seizures are partial seizures whose symptoms are primarily sensory and/or motor; usually the symptoms start in one part of the body and spread to other parts of the body as discharges spread through the sensory and motor areas of the brain.

• Complex partial seizures are often restricted to the temporal lobes; the motor symptoms of complex partial seizures vary in complexity from automatisms (simple, compulsive, repeated behaviors, such as tugging on a piece of hair) to long sequences of behavior that are out of context and slightly peculiar but are, for the most part, normal-appearing.

• Epileptics typically have no memory of the events of a complex partial seizure.

Generalized Seizures (see Figure 10.9 in Biopsychology) • Generalized seizures involve the entire brain; they may start from a focus and gradually spread, or they may begin almost simultaneously throughout the entire brain.

• Include tonic-clonic seizures (tonic-clonic, loss of balance and consciousness, tongue biting, incontinence, turning blue from hypoxia) and absence seizures (“little trouble”) (absence, three-per-second spike-and-wave).

• Absence seizures are more common in children and are associated with a disruption of consciousness rather than convulsions.

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Chapter 10: Brain Damage and Neuroplasticity •

Treatment options include anti-epileptic medication, vagal nerve stimulation, transcranial magnetic stimulation, the ketogenic diet, and surgery.

b. Parkinson’s Disease LO 10.9 Describe the symptoms of Parkinson’s Disease and some treatments for this disorder.

• • • • • • • •

Parkinson’s disease attacks 1% of the population over the age of 55; and it occurs slightly more often in males.

The first symptom is often a tremor or stiffness of the fingers (the same symptoms seen in many other long- and short-term disorders).

Symptoms of the full-blown disorder are tremor at rest, muscular rigidity, slowness of movement, and a masklike face.

There is no intellectual deterioration (no dementia). Though patients often display cognitive deficits.

Its cause is unknown, but it is associated with degeneration of dopamine neurons in the substantia nigra; these neurons project to the striatum of the basal ganglia through the nigrostriatal pathway.

It is treated with L-DOPA, the metabolic precursor of dopamine, though it is not a permanent solution.

Current data indicates that by the time a person becomes symptomatic, that irreversible damage has already occurred in the brain.

A controversial treatment currently available is deep brain stimulation of the subthalamic nucleus. Unfortunately, it is not without its side effects, including cognitive, speech and gait problems.

c. Huntington’s Disease LO 10.10 Describe the symptoms of Huntington’s disease, and explain the genetic basis.

• • • • •

Like Parkinson’s disease, it is a motor disorder; unlike Parkinson’s disease, it is inherited but rare, its cause is understood, and it is always associated with dementia.

Its main symptoms are complex jerky movements of entire limbs; dementia occurs later in the disease, which is always fatal.

Huntington’s disease is caused by a single dominant gene; 50% of all offspring of a Huntington’s parent will get it. The reason the disease has not disappeared is that the first symptoms do not appear until after the age of reproduction (at 40–50 years of age).

The abnormal gene responsible for Huntington’s disease produces an abnormal protein called huntingtin; its function in the brain is unknown.

Genetic testing is available to determine if an individual is a carrier of the gene.

d. Multiple Sclerosis (see Figure 10.12 in Biopsychology) LO 10.11 Deseribe the symptoms of multiple sclerosis and its risk factors.

• • •

MS is a disease of CNS myelin; degeneration of the myelin sheaths eventually leads to a breakdown of myelin and the associated axons and the development of areas of hard scar tissue throughout the CNS; sclerosis means “hardening.”

The symptoms depend on the location of the scars; but common symptoms are ataxia (loss of motor coordination), weakness, numbness, tremor, and poor vision.

Experimental allergic encephalomyelitis is an animal model of MS; it can be produced in animals by injecting them with myelin and a substance that stimulates the body’s immune

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Biopsychology, Tenth Edition

• •

reaction. This has led to the hypothesis that MS results from a faulty immune reaction against the body’s own myelin, perhaps resulting from an early infection or toxin.

There are often periods of partial recovery from the disease, but there are no exceptions to the generally worsening progression of the disorder.

Epidemiological studies have identified the following factors responsible for the etiology of multiple sclerosis: – A higher concordance rate in monozygotic twins (25%) than in dizygotic twins (5%), which indicates a modest role for genetic factors.

– The incidence is three times higher in females.

– The incidence is higher in Caucasians (.15%) than in other ethnic groups, such as native Asians and Africans.

– The incidence is higher among populations living in colder climates, as opposed to near the equator.

e. Alzheimer’s Disease (see Figures 10.13–10.14 in Biopsychology) LO 10.12 Describe the symptoms of Alzheimer’s disease, and evaluate the amyloid hypothesis.

•

• • • •

•

• • •

The first signs are a selective decline in memory (e.g., forgetfulness); during the intermediate stage there is increased emotional instability (e.g., anxiety) and loss of speech function.

Eventually, there is total dementia and an inability to perform even the most simple responses (e.g., swallowing); it is terminal.

Alzheimer’s disease can only be definitively diagnosed by autopsy and the discovery of amyloid plaques (clumps of degenerating neurons and an abnormal protein called amyloid), and tangles of neurofibrils within neurons.

Small lesions produced by microbleeds suggest that Alzheimer’s disease might be produced by vascular problems.

Loss of neurons is common; plaques, tangles, and neuron loss are often most common in areas involved in memory such as the hippocampus, amygdala, and entorhinal cortex.

Alzheimer’s appears to have a clear genetic component; people with an immediate family member suffering from Alzheimer’s disease are two times as likely to develop the disease if they live into their 80s.

– Three genes have been identified that contribute to an early-onset form of the disease but at least 15 genes contribute to the late-onset form.

A massive research effort is aimed at an effective treatment or cure for Alzheimer’s disease; early efforts have focused on treatments that increase acetylcholine function, as cholinergic neurons often die early in the course of Alzheimer’s disease. Unfortunately, these are largely ineffective.

Other treatments under consideration focus on reducing amyloid plaques. These have met with mixed results, although many researchers believe that Alzheimer’s disease must be diagnosed and treated earlier to be successful.

Researchers are trying to better understand the connection between Down Syndrome and Alzheimer’s in hopes of developing more treatments.

The pathogenic spread hypothesis is relatively new and proposes that neurodegenerative diseases result from the presence of misfolded proteins that initiate a chain reaction that causes other proteins to misfold.

3. Animal Models of Human Neurological Diseases a. Kindling Model of Epilepsy 9 ..

Chapter 10: Brain Damage and Neuroplasticity LO 10.13 Describe the kindling model of epilepsy, and explain the ways in which it models human epilepsy.

• •

• • • •

•

The typical kindling experiment begins with an animal (usually a rat) receiving a mild, brief electrical brain stimulation (usually to the amygdala) about once per day.

The first stimulation has no behavioral effect; however, after a few days of stimulations a mild convulsion is elicited. With further stimulation, the convulsions elicited by each stimulation become longer and longer and more and more generalized, and eventually produces a fully generalized convulsion.

Kindling can be produced by the periodic stimulation of many brain sites other than the amygdala; it can be produced by the periodic administration of initially subconvulsive doses of convulsive drugs and it can be elicited in many different species.

Kindling does not occur at all at short interstimulation intervals (less than 20 minutes or so) and it takes many more stimulations to kindle if the intervals are less than an hour or so.

The most interesting and important aspect of kindling is its permanence.

The kindling paradigm has been used as to study epilepsy in two ways: – The convulsions elicited in kindled animals have been used as an animal model of different types of human epilepsy; and – The physiological changes that underlie kindling have been used as an animal model of the development of epilepsy (epileptogenesis) sometimes observed after a head injury.

Kindled convulsions are usually not spontaneous; however, if animals are kindled long enough (e.g., 300 stimulations in rats), they will eventually become truly epileptic, and will have convulsions that recur spontaneously even after the stimulations have been curtailed.

b. Transgenic Mouse Models of Alzheimer’s Disease LO 10.14 Describe the transgenic mouse models of Alzheimer’s disease, and evaluate their efficacy.

• •

• • •

•

This is the most exciting advance in Alzheimer’s disease research in many years, since the area has needed a good animal model of the disease.

The problem is that only humans and a few nonhuman primates develop amyloid plaques, a hallmark of the disease; this has prevented researchers from studying the role of plaques in the neurodegeneration that is observed in Alzheimer’s disease. (Are plaques a cause or a consequence of the degeneration?)

In one example of the transgenic mouse model of Alzheimer’s disease, genes that accelerate human amyloid development are injected into fertilized mouse embryos.

As mice mature, their brains develop amyloid plaques with a distribution similar to that seen in human patients (e.g., highest in hippocampus and surrounding areas).

Unfortunately, these mice do not develop neurofibrillary tangles; in addition, the degree of memory impairment does not change as the mice mature and develop more plaques.

However, these mice have proven useful in the development of amyloid vaccines for use as a treatment for Alzheimer’s disease.

An attempt to overcome the absence of neurofibrillary tangles has been to inject into transgenic mice the genet mutation that promotes accumulation of the protein tau.

c. MPTP Model of Parkinson’s Disease LO 10.15 Describe the events that led to the discovery of the MPTP model of Parkinson’s disease, and evaluate the utility of this animal model.

•

This particular animal model grew out of a tragic human accident.

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Biopsychology, Tenth Edition • • • •

In 1982, several young people were admitted to hospitals with severe Parkinson’s symptoms; this was surprising because such severe cases are not usually seen before the age of 50.

It was discovered that all were opioid addicts who had recently used a synthetic heroin made by the same person; some of the batch was obtained, and it was found to contain a neurotoxin called MPTP. This suggested that Parkinson’s disease might be effectively studied in an MPTP animal model; it was quickly established that laboratory primates (but not rats) exposed to MPTP experienced a major loss of neurons in the substantia nigra and a reduction in dopamine.

In addition, most of these primates developed a Parkinson’s disease-like behavioral syndrome.

4. Responses to Nervous System Damage: Degeneration, Regeneration, Reorganization, and Recovery (see Figures 10.15–10.20 in Biopsychology) a. Neural Degeneration LO 10.16 Explain the various types of neural degeneration that ensue following axotomy.

•

•

This is a deterioration of the neuron following damage. There are two main types: – Anterograde degeneration involves distal segments of the axon and occurs rapidly following an axotomy; the entire segment of the axon that was separated from the cell body swells and within a few days breaks into fragments.

– Retrograde degeneration involves changes in the proximal segments of the axon from the site of damage back to the soma over a two- to three-day period. If early changes show an increase in the size, the neuron will likely regenerate the axon; if early changes include a decrease in size, the entire cell will probably degenerate and die.

Transneuronal degeneration is the spread of degeneration from damaged neurons to neurons on which they synapse. Anterograde transneuronal degeneration is when neurons postsynaptic to the damaged cell are affected. Retrograde transneuronal degeneration is when neurons that are presynaptic to the damaged cell are affected.

b. Neural Regeneration LO 10.17 Compare neural regeneration within the CNS and the PNS. • • • • • •

Is a regrowth of the damaged neurons: this occurs more readily in invertebrates than in higher vertebrates; is hit-or-miss in the PNS of mammals, and is almost nonexistent in the CNS of adult mammals.

In mammalian PNS regeneration, regrowth from the proximal stump of the damaged neuron begins two to three days after damage; if the myelin sheath is intact, regrowth may be guided through the myelin sheath and toward the original target.

However, if a segment of the nerve has been cut, the regenerating axons may grow into incorrect sheaths and thus to incorrect targets, or else the axon may grow in a tangled mass without direction.

Collateral sprouting is the growth of axon branches from adjacent healthy neurons and may occur at the site of degenerating neurons.

CNS neurons can regenerate if they are placed in the PNS, whereas PNS neurons cannot regenerate in the CNS; the secret to regeneration in the PNS appears to be the Schwann cells that form myelin sheaths in the PNS. Schwann cells promote regeneration by releasing both trophic factors (promote growth) and cell-adhesion molecules (guide growing axons to targets).

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Chapter 10: Brain Damage and Neuroplasticity c. Neural Reorganization LO 10.18 Describe three examples of cortical reorganization following damage to the brain, and discuss the mechanisms that might underlie such reorganization.

• •

• • •

Damage to sensory and motor pathways, the sensory and motor cortexes, and distortion of sensory experiences have all been used to study neural reorganization in adult mammals.

For example, Kaas et al., (1990) found that retinal lesions resulted in new visual receptive fields in areas of the primary visual cortex that had originally received input from the lesioned areas of retina. It was later learned that these changes begin within minutes of the retinal lesion.

In a similar vein, Sanes, Suner, and Donoghue (1990) found that transection of the motor neurons that controlled the vibrissae muscles of rats produced changes in the associated motor cortex areas so that they came to activate other parts of the face after a few weeks.

It has been shown that individuals who are blind have sensory cortices that show overrepresentation for audition and somatosensory inputs.

The reorganization of neural connections is believed to occur via two types of changes: – Reorganization may occur through release from inhibition previously unused connections.

– Gradual reorganization usually results from neural damage; this is believed to reflect the establishment of new connections via collateral sprouting.

Reorganization may also occur through neural degeneration, adjustment of dendritic trees, and adult neurogenesis.

d. Recovery of Function after CNS Damage LO 10.19 Describe the concept of “cognitive reserve,” and discuss the potential role of adult neurogenesis in recovery following CNS damage.

• • • •

A challenge to the study of recovery of function is to distinguish it from a decline in cerebral edema or the acquisition of compensatory behavioral strategies.

There is no evidence that hippocampal stem cells can migrate to sites of damage and contribute to recovery.

Cognitive reserve (related to education and intelligence) is important in the apparent recovery of cognitive function that is often observed. This seems to be due to the adoption of alternative strategies to solve a problem, rather than true recovery of function.

Researchers have found that the neurodegeneration normally caused by ischemia can be blocked by administration of viruses that release apoptosis inhibitor protein; this blocked the loss of hippocampal cells and poor performance in the Morris water maze that was observed in untreated control rats.

5. Neuroplasticity and the Treatment of CNS Damage a. Neurotransplantation as a Treatment for CNS Damage: Early Research LO 10.20 Discuss early work on neurotransplantation for the treatment of CNS damage.

• •

Based on successful transplants in the primate MPTP model, doctors bilaterally implanted fetal substantia nigra cells into the striatum of Parkinson’s patients.

Initial reports were promising, as many patients showed a reduction of symptoms; however, the results of a subsequent, large-scale double-blind evaluation suggest that as many as 15% of patients showing an initial positive response to the transplanted tissue develop side effects, such as uncontrollable writhing and chewing movements.

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Biopsychology, Tenth Edition • •

Other early clinical approaches involved implanting dopamine-releasing cells from the adrenal medulla.

Transplantation of Schwann cells sheaths has also been shown to promote axonal regeneration in the CNS, restoring motor function following lesions of corticospinal pathways.

b. Modern Research on Neurotransplantation LO 10.21 Discuss the methods and findings of modern research on neurotransplantation.

• • • •

The early failures of clinical transplantation have not stifled research in this field.

Recall that stem cells are pluripotent (can develop into many different types of mature cells).

However, they are not permanent sources for transplantation because they accumulate chromosomal abnormalities with repeated cell division.

Neurotransplantation can be effective via mechanisms other than replacing dead neurons: – Implants can stimulate remyelination, release neurotrophic factors, or differentiate into glia cells

c. Promoting Recovery from CNS Damage by Rehabilitative Training LO 10.22 Discuss methods of promoting recovery from CNS damage through rehabilitative treatment.

• •

• •

•

It has become clear that experience can facilitate the functional reorganization of the CNS following damage.

Treating Strokes – Small strokes often produce a core of damage, which is followed by a gradually expanding loss of function around this core. This latter loss can be reduced in motor cortex by rehabilitative training; recovery of function following damage to the hand area of motor cortex in primates is facilitated if the monkeys engage in manual tasks during their recuperation. There is less loss of tissue and greater recovery of manual dexterity.

Treating Spinal Injury – Following spinal cord injury in humans, people receiving rehabilitative training (physical and cognitive training) showed greater recovery of function (walking) than people that simply received conventional physiotherapy.

Benefits of Cognitive and Physical Exercise – Animals exposed to enriched environments demonstrate more dendritic branching, increased size and number of dendritic spines, increased rate of adult neurogenesis, and improved levels of neurotrophic factors. Physical exercise improves neurogenesis and reduces the formation of plaques associated with Alzheimer’s disease.

Treating Phantom Limbs – About 50% of amputees suffer from phantom limb pain; surgical interventions are notoriously poor at treating such pain, but it can be reduced by encouraging reorganization of the areas of somatosensory cortex that previously innervated the amputated limb.

< Return to Table of Contents

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Chapter 10: Brain Damage and Neuroplasticity

LECTURE LAUNCHERS Lecture Launcher 10.1: Visualizing a Brain Tumor Pinel begins Chapter 10 with the story of his own experience with a brain tumor. You can begin this series of lectures by discussing brain tumors in greater detail. A very nice summary of brain tumors, their diagnosis, and treatments is located at http://www.umm.edu; place “brain tumors primary” in the search bar. Click on the first link that comes from your search results.

Lecture Launcher 10.2: Identification and Treatment of Cerebral Aneurysms Students are usually amazed at the sight of a cerebral aneurysm, especially if you present them within the context of “Now how would you go about treating this type of brain pathology?” Your discussion will be greatly helped by the simple and well-illustrated overview of the different types of cerebral aneurysms and their surgical treatment (complete with animations) available at http://brainavm.uhnres.utoronto.ca/. From the homepage, click “For Patients,” the link for “Brain Vascular Disorders” and then select “Brain Aneurysms.”

Lecture Launcher 10.3: Apoptosis and Necrosis In Chapter 10, Pinel discusses the differences between apoptosis and necrotic cell death, with apoptosis being the preferred means of cell death due to the fact that it is less likely to involve other cells in the brain.

The processes of apoptosis and necrosis, and the reasons why apoptosis is preferred, are nicely illustrated in an animation available at http://www.susanahalpine.com/. Once on the homepage, select “animations” and scroll down the page to the link to “Cell death: Necrosis and Apoptosis.”

Lecture Launcher 10.4: Thinking Yourself Strong?

One problem with the idea of rehabilitative training is that patients sometimes lack the strength to engage in many of the activities that are required. However, researchers have recently demonstrated that at least some of the gains of rehabilitative training can be achieved if you simply imagine that you are using a limb.

Present this idea to your class and discuss its implications, both for normal activities (e.g., visualizing playing a guitar) and in therapeutic situations. For more information on this idea, see http://jn.physiology.org and place “the power of the mind” in the search bar. Click on the matching link.

Lecture Launcher 10.5: Introduction to Brain Tumors Beginning a lecture with a few interesting facts or connections to people the student might have heard about can entice students into wanting to know more about the topic. This list can come in handy for these introductions!

For example: There are over 120 different types of brain tumors, making effective treatment very complicated.

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Biopsychology, Tenth Edition Brain tumors in children are different from those in adults and are often treated differently. Although as many as 69 percent of children with brain tumors will survive, they are often left with long-term side effects.

Symptoms of a brain tumor can include headaches (headaches that wake you up in the morning), seizures in a person who does not have a history of seizures, cognitive or personality changes, eye weakness, nausea or vomiting, speech disturbances, or memory loss. While these are the most common symptoms of a brain tumor, they can also indicate other medical problems.

Bob Marley, 36, reggae singer Greg Morris, 62, Mission Impossible actor Deke Slayton, 47, astronaut George Gershwin, 36, composer Pat Paulsen, 69, comedian

Wilma Rudolph, 54, Olympic Gold medalist Mike Synar, 45, U.S. congressman Megan O’Connell, 30, international model Slim Pickens, 64, actor Gene Siskel, 53, movie critic

Web Links 10.2 National Brain Tumor Foundation 10.3 National Cancer Institute Lecture Launcher 10.6: Prevalence of Brain Injury Many students are already familiar with the term “traumatic brain injury” (TBI). According to one RAND Corporation report (Invisible Wounds of War), approximately 19.5 percent of troops returning from Iraq have experienced probable TBI. The effects of TBI are of major concern to the Veterans Administration and the Department of Defense.

Web Link 10.4 Traumatic Brain Injury Lecture Launcher 10.7: Phenylketonuria Some interesting facts: Low levels of tyrosine also lead to lowered production of the pigment melanin, so children with this condition tend to have fairer hair and greener eyes than other members of their family.

The excess phenylalanine, instead of being converted to tyrosine, is converted into phenylketones, which are excreted in the urine (phenylketone—uria (urine)) The sweat and urine of an affected child has a distinctive musty odor due to these ketones.

Amino acids are common in most foods. How is something like phenylketonuria treated?

“At first, the baby is fed a special formula that contains protein but no phenylalanine. Breast milk or infant formula is used sparingly to supply only as much phenylalanine as the baby can tolerate. Later, certain vegetables, fruits, some grain products (for example, certain cereals and noodles) and other lowphenylalanine foods are added to the diet, but no regular milk, cheese, eggs, meat, fish and other high protein foods are ever allowed. Since protein is essential for normal growth and development, the child must continue to have one of the special formulas that are high in protein and essential nutrients, but contain little or no phenylalanine. Diet drinks and foods that contain the artificial sweetener aspartame (which contains phenylalanine and is sold as NutraSweet or Equal) must be strictly avoided.”

Can students name products that have phenylalanine?

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Chapter 10: Brain Damage and Neuroplasticity

Web Links 10.6 Genes and Disease—PKU 10.7 PKU Lecture Launcher 10.8: Down Syndrome Since Down syndrome is relatively common—it occurs at a rate of 1 in 700 to 800 live births—many students know or have at least seen someone with this disorder. The distinctive physical characteristics have also served to make this a disorder that people know about. Down syndrome has also been represented in television programs and movies. One example is the character of Corky in the 1990s TV series, Life Goes On. Duo is an independent film starring Stephane Ginnsz. It is notable for featuring the first lead actor with Down syndrome.

Clips from the movie or TV show could be used to introduce the topic.

Another resource for images of Down syndrome children would be a movie, produced by a parent of a Down syndrome child, called Down Syndrome: The First 18 Months. < Return to Table of Contents

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Biopsychology, Tenth Edition

WEB LINKS Web Link 10.1: Gene Tests: Gene Reviews http://www.geneclinics.org Do a search for diseases with genetic factors for a detailed report on the genetic aspects of the disease.

Web Link 10.2: National Brain Tumor Foundation http://www.braintumor.org Limited but understandable information about tumors and treatment.

Web Link 10.3: National Cancer Institute Go to http://www.cancer.gov/ and place “what you need to know about brain tumors” in the search bar.

Select the link that comes up with that name.

Information about brain tumors from the National Cancer Institute.

Web Link 10.4: Traumatic Brain Injury Go to http://www.ninds.nih.gov/ and place “traumatic brain injury” in the search bar. Click on the link that is called “traumatic brain injury information page.” The National Institute of Neurological Disorders’ Web page on traumatic brain injury (TBI). An excellent summary of what it is, what causes it, why it is a problem, and possible treatments.

Web Link 10.5: Epilepsy Foundation Resources http://www.efa.org Web Link 10.6: Genes and Disease—PKU Go to https://ghr.nlm.nih.gov/ and place “PKU” in the search bar. Select the first link that comes from your search.

Includes information on how PKU occurs, how it is diagnosed, and how it is managed.

Web Link 10.7: PKU Go to http://www.marchofdimes.org/and place “PKU and your baby” in the search bar. Select the link with the matching title.

March of Dimes: Quick Reference and Fact Sheets. Outline of information on phenylketonuria.

Web Link 10.8: Down’s Syndrome and Alzheimer’s Go to http://www.alz.org and place “Down Syndrome and Alzheimer’s Disease” in the search bar. Select the link with the same name.

Possible relationship between Down Syndrome and Alzheimer’s Disease.

Web Link 10.9: NINDS Parkinson’s Disease Information Page Go to http://www.ninds.nih.gov/ and place “Parkinson’s Disease” in the search bar.

Web Link 10.10: Parkinson’s Disease Foundation: Understanding Parkinson’s Go to http://www.pdf.org/ and click on the tab titled “Understanding Parkinson’s.” Choose your topic from the menu at the bottom.

Comprehensive page on Parkinson’s disease.

Web Link 10.11: Parkinson’s Disease Foundation: Medications and Treatments 17 ..

Chapter 10: Brain Damage and Neuroplasticity Go to http://www.pdf.org/ and click on the link for “Understanding Parkinson’s.” From the drop down menu, select “What is Parkinson’s Disease?” Once on that page select “Medications and Treatments” from the menu listed on the left side of the page.

Detailed summary with interactions and side effects.

Web Link 10.12: Genetics Home Reference: Parkinson Disease Go to http://ghr.nlm.nih.gov/ and place “Parkinson’s Disease” in the search bar. Select the matching link.

Some clear explanations of the genetic differences between forms of Parkinson’s disease.

Web Link 10.13: Dystonia Go to https://www.verywell.com and place “dystonia” in the search bar. From there, you may select an overview or you may select to look at supportive therapies.

Web Link 10.14: Deep Brain Stimulation for Parkinson’s Go to http://www.ninds.nih.gov/ and place “deep brain stimulation for Parkinson’s” in the search bar. Select the link with the matching name.

Web Link 10.15: NINDS Huntington’s Disease Information Page Go to http://www.ninds.nih.gov/ and place “Huntington’s disease” in the search bar. Select the matching link.

Web Link 10.16: HDLighthouse http://hdlighthouse.org/ Information on Huntington’s disease, including news updates on recent discoveries.

Web Link 10.17: Huntington’s Disease Go to http://www.ninds.nih.gov/ and place “Huntington’s Disease” in the search bar. Select the information page for Huntington’s Disease.

Web Link 10.18: NINDS Alzheimer’s Disease Information Page Go to http://www.ninds.nih.gov/ and place “Alzheimer’s Disease” in the search bar. Select the information page for Alzheimer’s Disease.

Web Link 10.19: Inside the Brain: An Interactive Tour Go to http://www.alz.org/ and place “inside the brain” in the search bar. Select the first link titled “Inside the Brain: An Interactive Tour.”

A simple treatment, but some very nice illustrations.

Web Link 10.20: Alzheimer’s Research Forum http://www.alzforum.org/ Links to recent research topics and data.

Web Link 10.21: Diagnosis and Management of Multiple Sclerosis Go to http://www.aafp.org/ and place “diagnosis and management of multiple sclerosis” in the search bar.

Page down until you find a link that matches that same name.

Detailed information and references. Useful images.

Web Link 10.22: NINDS Multiple Sclerosis Information Page Go to http://www.ninds.nih.gov/ and place “multiple sclerosis” in the search bar. Select the link for the multiple sclerosis information page.

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Biopsychology, Tenth Edition Web Link 10.23: Herpes Simplex Virus Go to http://emedicine.medscape.com/ and place “herpes simplex encephalitis” in the search bar. Select the link with the matching name.

Not only can this virus lay dormant for years and then cause encephalitis, it can also do a great deal of damage to a fetus or newborn and can be deadly when someone has a compromised immune system as in AIDS. Web Link 10.24: Viral Infections Go to http://www.merck.com/ and place “rabies” in the search bar. Select the link with the same name.

“Symptoms appear when the rabies virus reaches the brain or spinal cord, usually 30 to 50 days after the person is bitten. However, this interval can vary from 10 days to more than a year. The closer the bite to the brain, the more quickly symptoms appear.

“Rabies commonly begins with a short period of depression, restlessness, a general feeling of illness (malaise), and a fever. However, in 20% of people, rabies begins with paralysis in the lower legs that moves up through the body. Restlessness increases, leading to uncontrollable excitement, and saliva production greatly increases. Spasms of the muscles in the throat and voice box occur because rabies affects the area in the brain that controls swallowing and breathing. The spasms can be excruciatingly painful. A slight breeze or an attempt to drink water can trigger the spasms. Thus, a person with rabies cannot drink. For this reason, the disease is sometimes called hydrophobia (fear of water).

“As the disease spreads through the brain, the person becomes more and more confused and very agitated.

Eventually, coma and death result. The cause of death can be blockage of airways, seizures, exhaustion, or widespread paralysis.” < Return to Table of Contents

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11 Learning, Memory, and Amnesia: How Your Brain Stores Information TABLE OF CONTENTS Chapter-at-a-Glance

2

Learning Objectives

3

Brief Chapter Outline

4

Teaching Outline

5

Lecture Launchers

14

Activities

17

Assignments

18

Web Links

19

Handouts

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Chapter 11: Learning, Memory, and Amnesia

CHAPTER-AT-A-GLANCE

Brief Outline Chapter Introduction (p. 272) 11.1 Amnesic Effects of Bilateral Medial Temporal Lobectomy (pp. 273–279) 11.2 Amnesia of Korsakoff’s Syndrome and 11.3 Alzheimer’s Disease (pp. 279–280) 11.4 Amnesia After Concussion: Evidence for Consolidation (pp. 280–283) 11.5 Evolving Perspective of the Role of the Hippocampus in Memory (pp. 283–288) 11.6 Neurons of the Medial Temporal Lobes and Memory (pp. 288–291) 11.7 Where Are Memories Stored? (pp. 291–294) 11.8 Synaptic Mechanisms of Learning and Memory (pp. 294-298) 11.9 Conclusion: Biopsychology of Memory and You (pp. 298-300)

Instructor’s Manual Resources Lecture Launchers 11.1, 11.8,11.9, Activity 11.1 Lecture Launcher 11.2 Lecture Launcher 11.3

Assignments 11.1, 11.2

Lecture Launchers 11.4, 11.10, 11.11, Activity 11.3 Lecture Launchers 11.5, 11.6, 11.7, Activity 11.2 Assignment 11.3

< Return to Table of Contents

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Biopsychology, Tenth Edition

LEARNING OBJECTIVES After completion of this chapter, the student should be able to: LO 11.1 LO 11.2 LO 11.3 LO 11.4 LO 11.5 LO 11.6 LO 11.7 LO 11.8 LO 11.9 LO 11.10 LO 11.11 LO 11.12 LO 11.13 LO 11.14 LO 11.15 LO 11.16 LO 11.17 LO 11.18 LO 11.19 LO 11.20 LO 11.21 LO 11.22

Describe the specific memory tests used to assess H.M.’s anterograde amnesia.

Describe three major scientific contributions of H.M.’s case.

Discuss what research on medial temporal lobe amnesias has taught us about learning and memory.

Describe the difference between semantic and episodic memories.

Describe the case of R.B. and the phenomenon known as transient global amnesia.

Describe the symptoms and etiology of the amnesia of Korsakoff’s syndrome.

Describe the symptoms and etiology of the amnesia of Alzheimer’s disease.

Summarize the effects of a closed-head injury on memory.

Describe the classic view of memory consolidation and some of the evidence it rests upon.

Contrast the view with the current view of memory consolidation.

Describe the delayed nonmatching-to-sample tests for monkeys and rats.

Describe the neuroanatomical basis for the object-recognition deficits that result from bilateral medial temporal lobectomy.

Describe hippocampal place cells and entorhinal grid cells and the relationship between these two cell types.

Describe the role of the hippocampus in spatial memory and the other types of memory it supports.

Define a concept cell, and describe the key properties of concept cells with reference to the experimental evidence.

Explain what an engram cell is, and describe how these cells were identified using optogenetics.

List the types of memories that are stored in each of the following structures: inferotemporal cortex, amygdala, prefrontal cortex, cerebellum, and striatum.

Describe the phenomenon known as long-term potentiation (LTP), and provide evidence for its role in learning and memory.

Describe the mechanisms underlying the induction of LTP. Describe four findings that have emerged from the study of the maintenance and expression phases of LTP. Define long-term depression (LTD) and metaplasticity.

Define infantile amnesia, and describe two experiments that investigated whether infantile amnesia extends to implicit memories.

Discus the findings on the efficacy of smart drugs.

< Return to Table of Contents

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Chapter 11: Learning, Memory, and Amnesia

BRIEF CHAPTER OUTLINE Lecture Launcher 11.1: Using Models to Describe H.M.’s Surgery 1. Amnesic Effects of Bilateral Medial Temporal Lobectomy a. Formal Assessment of H. M’s Anterograde Amnesia: Discovery of Unconscious Memories b. Three Major Scientific Contributions of H.M.’s Case c. Medial Temporal Lobe Amnesia d. Semantic and Episodic Memories e. Effects of Global Cerebral Ischemia on the Hippocampus and Memory Lecture Launcher 11.2: A Neural Prosthesis?

2. Amnesia of Korsakoff’s Syndrome and 3. Alzheimer’s Disease a. Amnesia of Korsakoff’s Syndrome b. Amnesia of Alzheimer’s Disease Lecture Launcher 11.3: Do Coaches Take Concussions Seriously?

4. Amnesia after Concussion: Evidence for Consolidation a. Posttraumatic Amnesia b. Gradients of Retrograde Amnesia and Memory Consolidation 5. Evolving Perspective of the Role of the Hippocampus in Memory a. Animal Models of Object-Recognition Amnesia: The Delayed Nonmatching-to-Sample Test b. Neuroanatomical Basis of the Object-Recognition Deficits Resulting from Medial Temporal Lobectomy 6.

Neurons of the Medial Temporal Lobes and Memory a. Hippocampal Place Cells and Entorhinal Grid Cells b. Comparative Studies of the Hippocampus and Spatial Memory c. Jennifer Aniston Neurons: Concept Cells d. Engram Cells Lecture Launcher 11.4: Rat Going for a Swim 7. Where Are Memories Stored? a. Five Brain Areas Implicated in Memory Lecture Launcher: 11.5: Long-Term Potentiation: A Model of the Cellular Basis of Memory?

8. Synaptic Mechanisms of Learning and Memory a. Long-Term Potentiation b. Induction of LTP: Learning c. Maintenance and Expression of LTP: Storage and Recall d. Variability of LTP 9. Conclusion: Biopsychology of Memory and You a. Infantile Amnesia b. Smart Drugs: Do They Work? < Return to Table of Contents 4 ..

Biopsychology, Tenth Edition

TEACHING OUTLINE • • • • • • • • •

Learning deals with how experience changes the brain, and memory refers to how these changes are stored and later reactivated.

Much has been learned about the neural mechanisms of memory by studying amnesic patients.

H.M. suffered from severe, intractable epilepsy; he seemed to have epileptic foci in both medial temporal lobes.

Because unilateral medial temporal lobectomy had proven successful in patients with one epileptic focus, a bilateral medial temporal lobectomy was prescribed for H.M.; this included the removal of the hippocampus and the amygdala.

In some respects, the operation was a success: H.M.’s convulsions were reduced in severity and frequency, his I.Q. increased from about 104 to about 118, and he remained an emotionally stable individual with generally superior psychological abilities.

There is one exception to this otherwise rosy picture: H.M. suffered from devastating amnesia as a result of his operation.

H.M. has minor retrograde amnesia (amnesia for events before his surgery) for events within the two years preceding the surgery.

He has normal memory for remote events and normal short-term memory (his digit span is about six).

However, he cannot form long-term memories for events that occurred after his surgery (anterograde amnesia); for example, he has no memory of his new home, his new job, or new friends.

1. Amnesic Effects of Bilateral Medial Temporal Lobectomy (see Figures 11.1–11.4 in Biopsychology) a. Formal Assessment of H.M.’s Anterograde Amnesia: Discovery of Unconscious Memories LO 11.1 Describe the specific memory tests used to assess H.M.’s anterograde amnesia.

•

• • •

• •

At first, it was assumed that H.M. could not form long-term memories at all, but objective testing revealed that H.M. could demonstrate his retention of certain types of tasks by his improved performance on them, although he has no conscious recollection of previously practicing them.

H.M.’s deficits can be described in terms of his performance on seven objective tests of memory.

Digit Span +1 Test: After 25 trials with the same series of digits, he could do only seven digits, just one more than his normal memory span.

Block-Tapping Memory-Span Test: His block-tapping memory-span was normal; but he could not extend it, even by one, when the same sequence was repeated for twelve trials. This test helped show that H.M. had global amnesia-amnesia for information presented in all sensory modalities.

Mirror-Drawing Test: He displayed substantial savings with no conscious recall of previous practice.

Incomplete-Pictures Test: This test is a nonsensorimotor test of memory. After seeing five sets of twenty line drawings of varying completeness, he displayed substantial savings with no conscious recall of the drawings.

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Chapter 11: Learning, Memory, and Amnesia •

Pavlovian Conditioning: Tones and a puff of air to the eye were presented to H.M.; he blinked in response. Two years later, he retained this conditioned pairing almost perfectly, although he had no conscious awareness of his previous training.

b. Three Major Scientific Contributions of H.M.’s Case LO 11.2 Describe the three major scientific contributions of H.M.’s case.

H.M.’s case had the following significant influences on the study of memory: • It showed that the medial temporal lobes are important for memory.

• It led to the discovery that bilateral temporal lobectomy abolished H.M.’s ability to form certain kinds of long-term memories without disrupting his performance on STM or his remote memory (memory for experiences in the distant past). This suggested that there were 3 different modes of memory storage. H.M.’s problems were with consolidating memories (moving memories from short-term to long-term memory).

• It revealed that amnesic patients might claim no recollection of a previous experience, while demonstrating memory for it by improved performance. This led to the creation of two distinct categories of memories: explicit and implicit memories. c. Medial Temporal Lobe Amnesia LO 11.3 Discuss what research on medial temporal lobe amnesias has taught us about learning and memory.

• • • •

• •

Medial temporal lobe amnesia occurs when a patient has preserved intellectual functioning and mnemonic deficits.

H.M.’s ability to form implicit, but not explicit, long-term memories is often seen in cases of medial temporal lobe amnesia.

Tests have developed to assess implicit memory, called repetition-priming tests.

Repetition priming tests are used to assess implicit memory; patients are shown a list of words and some time later they are shown a series of word fragments and asked to complete the words.

Amnesic patients do as well on this task as control subjects, even though they do not remember ever seeing the original list of words.

The fact that implicit memories are intact, while explicit memories are compromised, in patients suffering from medial temporal lobe amnesia raises the question, “Why do we have two memory systems, one conscious, and the other unconscious?”

The answer seems to be flexibility; implicit memories do not transfer well to different contexts, whereas explicit memories can.

d. Semantic and Episodic Memories LO 11.4 Describe the difference between semantic and episodic memories.

• •

Explicit memories are divided into two categories: episodic and semantic memories.

Recent research has suggested that problems with episodic memory (memories for the events of one’s own life) are more common than problems with semantic memory (memories for general facts or information) in patients suffering from medial temporal lobe amnesia.

e. Effects of Global Cerebral Ischemia on the Hippocampus and Memory LO 11.5 Describe the case of R.B. and the phenomenon known as transient global amnesia.

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Biopsychology, Tenth Edition The Case of R.B. • R.B. suffered ischemia-produced brain damage during heart surgery; subsequently, R.B. displayed a pattern of amnesic deficits similar to, although less severe than, those of H.M. • Shortly after testing, R.B. died and postmortem examination revealed damage to the pyramidal cell layer of the CA1 hippocampal subfield, but no other obvious damage.

• This supported the original hypothesis that H.M.’s deficits were attributable to his hippocampal damage, although there might have been subtle damage to other regions.

• A stroke can sometimes produce transient global amnesia, which is characterized by sudden onset and severe anterograde amnesia lasting 4–6 hours.

• DTI studies have identified damage to the CA1 subfield following transient global amnesia.

(Figure 11.4 in Biopsychology) 2. Amnesia of Korsakoff’s Syndrome LO 11.6 Describe the symptoms and etiology of the amnesia of Korsakoff’s syndrome.

• • • • • • • • •

Individuals who chronically consume alcohol develop a pattern of behavioral disorders commonly referred to as Korsakoff’s syndrome believed to result from a thiamine deficiency.

In addition to severe anterograde amnesia, Korsakoff’s patients suffer from a severe retrograde amnesia.

Although their retrograde amnesia is more severe for recent memories, it also affects their memory for events occurring many years before the diagnosis of their case (i.e., for remote events).

This temporal gradient is usually assumed to reflect a gradient of retrograde amnesia; however, it could reflect the insidious development of anterograde deficits prior to diagnosis—or a combination of both.

The brain damage associated with Korsakoff’s amnesia is diffused, but the amnesia is usually attributed to medial diencephalic damage, particularly to the mediodorsal nuclei of the thalamus.

Support for the role of diencephalic structures in mnemonic function comes from the patient N.A. who had medial diencephalic amnesia.

N.A. was in the Air Force. One day, he was accidentally stabbed in the brain through the right nostril by a friend with a fencing foil; he suffered both retrograde and anterograde amnesia.

The foil penetrated the cribriform plate; a subsequent MRI revealed extensive damage in medial diencephalon, including the mediodorsal thalamic nuclei and the mammillary bodies.

Despite this evidence, it is unlikely that Korsakoff’s amnesia is due to damage to any single brain region.

3. Amnesia of Alzheimer’s Disease LO 11.7 Describe the symptoms and etiology of the amnesia of Alzheimer’s disease.

• This is a major cause of amnesia; the first noticeable symptom is often a mild loss of memory.

• The disease is progressive; eventually, the dementia becomes severe enough to completely incapacitate the patient.

• Considerable attention has been focused on predementia Alzheimer’s patients; in addition to both anterograde and retrograde amnesia, these patients often display deficits in short-term memory and some forms of implicit memory (those involving verbal or perceptual material, but not sensorimotor learning).

• Pathological changes include reduced levels of the neurotransmitter acetylcholine; these changes suggested that acetylcholine plays a role in the amnesia observed in Alzheimer’s patients. This reduction in acetylcholine occurs because of degeneration of the basal forebrain.

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Chapter 11: Learning, Memory, and Amnesia

4. Amnesia after Concussion: Evidence for Consolidation (see Figures 11.5–11.6 in Biopsychology) a. Posttraumatic Amnesia LO 11.8 Summarize the effects of a closed-head injury on memory.

• • •

Blows to the head can lead to a disturbance of consciousness (concussion), a complete loss of consciousness (coma), and amnesia; the memory loss attributable to a nonpenetrating blow to the head is called posttraumatic amnesia.

Patients with posttraumatic amnesia generally have both anterograde and retrograde amnesia; in general, the anterograde amnesia is longer than the period of coma that produced it, while the duration of the coma lasts longer than the period of retrograde amnesia that it produced.

Islands of memory are surviving memories for isolated events that occurred during periods for which other memories have been wiped out.

b. Gradients of Retrograde Amnesia and Memory Consolidation LO 11.9 Describe the classic view of memory consolidation and some of the evidence it rests upon. Contrast that view with the current view of memory consolidation.

• • • •

The retrograde amnesia seen after concussion or coma is typically worse for the most recent memories; this led to the suggestion that older memories are stored in a more permanent form through the process of consolidation.

Electroconvulsive shock (ECS) has been used to study the process of consolidation; this has led to the belief that consolidation is a long-term process that may take years to complete.

Figure 11.6 represents the long gradient of ECS-produced retrograde amnesia.

The current view is that consolidation may last indefinitely, with memories continually updated and linked each time they are activated.

Hippocampus and Consolidation • The standard consolidation theory or dual-trace theory suggests that the hippocampus holds a memory until it has been stored elsewhere in cortical regions.

• The current view is that the hippocampus and other structures play a role in storing a memory every time it is recalled. Ongoing recall makes memories more resistant to hippocampal damage.

• An engram is a change in the brain that stores a memory. Each time an experience is repeated or the engram is recalled, it becomes more resistant to disruption.

Reconsolidation • Recently, the phenomenon of reconsolidation has attracted renewed attention. Apparently, each time a memory is retrieved, it is temporarily held in labile short-term memory, where it is susceptible to posttraumatic amnesia until it is reconsolidated.

5. Evolving Perspective of the Role of the Hippocampus in Memory • Early attempts to develop an animal model of medial temporal lobe amnesia were largely unsuccessful.

• In part, this was because researchers did not know that H.M.’s amnesia was restricted to explicit long-term memory, and most animal memory tests of the time focused on tests of implicit memory.

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Problems developing an animal model of medial temporal lobe epilepsy were also due to the fact that researcher’s attention focused almost entirely on the hippocampus, thus ignoring the potential contribution of the other structures that were damaged during H.M.’s surgery.

a. Animal Models of Object-Recognition Amnesia: The Delayed Nonmatching-to-Sample Test (see Figure 11.7–11.9 in Biopsychology) LO 11.10 Describe the delayed nonmatching-to-sample tests for monkeys and rats.

Monkeys • An animal model of H.M. was developed in monkeys in the 1970s.

• A monkey with bilateral medial temporal lobectomies had major problems forming long-term memories for an object encountered in the delayed nonmatching-to-sample test (DNMTS).

• In this test, a monkey is presented with a distinctive object, under which it finds food.

• After a delay, the monkey is presented with two test objects; the sample and an unfamiliar one.

• The monkey must remember the sample, so that it can select the unfamiliar one to get the reward.

• Monkeys with lesions had major object-recognition deficits after several minutes.

Rats (see Figures 11.10–11.13 in Biopsychology) • The rat hippocampus can be lesioned with little damage to surrounding structures.

• The Mumby box apparatus allows a version of the nonmatching-to-sample paradigm for rats.

• Remarkably, the performance of rats is not substantially different from that of monkeys at retention intervals of up to a minute. b. Neuroanatomical Basis of the Object-Recognition Deficits Resulting from Medial Temporal Lobectomy (see Figure 11.13 in Biopsychology) LO 11.11 Describe the neuroanatomical basis for the object-recognition deficits that result from bilateral medial temporal lobectomy.

• • •

In the early 1990s, researchers began to question the role of the hippocampus in the memory deficits observed following medial temporal lobectomy.

They found that bilateral removal of the medial temporal cortex consistently produces severe and permanent deficits for object recognition. In contrast, bilateral removal of the hippocampus produces only modest deficits and bilateral destruction of the amygdala produces none.

Data suggest that damage to brain structures other than the hippocampus contributes to the amnesia observed in patients following global cerebral ischemia.

6. Neurons of the Medial Temporal Lobes and Memory • Although the hippocampus may not be critical to the performance of the DNMTS test, it does appear to be involved in the mediation of spatial memory.

Two Tests of Rodent Spatial Memory • The Morris water maze test requires rats to learn the location of an invisible stationary platform and find it when swimming in opaque (usually milk-white) water; rats with hippocampal lesions have great difficulty with this task, whereas control rats without hippocampal damage easily learn the task.

• In the radial arm maze test, there is a central chamber with as many as eight alleys or “arms” radiating from it. During each test, a few of the eight arms of the apparatus are baited with some kind of reward. Intact rats learn to visit only the baited arms (this is referred to as reference memory), rats with hippocampal lesions show deficits in reference memory in that 9 ..

Chapter 11: Learning, Memory, and Amnesia they do not exclusively visit baited arms. In addition, they show deficits in working memory as they repeatedly visit unbaited arms during each test. a. Hippocampal Place Cells and Entorhinal Grid Cells LO 11.12 Describe hippocampal place cells and entorhinal grid cells and the relationship between these two cell types.

• • • • • • •

Evidence for the role of the hippocampus in spatial memory comes from the existence of hippocampal place cells; these cells fire when a rat is placed in a specific location (in the place field), but only after the rat becomes familiar with that location.

Each place cell has a place field in a different part of the environment.

By placing a rat in an ambiguous situation, yet in a familiar test environment, it is possible to determine where the rat “thinks” it is from the route it takes to get to the location previously reinforced.

The entorhinal cortex is a major source of neural signals to the hippocampus.

How hippocampal cells obtain their spatial information comes from the discovery of grid cells, entorhinal neurons that have an extensive array of evenly spaced place fields.

There are other types of neurons in the entorhinal cortex associated with spatial location.

For example: head-direction cells, tuned to the direction of head orientation, and border cells, which fire when the subject is near the borders of an environment.

b. Comparative Studies of the Hippocampus and Spatial Memory (see Figure 11.14 in Biopsychology) LO 11.13 Describe the role of the hippocampus in spatial memory and the other types of memory it supports.

• • • •

Comparative research has revealed that the hippocampus plays a role in the spatial memory of many different species.

For example, Sherry and his colleagues (1989) have reported that food-caching birds tend to have larger hippocampi than noncaching species.

Research on a variety of species indicates that the hippocampus plays a role in spatial memory, but the evidence from primates has been less consistent.

This may be because spatial memory in humans and monkeys is often tested while they remain stationary and make judgments on a computer screen—whereas the spatial memory in rats, mice, and birds is typically studied as the subjects navigate their environment.

c. Jennifer Aniston Neurons: Concept Cells LO 11.14 Define a concept cell, and describe the key properties of concept cells with reference to the experimental evidence.

•

•

Recording electrodes implanted in the medial temporal lobes of epileptic patients have found neurons that respond to very specific test objects or individuals. For instance, they discovered individual cells that fire in response to seeing a familiar face. These are called Jennifer Aniston neurons.

These concept cells might be part of larger circuits that store episodic memories that comprise the semantic components represented by each cell.

d. Engram Cells LO 11.15 Explain what an engram cell is, and describe how these cells were identified using optogenetics.

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•

•

It’s a two-stage process to identify engram cells. The tagging stage requires that the neurons that are active during the learning task be induced to express opsins. During the manipulate stage, the previously active neurons are now either inhibited or excited by using light to influence them.

Engram cells are cells believed to hold memories in the brain.

7. Where Are Memories Stored? (see Figure 11.17 in Biopsychology) a. Five Brain Areas Implicated in Memory LO 11.16 List the types of memories that are stored in each of the following structures: inferotemporal cortex, amygdala, prefrontal cortex, cerebellum, and striatum.

Along with the hippocampus, medial temporal cortex, mediodorsal nucleus of the thalamus, and the basal forebrain, the following regions are also believed to play a role in memory storage: •

Inferotemporal Cortex: As an area of secondary sensory cortex, this area is believed to play a role in the storage of long-term visual memories.

•

Amygdala: This area is involved in memories of the emotional significance of an event; lesions here impair fear conditioning or startle responses.

•

Prefrontal Cortex: Damage in this area does not produce a gross memory defect, but it does impair memory of the temporal order of events and also working memory.

•

Cerebellum and Striatum: These areas are involved in implicit memories of sensorimotor learning; the role of the cerebellum in the conditioned eyeblink response has been intensely studied, and the striatum is believed to be involved in habit learning.

8. Synaptic Mechanisms of Learning and Memory (see Figures 11.18–11.20 in Biopsychology) a. Long-Term Potentiation LO 11.17 Describe the phenomenon known as Long-term potentiation (LTP), and provide evidence for its role in learning and memory.

• •

• • •

LTP is interesting because it is the kind of change that was postulated by Hebb in 1949 to underlie memory.

In an LTP experiment, a brief period of intense high-frequency stimulation enhances the subsequent response of postsynaptic neurons to low-intensity stimulation of the presynaptic neurons. This enhancement can last for weeks depending on the number, duration, frequency, and intensity of the inducing stimulations.

LTP has frequently been studied in terms of changes in the response of neurons in the granulecell layer of the rat hippocampal dentate gyrus following intense high-frequency perforant path stimulation.

The co-occurrence of firing in presynaptic and postsynaptic cells is critical in LTP and many pieces of evidence support the idea that LTP is related to the neural mechanisms of learning and memory.

LTP has two qualities that fit with the type of synaptic changes that Hebb suggested would underlie learning: it is reasonably permanent, and it occurs only when both the presynaptic and the postsynaptic neurons were simultaneously active. This need for co-occurrence of activation is called Hebb’s postulate for learning.

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LTP is usually conceived of as occurring in three phases: induction, maintenance, and expression.

b. Induction of LTP: Learning LO 11.18 Describe the mechanisms underlying the induction of LTP. • •

•

The NMDA (N-methyl-D-aspartate) glutamate receptor has been the focus of most LTP research.

Interestingly, NMDA-mediated activation of postsynaptic neurons requires that the postsynaptic cell already be depolarized by concurrent activation by non-NMDA receptors; this requirement for co-occurrence of activity provides further support for Hebb’s postulate and the putative role of LTP in learning.

Full activation of NMDA receptors allows Ca2+ ions to enter postsynaptic neurons; this Ca2+ influx is believed to activate protein kinases that are responsible for the induction of LTP.

c. Maintenance and Expression of LTP: Storage and Recall LO 11.19 Describe four findings that have emerged from the study of the maintenance and expression phases of LTP. The maintenance and expression of LTP are due to both presynaptic and postsynaptic changes: • LTP develops only at specific presynaptic inputs (that are active during periods of postsynaptic depolarization), due to postsynaptic dendritic spines that restrict the movement of Ca2+ in the postsynaptic neuron to only those synapses that are activated by high-frequency stimulation.

• LTP activates numerous transcription factors that are responsible for the structural changes that accompany LTP. Researchers have documented increases in the number and size of synapses, dendritic spines, and in the number of postsynaptic receptors that exist following the induction of LTP. • It’s been found that numerous transcription factors are activated by neural activity in LTP. d. Variability of LTP LO 11.20 Define long-term depression (LTD) and metaplasticity.

• •

LTD (Long-term Depression) is the flip side of LTP and occurs in response to prolonged lowfrequency stimulation of presynaptic neurons.

Metaplasticity refers to the fact that LTP and LTD induction can be modulated by prior synaptic activity.

9. Conclusion: Biopsychology of Memory and You a. Infantile Amnesia LO 11.21 Define infantile amnesia, and describe two experiments that investigated whether infantile amnesia extends to implicit memories.

• • •

Infantile amnesia refers to the fact that we remember virtually nothing of events in our infancy.

The question begs: Do normal children who fail explicitly to recall or recognize things in early childhood display preserved explicit memories of those events?

Studies (skin conductance findings and recognition of pictures) reveal that they do.

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Biopsychology, Tenth Edition b. Smart Drugs: Do They Work?

LO 11.22 Discuss the findings on the efficacy of smart drugs.

• • •

Nootropics, or smart drugs, are substances that are thought to improve memory.

They include: ginko biloba, ginseng, multivitamins, glucose, cholinergic agonists, Piracetam, antioxidants, phospholipids, and many more.

The following conclusions can be drawn: o Most research has been done on nonhuman or humans with memory problems. o Research with humans is of low quality because it uses few participants, poor controls, and little effort is made to differentiate among the different kinds of memory. o The few positive findings are difficult to replicate and generalize. o In sum, there is not enough evidence to justify the claims that they improve memory.

Posttraumatic Amnesia and Episodic Memory • Posttraumatic amnesia occurred to one biopsychologist (R.M.) who experienced a skiing accident.

• He suffered retrograde and anterograde amnesia; he was trapped in the present.

• Curiously enough, he remembered the case of H.M., who had a similar fate.

• Fortunately, R.M. recovered to speak of the horrors of posttraumatic amnesia. < Return to Table of Contents

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Chapter 11: Learning, Memory, and Amnesia

LECTURE LAUNCHERS Lecture Launcher 11.1: Using Models to Describe H.M.’s Surgery To help students appreciate what a “radical bilateral medial temporal lobectomy” means, use a pull-apart plastic model of a brain (for a smaller class) or else a program like The Digital Anatomist (Go to http://www9.biostr.washington.edu/ and click on the link for the “Neuroanatomy Interactive Atlas” to demonstrate the extent of H.M.’s surgery. In particular, emphasize its bilateral nature and the various cortical and subcortical structures that were damaged. For more details about H.M., use the article “The Day His World Stood Still” from the Brain Connection site at http://www.brainconnection.com/. Place “The Day His World Stood Still” in the search bar and page down to the link matching that name.

Lecture Launcher 11.2: A Neural Prosthesis?

Some of the most interesting research in biopsychology has focused on ways to ameliorate the cognitive impairments associated with damage to structures like the hippocampus. None has been more interesting than the work of Dr. Ted Berger and his colleagues. Over the last fifteen years, they have developed a “neural prosthesis,” or an electronic chip designed to mimic the information processing abilities of the hippocampus. Listen to Dr. Berger describe his work by going to You Tube and searching “Theodore Berger Neuroengineering.” When discussing this work, ask your class about the ethical dilemmas facing this type of research. Is it akin to the implantation of an artificial heart or kidney, or is there something “special” about the brain?

Lecture Launcher 11.3: Second-Impact Syndrome Second-Impact Syndrome occurs when a player returns to the game before a concussion is fully healed. Us this video to begin a conversation on the changes we are seeing in sports today with regard to how they view concussions and whether or not enough is being done to protect athletes. Go to You Tube and search “Second-Impact Syndrome” and select the link to the Preston Plevretes Story.

Lecture Launcher 1.4: Rat Going for a Swim To help students understand the nature of the Morris Water Maze task, you can present the three videos, each of which shows one stage of a rat’s acquisition of the task. To find the videos, place “Short Videos of Morris Water Maze” in your browser. Select the link associated with the Cyclotron Research Center in Belgium.

Lecture Launcher 11.5: Long-Term Potentiation: A Model of the Cellular Basis of Memory?

The phenomenon of long-term potentiation (LTP) has attracted an incredible amount of research attention, as brain scientists of various backgrounds try to unravel the biological bases of long-term memory.

Animations on the following Web page illustrate some basics of this phenomenon: http://www.learner.org/ and place “LTP” in the search bar. Select the link associated with “Unit 10 Neurobiology.”

Lecture Launcher 11.6: Memory Systems Present different types of memory as being related to different biological systems or involving different parts of the brain and nervous system. Use a diagram of the brain to make these areas more explicit.

ABSTRACT: “The operation of different brain systems involved in different types of memory is described. One is a system in the primate orbitofrontal cortex and amygdala involved in representing rewards and punishers, and in learning stimulus-reinforcer associations. This system is involved in emotion and motivation. A second system in the temporal cortical visual areas is involved in learning invariant representations of objects. A third system in the hippocampus is implicated in episodic memory and in spatial function. Fourth, brain systems in the frontal and temporal cortices involved in short-term memory are described. The approach taken provides insight into the neuronal operations that take place in each of these brain systems, and has the aim 14 ..

Biopsychology, Tenth Edition of leading to quantitative biologically plausible neuronal network models of how each of these memory systems actually operates.”

Rolls, E. T. (2000). Memory Systems and the Brain. Annual Review of Psychology.

Lecture Launcher 11.7: Long-Term Potentiation Research Reading the literature in this area is not particularly easy. Students will do better if given support in reading through an article. Choose an article that you are comfortable with. (Several are suggested here.) Make copies of the article available online, in the library on reserve, or through class handouts.

The online articles provide the advantage of electronic editing. You can save the article as a word processing document. Most programs, such as Microsoft Word, have editing functions that allow the addition of marginal notes and line numbering. As instructor, you can go through the article, adding comments and term definitions, or you can make the article available with line numbering and wide margins to allow students to add their own notes.

Web Links 11.2 Long-Term Potentiation: What’s Learning Got To Do With It? 11.3 Long-term Potentiation and Contextual Fear Conditioning Increase Neuronal Glutamate Uptake 11.4 Review of Long-Term Potentiation: A Decade of Progress?

Lecture Launcher 11.8: Testing Motor Memory H.M. is the classic case study on anterograde amnesia. Your students may be interested in learning more about H.M. The Tower of Hanoi is one puzzle used to test the anterograde amnesia for H.M. Your students can get a feeling for what this game involves in this online version.

Web Link 11.7 The Day His World Stood Still 11.10 Tower of Hanoi Game Lecture Launcher 11.9: Case Studies Discussing real people with memory disorders can help students to see the value in learning the material.

Several interesting presentations of material are available, including media where the student can actually see, hear, and observe the results of the problem.

If you are going to discuss case histories, I strongly recommend you read the article by Elizabeth Loftus on “Jane Doe.” Rosenbaum, R. S., Köhler, S., Schacter, D. L., Moscovitch, M., Westmacott, R., Black, S. E., Gao, F. & Tulving, L. (2004). The case of K.C.: contributions of a memory-impaired person to memory theory. Neuropsychologica. K.C. has brain damage that includes large bilateral hippocampal lesions. He has severe anterograde amnesia. A good deal of his general knowledge of the world, including knowledge about himself, is preserved, but he is incapable of recollecting any personally experienced events. This article documents the brain damage using MRI-based quantitative measurements as well as describing his specific memory loss. HM is the classic case of anterograde amnesia. His symptoms and life are outlined in a number of publications.

Lecture Launcher 11.10: Memory in the Movies Bring in movie clips or describe scenarios when someone has lost his or her memory. Do the symptoms fit with the information about brain damage and loss of specific aspects of memory? How does amnesia from

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Chapter 11: Learning, Memory, and Amnesia hippocampal damage compare to a fugue state? What would be required to implant memories in a human brain?

For example, the movie Memento has both realistic and fictional symptoms as portrayed in the main character. You may wish to show relevant clips from the movie in class.

Other possible movies to explore are: The Bourne Identity Memento Total Recall The Man without a Past Hitchcock’s Spellbound Web Link 11.14 Memory Loss at the Movies Lecture Launcher 11.11: The Biology of Induced Memory The effect of disrupting protein synthesis and thereby disrupting a memory has almost science fiction types of implications. An excerpt from a popular press report on some of this research follows. “Imagine the possible benefit for people traumatized by haunting memories of terror or tragedy. The day may come when the cure is recalling the trauma, and then erasing it with a shot.” Dr. Karim Nader discovered that a fear memory induced in a rat and reactivated after 1–12 days of storage in the outer part of the brain could be eradicated with a shot of anisomycin, a protein-synthesis inhibitor.

The findings were based on earlier work identifying the amygdala as a site at which neural changes that underlie auditory fear learning occur. Current theories suggest that memories are processed by our brain initially as fragile short-term memories (STM) and then get stored more permanently as long-term memories (LTM). The transition from STM to LTM is mediated by the production of proteins. Nader found that fear experiences stored in the amygdala, when retrieved, return to a state that again requires protein synthesis in order to be restored. If you reactivate the fear memory and block the production of protein in the amygdala immediately afterwards, the memory is lost.

Systems consolidation theory suggests that the hippocampus also has a time-limited role in memory storage, after which the memory is independent of the hippocampus. This is why amnesiacs such as H.M., who have damage to their hippocampus, can remember events that happened a few years ago but can’t remember recent events.

Professors Nader and Ledoux showed that intra-hippocampal infusions of the protein synthesis inhibitor anisomycin caused amnesia for a consolidated hippocampal-dependent contextual fear memory, but only if the memory were reactivated prior to infusion. “In fact, we found that if you lesion the hippocampus 45 days after conditioning, there is no effect with the drug.”

• •

What are the implications for “False Memory Syndrome”?

What are the implications for EMDR Therapy or other therapeutic procedures?

Web Link 11.6 The Biology of Induced Memory

< Return to Table of Contents

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ACTIVITIES Activity 11.1: Getting a Feel for the Extent of H.M.’s Deficits To help students appreciate how severe H.M.’s memory deficits are, have one student come to the front of the class and administer a Digit Span +1 test (see page 274) to that student. Alternatively, have a student administer the test to you. Once the administration is complete, compare their scores to the average score that H.M. obtains on this task (i.e., less than eight digits after 25 trials).

Activity 11.2: Long-Term Potentiation Model The most difficult concepts in this chapter relate to long-term potentiation. There are many steps and components and the concepts involved are quite abstract. The best way to facilitate understanding is to make the concepts as visible and concrete as possible so that students can visualize the process. One way to do this is to have the students act out the long-term potentiation in a group of cells. If you have used the transmission skits in earlier chapters, this more complex model can be worked out in class. Have the students figure out who the players need to be, such as the cell membrane, calcium, magnesium, glutamate, etc. This might take an entire class period before the model is up and working, but the students will have a much better understanding than if they had simply listened to a lecture reiterating the material from the text.

Activity 11.3: Testing Your Memory Have the students try out some of the online memory games. Lead a class discussion on how the game relates to the brain structures that you have been discussing. What kind of brain damage would lead to problems with this game?

Web Link 11.1 The Memory Exhibition < Return to Table of Contents

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ASSIGNMENTS Assignment 11.1: Reading Primary Sources Reading some of the original literature on learning is a good way to tie the history of the discipline to current learning. Original articles by Hebb, Lashley and Watson can give students a review of learning while assisting them in reading original research.

References Hebb, Donald O. (1955). Drives and the C.N.S. (conceptual nervous system). Psychological Review, 62, 243–254. Available at http://psychclassics.yorku.ca/ and select “Hebb” from the alphabetical listing of authors.

Lashley, Karl S. (1930). Basic neural mechanisms in behavior. Psychological Review, 37, 1–24.

Available at http://psychclassics.yorku.ca/ and select “Lashley” from the alphabetical listing of authors.

Watson, John B. & Rayner Rosalie (1920). Conditioned Emotional Reactions. First published in Journal of Experimental Psychology, 3(1), 1–14. Available at http://psychclassics.yorku.ca/ and select “Watson” from the alphabetical listing of authors.

Rolls, E. T. (2000) Memory Systems and the Brain. Annual Review of Psychology.

Assignment 11.2: Diagnosis Case Studies This handout includes several mini-case studies that can get students thinking about the different aspects of memory.

Handout 11.1 Diagnosis Case Studies Assignment 11.3: Memory Games See Activity 11.3: Testing Your Memory. < Return to Table of Contents

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WEB LINKS Web Link 11.1: The Memory Exhibit Place “The memory exhibition Exploratorium” in your web browser. Click on the link called “The Memory Exhibition: Memory Games and More” from your search results. This link goes to the index, which includes links to memory games (Memory Solitaire, Tell Yourself a Story, Wander Around Your House, and Memory Party Game) as well as information and illustrations about a man who painted his childhood home from memory, comparing the paintings with the real locations.

Web Link 11.2: Long-Term Potentiation: What’s Learning Got to Do With It? Place “Long-term Potentiation: What’s Learning Got to Do With It?” in the search bar of your browser.

Select the link from http://www.neuroscience.brown.edu from your search.

ABSTRACT: “Of principal interest to those who study LTP, particularly LTP in the mammalian hippocampus, is its presumed role in the establishment of stable memories, a role consistent with “Hebbian” descriptions of memory formation. Other characteristics of LTP, including its rapid induction, persistence, and correlation with natural brain rhythms, provide circumstantial support for this connection to memory storage. Nonetheless, there is little empirical evidence that directly links LTP to the storage of memories...As an alternative to serving as a memory storage device, we propose that LTP may serve as a neural equivalent to an arousal or attention device in the brain.”

Shors, T. J. and Matzel, L. D. (1997) Long-Term Potentiation: What’s Learning Got to Do With It? Web Link 11.3: Long-Term Potentiation and Contextual Fear Conditioning Increase Neuronal Glutamate Uptake Go to http://www.nature.com/ and place the full title of the article as listed above in the search bar. Scroll down to select the link with the matching name.

ABSTRACT: “Induction and expression of long-term potentiation (LTP) in area CA1 of the hippocampus require the coordinated regulation of several cellular processes. We found that LTP in area CA1 was associated with an N-methyl-D-aspartate (NMDA) receptor-dependent increase in glutamate uptake. The increase in glutamate uptake was inhibited by either removal of Na+ or addition of D,L-threohydroxyaspartate. Dihydrokainate (DHK), a specific inhibitor of the glial glutamate transporter GLT–1, did not block the increase in glutamate uptake. LTP was also associated with a translocation of the EAAC1 glutamate transporter from the cytosol to the plasma membrane. Contextual fear conditioning increased the maximum rate (Vmax) of glutamate uptake and membrane expression of EAAC1 in area CA1. These results indicate that regulation of glutamate uptake may be important for maintaining the level of synaptic strength during long-term changes in synaptic efficacy.”

Jonathan Levenson, Edwin Weeber, Joel C. Selcher, Lorna S. Kategaya, J. David Sweatt & Arnold Eskin.

February 2002, Volume 5, Number 2, pp. 155–161. Published online: 14 January 2002, doi:10.1038/nn791 Web Link 11.4: Review of Long-Term Potentiation: A Decade of Progress?

By Robert C. Malenka & Roger A. Nicoll.

Place “Review of Long-Term Potentiation: A Decade of Progress” in your browser. Click on the link to the PDF file associated with the Silva Lab. Web Link 11.5: Hippocampus Neuron Photos Go to http://faculty.washington.edu/ and place “Hippocampus Neurons” in the search bar. Select the link sharing the same name.

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Chapter 11: Learning, Memory, and Amnesia Web Link 11.6: The Biology of Induced Memory Go to http://www.sciencedaily.com/ and place “The Biology of Induced Memory” in the search bar. Select the link with the same name.

Source: McGill University Date: 2002–12–11 “Imagine the possible benefit for people traumatized by haunting memories of terror or tragedy. The day may come when the cure is recalling the trauma, and then erasing it with a shot,” wondered Dallas Morning News reporter Tom Siegfried (Aug. 28, 2000), commenting on Dr. Karim Nader’s discovery that a fear memory induced in a rat and reactivated after 1–12 days of storage in the outer part of the brain, could be eradicated with a shot of anisomycin, a protein-synthesis inhibitor.

Web Link 11.7: The Day His World Stood Still, by Joanna Schaffhausen Go to http://brainconnection.brainhq.com/ and place “The Day His World Stood Still” in the search bar.

Scroll to the bottom of the page and click on the link with the same name as what you searched for.

A nice summary of the case of H.M. with some description of his current life.

Web Link 11.8: Deconstructing Henry Go to http://www.brainandsociety.org/ and click on the link for “Patient HM.” H.M. donated his brain to science. This site provides access (you must fill in form and have the link emailed to you) to a 3D model of HM’s brain along with the current status of research on his brain. They outline the challenge of finding that H.M. did actually have a partially intact hippocampus upon post mortem examination.

Web Link 11.9: Case Study (H.M.) Place “Big Picture Education” in your browser and select the matching link. Once there, place “Case Study of the Brain HM” and select the matching link. Well-written summary of the life of HM. Web Link 11.10: Tower of Hanoi Game Place “Tower of Hanoi” in your web browser. Select the link from “Math is Fun.” Web Link 11.11: Alzheimer’s Association http://www.alz.org The Alzheimer’s Association is the only national voluntary health organization dedicated to conquering Alzheimer’s disease through research, and to providing education and support to those affected by the disease.

Web Link 11.12: Alzheimer’s Disease Education and Referral http://www.alzheimers.org/ The ADEAR Center is a service of the National Institute on Aging (NIA). The NIA is one of the National Institutes of Health, under the U.S. Department of Health and Human Services.

Web Link 11.13: The Institute for Brain Aging and Dementia http://www.alz.uci.edu/ This site provides information on dementia, an on-line educational preview of diagnostic tools for dementia.

Web Link 11.14: Memory Loss at the Movies Go to http://www.memorylossonline.com/ and click on the link for “past issues.” From that search, click on Spring 2002. Once there, select the link for “Memory Loss at the Movies.”

This discussion of the movie Memento points out realistic and fictional symptoms as portrayed in the main character.

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Biopsychology, Tenth Edition Web Link 11.15: The Brain’s Navigational Place and Grid Cell System Go to http://www.nobelprize.org and place “Nobel Prize in Physiology or Medicine 2014” in the search box. Select the link that leads you to the award to John O’Keefe. From that page click on the link “Advanced Information” and click on the primary link on that page. It will take you to a PDF paper about the spatial navigation system in the brain.

Web Link 11.16: Identification and Manipulation of Memory Engram Cells Go to http://symposium.cship.org/ and place “engram” in the search bar. Select the link that comes up titled “Identification and Manipulation of Memory Engram Cells.”

How memories are formed and stored in the brain remains a fascinating question in neuroscience. Here they discuss the memory engram theory, their recent attempt to identify and manipulate memory engram cells in the brain with optogenetics, and how these methods are used to address questions such as how false memory is formed and how the valence of a memory can be changed in the brain. < Return to Table of Contents

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Chapter 11: Learning, Memory, and Amnesia

HANDOUTS Handout 11.1: Diagnosis Case Studies Name: ________________________________________ Section: ___________ Date: ____________ For the following brief descriptions, indicate the type of memory the individual is having difficulty with and describe the location of brain damage that might create this kind of behavior.

When Mr. Smith is handed a toothbrush, he bangs it on the table and brushes the bristles against his thumb.

He does not know what to do with it, though he knows it is called a toothbrush.

Lottie Lockheart has been having difficulty finding her way home since her family moved to a new neighborhood. She often calls a taxi because, while she can remember the new address, when she starts to walk home, she is not sure where she is or which direction to turn.

Knowing that Ziggy was in jail, the attorney asks “Ziggy the Rat” where he was on the night of Thursday, April 17, 2003. Ziggy confidently answers that he was at Otto’s Bar and Grill, because that was a Thursday and he always goes to Otto’s for the Thursday night “all you can eat” spaghetti and beer.

Virgil’s mother and youngest sister stop to visit him. He expresses concern for how old his mother is looking, but he has to be introduced to his thirteen-year-old sister, the other survivor of the accident twelve years ago.

Grandpa Lew has been practicing playing Tetris (a digital game). Although he doesn’t remember ever playing the game, he is now good enough to beat his granddaughter over half of the time.

Jojo got an A on this week’s spelling test in his third grade class. Even though he is doing well in most of his school subjects, Jojo’s mother brings him to school every day and takes him directly to the classroom so he does not get lost.

Nate has been a resident of the county mental hospital for fifteen years now. He has a favorite book of short jokes and wise sayings that he has asked people to write down for him. He reads the book every day and laughs when he reads a joke as if he is seeing it for the first time.

Ole is one of the janitors at Maple Thorne Middle School. He sweeps the halls and does other tasks with his friend Nels, who keeps track of what needs to be done and what has been completed.

Amy has been going to see her grandmother every week for the past year and playing a simple card game with her. Although Grandma Tiny does not know her name, she now smiles and sits down at the card table when she sees Amy come in the room.

Ramah is choosing movies for the evening entertainment. He asks cousin Ravi if he has seen any of the movies that look interesting. Ramah has noticed that if he says the name of a movie, such as Top Gun, his cousin will also report having seen movies with names such as Young Guns and Gun for Hire. < Return to Table of Contents

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12 Hunger, Eating, and Health: Why Do Many People Eat Too Much?

TABLE OF CONTENTS Chapter-at-a-Glance

2

Learning Objectives

3

Brief Chapter Outline

4

Teaching Outline

5

Lecture Launchers

14

Activities

17

Web Links

18

Handouts

20

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Chapter 12: Hunger, Eating, and Health

CHAPTER-AT-A-GLANCE

Brief Outline Chapter Introduction (p. 303) 12.1 Digestion, Energy Storage, and Energy Utilization (pp. 304–306) 12.2 Theories of Hunger and Eating: Set Points versus Positive Incentives (pp. 306–309) 12.3 Factors That Determine What, When, and How Much We Eat (pp. 309–313) 12.4 Physiological Research on Hunger and Satiety (pp. 313–318) 12.5 Body Weight Regulation: Set Points versus Settling Points (pp. 318– 322) 12.6 Human Obesity: Causes, Mechanisms, and Treatments (pp. 322– 326) 12.7 Anorexia and Bulimia Nervosa (pp. 326–330)

Instructor’s Manual Resources Lecture Launcher 12.1, Activity 12.1 Lecture Launcher 12.5, Handout 12.2 Lecture Launcher 12.4

Activity 12.2

Lecture Launchers 12.2, 12.6, Handout 12.1 Lecture Launchers 12.3, 12.7

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LEARNING OBJECTIVES After completion of this chapter, the student should be able to:

LO 12.1 LO 12.2 LO 12.3 LO 12.4 LO 12.5 LO 12.6 LO 12.7 LO 12.8 LO 12.9 LO 12.10 LO 12.11 LO 12.12 LO 12.13 LO 12.14 LO 12.15 LO 12.16 LO 12.17 LO 12.18 LO 12.19 LO 12.20 LO 12.21 LO 12.22 LO 12.23 LO 12.24 LO 12.25

Summarize the process of digestion, and explain how energy is stored in the body.

Explain the three phases of energy metabolism.

Describe the set point assumption, and describe the glucostatic and lipostatic set-point theories of hunger and eating. Also, outline three problems with set-point theories of hunger and eating.

Describe the positive-incentive perspective on hunger and eating.

Describe at least two factors that determine what we eat.

Describe at least two factors that influence what we eat.

Describe the various factors that influence how much we eat.

Explain the nature of the relationship between blood glucose levels and hunger and satiety.

Critically evaluate the concept of hypothalamic hunger and satiety centers.

Describe the role of the gastrointestinal tract in satiety.

Describe the discovery of the hunger and satiety peptides, and name several.

Describe the role of serotonin in satiety.

Describe the symptoms and etiology of Prader-Willi syndrome.

Evaluate the evidence for set-point assumptions about body weight and eating.

Compare and evaluate set-point and settling-point models of body-weight regulation.

Explain why there is cause for concern surrounding the obesity epidemic.

Describe, from an evolutionary perspective, why there is a current epidemic of obesity.

Give some reasons as to why some people become obese whereas others do not.

Explain why weight-loss programs are typically ineffective.

Explain how leptin and insulin are feedback signals for the regulation of body fat.

Describe two sorts of treatments for obesity.

Describe the symptoms of anorexia nervosa and bulimia nervosa.

Explain how anorexia and bulimia are, and are not, related.

Explain why those starving due to anorexia do not appear to be as hungry as they should be.

Explain how anorexia might result from conditioned taste aversions.

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Chapter 12: Hunger, Eating, and Health

BRIEF CHAPTER OUTLINE Lecture Launcher 12.1: The Body Mass Index 1. Digestion, Energy Storage, and Energy Utilization a. Digestion and Energy Storage in the Body b. Three Phases of Energy Metabolism 2. Theories of Hunger and Eating: Set-Points versus Positive Incentives a. Set-Point Assumption b. Positive-Incentive Perspective 3. Factors That Determine What, When, and How Much We Eat a. Factors That Influence What We Eat b. Factors That Influence When We Eat c. Factors That Influence How Much We Eat 4. Physiological Research on Hunger and Satiety a. Role of Blood Glucose Levels in Hunger and Satiety b. Myth of Hypothalamic Hunger and Satiety Centers c. Role of the Gastrointestinal Tract in Satiety d. Hunger and Satiety Peptides e. Serotonin and Satiety f. Prader-Willi Syndrome: Patients with Insatiable Hunger 5. Body Weight Regulation: Set-Points versus Settling Points a. Set-Point Assumptions about Body Weight and Eating b. Set-Points and Settling Points in Weight Control Lecture Launcher 12.2: Is Obesity a Social Phenomenon?

6. Human Obesity: Causes, Mechanisms and Treatments a. Obesity: Who Needs to Be Concerned? b. Obesity: Why Is There an Epidemic? c. Why Do Some People Become Obese While Others Do Not? d. Why Are Weight-Loss Programs Often Ineffective? e. Leptin and the Regulation of Body Fat f. Treatment of Obesity Lecture Launcher 12.3: Body Image Distortion in Anorexia 7. Anorexia and Bulimia Nervosa a. Anorexia and Bulimia Nervosa b. Relation between Anorexia and Bulimia c. Anorexia and Positive Incentives d. Anorexia Nervosa: A Hypothesis < Return to Table of Contents

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TEACHING OUTLINE 1. Digestion, Energy Storage, and Energy Utilization (see Figures 12.1–12.3 in Biopsychology) a. Digestion and Energy Storage in the Body LO 12.1 Summarize the process of digestion, and explain how energy is stored in the body.

• • • • • •

Digestion is the gastrointestinal process of breaking down food and absorbing its constituents into the body.

Gut microbiome (the bacteria and other organisms that live inside our gastrointestinal tract) help break down food).

The primary purpose of eating is to supply the body with the energy that it needs to survive.

Energy is available in three forms: (1) lipids (fats), (2) amino acids (broken down from proteins), and (3) glucose (simple sugar byproducts of carbohydrates).

Energy is stored in the form of fats, glycogen, and proteins.

The usual form energy is stored in is fats because 1 gram of fat can store almost twice as much energy as a gram of glycogen, and glycogen would retain too much water as it is stored.

b. Three Phases of Energy Metabolism (see Figure 12.3 in Biopsychology) LO 12.2 Explain the three phases of energy metabolism.

Energy metabolism is controlled by two pancreatic hormones: insulin and glucagon. Energy metabolism occurs in three phases: • The cephalic phase: This is a preparatory phase; it begins with the sight, smell, and even thought of food. Insulin is released by the pancreas to promote glucose use and storage.

• The absorptive phase: This is when energy is absorbed into the bloodstream; insulin is released by the pancreas to promote glucose use and storage.

• The fasting phase: This is when body utilizes energy stores; glucagons are released by the pancreas to promote the use of free fatty acids and ketones by the body.

Role of Insulin • Promotes use of glucose as primary source of energy, promotes the conversion of bloodborne fuels to forms that can be stored (glucose to glycogen and fats/amino acids to proteins), and promotes the storage of glycogen in liver and muscle, fat in adipose tissue and proteins in muscle.

2. Theories of Hunger and Eating: Set-Points versus Positive Incentives (see Figure 12.4 in Biopsychology) a. Set-Point Assumption LO 12.3 Describe the set-point assumption, and describe the glucostatic and lipostatic setpoint theories of hunger and eating. Also, outline three problems with set-point theories of hunger and eating.

• •

Research on feeding has been heavily influenced by the idea of a feeding set-point, based around the idea of a homeostatic, negative feedback system regulating feeding.

Homeostasis − A stable internal environment that is critical to survival.

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The set-point theory was necessary when the brain was assumed to be immutable and energy resources needed to be high. Thinking creatively, outside the box, requires a revision in our long-held assumptions.

Since we now know the brain is plastic, capable of considerable adaptation, there is no logical imperative for the set-point regulation of eating.

Glucostatic and Lipostatic Set-Point Theories of Hunger and Eating • Research on feeding has been strongly influenced by the idea that feeding is controlled by deviations from two different set points: a set point for blood glucose (short-term regulation) and a set point for body fat (long-term regulation).

• The glucostatic and lipostatic theories were viewed as complementary, not mutually exclusive.

• The glucostatic theory accounted for meal initiation and termination, whereas the lipostatic theory accounted for long-term regulation.

Problems with Set-Point Theories of Hunger and Eating There are many problems with set-point models of feeding: • They cannot explain the current epidemic of eating disorders in our society.

• They are inconsistent with current ideas about evolutionary pressures related to eating.

• Eating does not seem to be sensitive to changes in body fat or the caloric status of an individual prior to a meal.

• They fail to recognize the role that factors like taste, learning, or social factors play in eating. b. Positive-Incentive Perspective LO 12.4 Describe the positive-incentive perspective on hunger and eating.

• • •

Developed in response to shortcomings with set-point theories of feeding; positive-incentive perspectives emphasize the idea that animals eat not because of deviations from some internal energy set-point, but because of the anticipated pleasure of eating.

In this sense, feeding is a lot like sexual behavior; we do it because we crave it, not because we are trying to match a set-point.

According to positive incentive theories, animals eat in response to a host of factors—preferred flavors, past experiences with a food, the time since your last meal, whether or not other people are eating, etc.

3. Factors That Determine What, When, and How Much We Eat (see Figure 12.5 in Biopsychology) a. Factors That Influence What We Eat LO 12.5 Describe at least two factors that determine what we eat.

• • • •

In general, animals are born with a preference for sweet and salty tastes (typically high-energy foods rich in vitamins and minerals) and with an aversion to bitter tastes.

They learn to avoid any taste followed by illness (conditioned taste aversion) or to prefer tastes that improve their health (conditioned taste preference).

Humans and other animals learn to prefer flavors associated with mother’s milk, as well as foods that they have seen their conspecifics eating.

When an animal is sodium deficient, it develops a craving for sodium salt; however, when it becomes deficient in a vitamin or another mineral, it must learn to consume foods that are rich in the missing nutrient. This becomes a problem when an animal is faced with a multitude of food possibilities, as humans often are.

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For example, when thiamin (Vitamin B1) deficient rats were offered two different diets, one of which had thiamin, within a few days all preferred the thiamin diet; however, when they were offered ten new diets, few learned to consume the one with thiamin.

b. Factors That Influence When We Eat LO 12.6 Describe at least two factors that influence when we eat.

• • • • •

• •

When food is readily available, most mammals eat many small meals a day.

By contrast, most humans choose to eat a few large meals at regular times; in fact, many people feel ill if they miss a scheduled meal.

According to Woods, a key to understanding hunger is that eating stresses the body.

This is due to the fact that animals will enter the cephalic phase of feeding as the mealtime approaches; the malaise that you feel occurs when insulin is released and blood glucose levels fall in expectation of the coming meal.

Recent research by Weingarten and his colleagues suggests that nondeprived humans and animals learn to become hungry when they are used to eating, not when they have an energy deficit—nondeprived humans and animals do not normally have energy deficits when they begin meals.

Weingarten fed deprived rats six small meals per day of a highly palatable liquid diet at irregular intervals for eleven days; a buzzer-and-light conditional stimulus came on before each meal and stayed on during it.

Next, Weingarten gave these same rats continuous access to the palatable liquid diet; despite the fact that they consumed large quantities of the liquid diet throughout the day, each time the buzzer and light were presented the rats consumed a meal.

c. Factors That Influence How Much We Eat LO 12.7 Describe the various factors that influence how much we eat.

• • •

• • • •

4.

Satiety signals based on volume of food intake and its nutritive density influence how much we eat; to a point, animals will adjust their eating to keep food intake and body weight stable.

Sham eating studies indicate that signals from the gut or blood are not necessary to terminate eating; in sham eating studies, food is chewed and swallowed, but it leaves the body before it enters the stomach.

Set-point theory suggests that sham-eaten meals should be huge, as there cannot be a satiety signal generated as food intake meets caloric requirements. That is not the case, as the size of these meals seems to depend more on an animal’s previous experience with the food than with its immediate effects on the body.

Eating a small amount of food prior to a meal often increases the size of that meal. This is known as the appetizer effect.

Serving size impacts how much we eat (larger servings lead to more eating).

Eating in the company of others (social influence) often influences the serving size of the meal that is eaten.

The variety of foods available at a meal also influences meal size; the greater the variety, the more food that is eaten. This is due to sensory-specific satiety. This is one reason why body weight tends to increase when a human being or other animal is faced with a cafeteria-style diet.

Physiological Research on Hunger and Satiety (see Figures 12.6–12.10 in Biopsychology) a. Role of Blood Glucose Levels in Hunger and Satiety 7 ..

Chapter 12: Hunger, Eating, and Health LO 12.8 Explain the nature of the relationship between blood glucose levels and hunger and satiety.

• • •

In spite of a long history, research on the role of blood glucose in eating has had a mixed history.

In the 1990s, Campfield and Smith found that blood glucose levels dropped sharply about ten minutes before a meal was initiated, suggesting that this drop might be linked to eating.

Four pieces of evidence that the decline in blood glucose is triggered by eating: − Time course of glucose decline is not consistent with a gradual decline in the body’s energy. − Eliminating the premeal drop in glucose does not eliminate the meal. − If an expected meal is not served, glucose returns to its previous level. − Glucose levels in the brain stay relatively constant.

b. Myth of Hypothalamic Hunger and Satiety Centers (See Figures 12.6−12.8 in Biopsychology) LO 12.9 Critically evaluate the concept of hypothalamic hunger and satiety centers.

• •

• • •

• •

In the 1950s, studies in which various areas of the rat hypothalamus were lesioned or stimulated seemed to suggest that it contained the hypothesized hunger and satiety centers.

Large bilateral lesions of the ventromedial hypothalamus (VMH) produced hyperphagia and gross obesity. After the lesion, the rats were extremely hyperphagic and gained weight rapidly (dynamic phase); after several weeks hyperphagia was only slight and a new, very high body weight was maintained (static phase).

By contrast, large bilateral lesions of the lateral hypothalamus (LH) rendered rats aphagic and adipsic; if force fed and then maintained on highly palatable wet diets, they eventually recovered to the point that they could maintain themselves on laboratory chow and water.

Although the idea of VMH satiety and LH feeding centers in the brain was attractive, it has proven to be false.

For example, it turns out that the hypothalamus is primarily involved in energy metabolism, not food intake. VMH lesions increase blood insulin levels; this increases the production of body fat (lipogenesis) and forces animals to eat more in order to maintain glucose blood levels for their immediate energy requirements.

In addition, VMH lesions are not due to damage to the VMH itself, but instead to damage to the ventral noradrenergic bundle or the axons of the paraventricular nucleus of the hypothalamus.

The idea that the LH is a center specific to feeding no longer warrants serious consideration, whereas, the new target of research is the arcuate nucleus.

c. Role of the Gastrointestinal Tract in Satiety LO 12.10 Describe the role of the gastrointestinal tract in satiety.

• • •

The first influential study of the physiological basis of hunger was conducted in 1912 by Canon and Washburn; Washburn swallowed a balloon on the end of a thin tube, the balloon was partially inflated, and a pressure gauge was attached to the other end of the tube.

Each time that he had a large stomach contraction, Washburn reported a pang of hunger; this led to the view that stomach contractions are a major factor in hunger.

The finding that animals whose stomachs had been completely removed ate enough to maintain their body weights discredited this view. In addition, people with no stomachs report feeling hungry and maintain their body weights; they eat less per meal, but they eat more meals.

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In the 1980s, Koopmans used a second-stomach preparation to implicate the gut in feeding behavior; rats that have had a second stomach implanted into their peritoneum eat less when the second stomach is loaded with food, even though the stomach is not innervated nor are the nutrients able to be absorbed into the bloodstream.

d. Hunger and Satiety Peptides LO 12.11 Describe the discovery of the hunger and satiety peptides, and name several.

• • •

There is considerable evidence that peptides released by the gut can serve as satiety signals in the brain; for example, CCK, bombesin, glucagons, alpha-melanocyte-stimulating hormone, and somatostatin all appear to reduce food intake (known as satiety peptides).

Neuropeptide Y, galanin, orexin-A, and ghrelin appear to increase appetite.

Research on the role of different peptides in feeding has indicated that the neural system that controls feeding responds to many different types of signals, and has refocused interest in the hypothalamus (which possesses receptors for many of these peptides).

e. Serotonin and Satiety LO 12.12 Describe the role of serotonin in satiety.

• •

f.

Serotonin also plays a role in satiety; serotonin agonists reduce food intake, even when the food is highly palatable.

There is also considerable interest in developing serotonergic agonists that suppress appetite without the side effects seen with conventional serotonin agonists.

Prader-Willi Syndrome: Patients with Insatiable Hunger LO 12.13 Describe the symptoms and etiology of Prader-Willi Syndrome.

• • • •

Prader-Willi results from an accident of chromosomal (#15, inherited from the father) replication.

Patients experience insatiable hunger, little or no satiety, and an exceptionally slow metabolism.

Other physical and neurological symptoms include: weak muscles, small hands and feet, feeding difficulties in infancy, tantrums, compulsivity, and skin picking.

If untreated, most patients become extremely obese at a young age and often die.

5. Body Weight Regulation: Set Points versus Settling Points (see Figures 12.11 and 12.12 in Biopsychology) a. Set-Point Assumptions about Body Weight and Eating LO 12.14 Evaluate the evidence for set-point assumptions about body weight and eating.

• • •

Set-point theories cannot account for the large changes in body weight that are common in adults, or the wave of obesity that is currently sweeping fast-food societies.

Set-point theories cannot account for the fact that animals that eat a free-feeding diet are typically less healthy than animals on a calorie-restricted diet; in both humans and animals, those who eat less have greater longevity and less likelihood of a variety of diseases.

The enhanced health of animals maintained on a calorie-restricted diet is not related to a decrease in body fat; rather, it is believed that a by-product of energy metabolism accumulates in cells and accelerates the rate of aging and its attendant health problems.

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Set-point theory cannot account for the fact that the body seems to control its fat levels by altering its metabolism, rather than its food intake.

The mechanism for this control is called diet-induced thermogenesis; increases in body fat increase body temperature, which leads to increased food intake so that the body temperature can be maintained.

b. Set-Points and Settling Points in Weight Control LO 12.15 Compare and evaluate set-point and settling-point models of body-weight regulation.

•

• • • • •

The inability of set-point theories to accurately describe feeding behavior and body weight has led researchers to consider the idea that body weight tends to drift around a natural settling point, or level at which all of the various factors that influence food intake and energy expenditure achieve a balance.

From this perspective, body weight is stable as long as there are no long-term changes in the factors that influence it.

The leaky-barrel model illustrates the ideas behind a settling-point theory of body weight regulation.

According to settling point models, the stability of body weight is a function of the stability of the various factors that influence energy intake and output; if these are changed, their impact is limited by negative feedback.

The strength of this model is that it accounts for the homeostasis of body weight without having to postulate a fixed set point, and it can also account for instances in which there are long-term changes in body weight, which a strict set-point model cannot.

The most significant aspect of a settling-point based model of food intake is that it better describes what we know about the regulation of food intake and body weight.

5. Human Obesity: Causes, Mechanisms and Treatments (see Figures 12.13–12.15 in Biopsychology) a. Obesity: Who Needs to Be Concerned?

LO 12.16 Explain why there is a concern surrounding the obesity epidemic.

• • •

Everyone needs to be concerned about obesity.

Weight also tends to increase with aging; many people who are slim as youths develop serious weight problems as they age.

Because of the correlation between obesity and health problems, there is great concern for the next generation.

b. Obesity: Why Is There an Epidemic?

LO 12.17 Describe, from an evolutionary perspective, why there is a current epidemic of obesity.

• •

•

Rates of obesity have doubled in the last century; this increased incidence represents a significant health problem in many “fast-food” societies.

One reason why obesity has become so common is that evolution has led to animals to prefer high-calorie foods, to eat to maximum capacity, to store as much energy as possible as fat, and to use calories as efficiently as possible. However, this pattern of ingestion is not adaptive in a setting in which food shortages are rare and highly palatable food is easily available.

In addition, social factors have encouraged humans to tend to eat at set times, rather than when we are hungry, and to eat in a way that maximizes our food intake.

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All of these factors lead humans to appallingly high levels of food intake and, thus, to increased incidence of obesity in many societies.

c. Why Do Some People Become Obese While Others Do Not? LO 12.18 Give some reasons as to why some people become obese whereas others do not.

•

• •

Other factors help to determine whether a given individual will become obese. These include an individual’s unique food preferences, the role of social factors in an individual’s feeding patterns, differences in basal metabolism, differences in consumption and energy expenditures, genetic differences, and differences in nonexercise activity thermogenesis (NEAT).

Differences in gut microbiome composition may play a role in obesity. Research shows that animals exposed to microbiome of other obese animals will gain weight and store greater amounts of body fat.

About 100 human chromosome loci have been linked to obesity and there is evidence that transgenerational epigenetic effects can predispose subsequent generations to obesity.

d. Why Are Weight-Loss Programs Typically Ineffective?

LO 12.19 Explain why weight-loss programs are typically ineffective.

•

•

From the perspective of settling-point models of weight regulation, weight-loss programs are largely unsuccessful because once the program ends, and an individual resumes the lifestyle factors that initially determined their weight, their eating habits and energy expenditures will lead to their body weight returning to pre-diet levels (see Figure 12.13).

Increased exercise by itself is not an efficient means of weight loss, because physical activity normally accounts for just a small amount of a person’s total caloric expenditures.

e. Leptin and the Regulation of Body Fat LO 12.20 Explain how leptin and insulin are feedback signals for the regulation of body fat.

• •

• • • • • •

In the early 1950s, a spontaneous mutation produced a strain of genetically obese mice called ob/ob mice; these mice eat more than normal, weigh three times as much as a normal mouse, store fat more effectively than normal mice, and burn fat more efficiently.

Researchers in the 1990s found that these mice cannot produce leptin, a hormone produced by fat cells that appears to serve as a negative feedback signal for fat deposition in the body.

Leptin levels are positively correlated with fat deposits in humans; low doses of leptin reduce eating and body fat in mice and there are leptin receptors in the brain.

Unfortunately, most humans have high circulating levels of leptin and leptin injections do not reliably reduce body fat in obese humans. Thus, other feedback signals must also be involved in the control of eating in humans.

These signals include insulin; it is also positively correlated with body fat; there are insulin receptors in the brain, and low doses of insulin injected in the brains of lab animals reduce eating and body weight.

Insulin-deficient individuals are not obese; they cannot convert their food to fat, and most excess calories are simple excreted.

Why does the body have two fat feedback signals?

Leptin appears to be correlated with subcutaneous fat, whereas insulin is correlated with visceral fat.

Both peptides have receptors (neuropeptide Y and melanocortins) distributed in high concentrations in the hypothalamus: the arcuate nucleus.

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f.

Leptin administration can help humans who have low levels of leptin already in their body to maintain a reasonable weight.

Treatment of Obesity LO 12.21 Describe two sorts of treatments for obesity.

• • • • • •

Serotonergic agonists have been found to reduce the urge to eat high-calorie foods, reduce the consumption of fat, reduce the subjective intensity of hunger, decrease the size of meals, reduce snacking and bingeing.

Gastric bypass surgical treatment for extreme obesity involves short-circuiting the normal path of food through the digestive tract, so that its absorption is reduced.

This is the most common surgical procedure to treat obesity.

An alternative surgical treatment is the gastric band procedure.

This involves surgically positioning a hollow silicone band around the stomach to reduce the flow of food through it; the circumference of the band can be adjusted and the band can be removed (see Figure 12.15).

However, the key to any weight loss is a permanent change in lifestyle.

6. Anorexia and Bulimia Nervosa a. Anorexia and Bulimia Nervosa LO 12.22 Describe the symptoms of anorexia nervosa and bulimia nervosa.

• • • •

Anorexia nervosa is a disorder of underconsumption of food.

Anorexics eat so little that they experience health-threatening weight loss; in about 4% of diagnosed cases, complications from starvation result in death and there is a high rate of suicide among persons with anorexia.

Bulimia nervosa is a related condition in which individuals binge-eat and purge in the absence of extreme weight loss.

The mortality rate for bulimia is about 4 percent.

b. Relation Between Anorexia and Bulimia LO 12.23 Explain how anorexia and bulimia are, and are not, related.

• Persons with anorexia often require treatment for reduced metabolism, bradycardia, hypotension, hypothermia, and anemia. Persons with bulimia often require treatment for irritation and inflammation of the esophagus, vitamin and mineral deficiencies, electrolyte imbalance, dehydration, and acid reflux.

• Anorexia and bulimia might be variants of the same disorder. Both anorexics and bulimics have distorted body images, are comorbid with obsessive-compulsive disorder and depression, and patients seem to straddle the two diagnoses or flip-flop between the two. c. Anorexia and Positive Incentives LO 12.24 Explain why those starving due to anorexia do not appear to be as hungry as they should.

• •

An alternative is suggested by a positive-incentive model of eating and weight control. From this perspective, eating food is not a positive incentive for anorexics, even though they are essentially starving themselves. Thus, there is no motivation for them to eat.

This stands in stark contrast to the normal response to starvation, which greatly increases the positive-incentive qualities of food.

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People with anorexia are often very interested in thinking and talking about food (high positiveincentive value), but actually eating food has low-incentive value.

d. Anorexia Nervosa: A Hypothesis LO 12.25 Explain how anorexia might result from conditioned taste aversions.

• • • • • •

Woods and colleagues have offered an alternative hypothesis of anorexia.

At the beginning of meals, people are normally in homeostatic balance, and this balance is disrupted by the infusion of calories.

In people who eat little, the aversive effects of meals are much greater.

Further support for this hypothesis comes from the findings that starving concentration camp victims found eating noxious.

Meals consumed by anorexics may produce a variety of conditioned taste aversions that reduce the motivation to eat.

A potential treatment may be to give anorexics small amounts of food intermittently throughout the day.

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Chapter 12: Hunger, Eating, and Health

LECTURE LAUNCHERS Lecture Launcher 12.1: The Body Mass Index A common measure of human obesity is the Body Mass Index, or BMI. It is sometimes fun (or distressing) to present a BMI chart to your class and allow them to see where they rate. A BMI calculator and rating scale is available at http://www.nhlbi.nih.gov/. Once on that page, place “calculate your BMI” in the search box and select the matching result from the list. Make sure that they understand all of the caveats that accompany the BMI; for a good summary of these, read the information available at http://www.halls.md/.

Once there, scroll to the bottom to the link for the body mass index.

Lecture Launcher 12.2: Is Obesity a Social Phenomenon?

Recent research has demonstrated that obesity can spread through social networks in complex ways. There is a wonderful animation of this effect complete with time-slider at http://content.nejm.org/. Once there place “Spread of Obesity in a Large Social Network” in the search bar. Select the link that shares that same name. Please note: You might require a subscription through your academic institution to access this content.

Lecture Launcher 12.3: Body Image Distortion in Anorexia For a powerful illustration of the significant body image distortion that accompanies anorexia and bulimia, show the following video clip that has been posted on YouTube: Go to http://www.youtube.com and place “Media Distortion of Body Image” and click on the matching link.

Lecture Launcher 12.4: Weird Food People often eat things in one culture that people in another culture find disgusting. All of these things provide some of the nutrients needed for survival. Why are some things found to be edible and others not consumed or consumed under unusual circumstances?

Can you use what you know about the biology of eating and drinking to explain people’s tastes for the foods listed here?

Try “Ray’s List of Weird and Disgusting Foods” for some ideas.

Netherlands: Salted Horsemeat Sandwiches, Raw Salted Herring, Peanut Butter Sauce on French Fries France: Escargot, Tripe, Frog’s Legs, Steak Tartare, Brains, Truffles Mediterranean: Sheep’s head (the whole thing, cooked and skinned, including the eyeballs), Octopus, Cicada, Octopus and Squid in Ink. Africa: Blood fresh from living livestock, Grasshoppers, Okra, Urine, Clay, Goat’s Head China: Bird’s Nest Soup, Breast Milk, Sea Cucumber, Jellyfish, Rat, Snake, Drunken Shrimp, Jelled Blood, Bear Paws, Tiger Testicles, Owl Soup, Thousand-Year Eggs, Fish Australia: Vegemite, Marmite, Kangaroo, Witchety Grub, Beetroot, Honey Ants Japan: Fugu, Sashimi, Tofu, Miso, Seaweed, Crickets Arctic Alaska: Blubber, Stinkheads U.S. in general: Spam, Chewing Gum, Iceberg Lettuce, Bread, Beer, Peanut Butter U.S. Northwest: Geoduck Clams U.S. West: Prairie Oysters, Fried Pork Rinds, Blood-Rare Steak, Rattlesnake U.S. Midwest: White Castle Sliders, Jell-O Salad, Fruitcake, American Cheese Food Product (such as Velveeta) in Fried Cheese Balls, Cincinnati Greek Chili U.S. South: Grits, Crawfish, Hog Maws and Snouts, etc., Dropped Fowl, Chicken Feet Chitterlings, Iced Tea, Ramps, Turkey Deep-Fried Whole (Fried Everything) Chicken-Fried Steak, Dill Pickles Fried 14 ..

Biopsychology, Tenth Edition U.S. East: Souse, Pork Loaf U.S. Northeast: Scrapple, Cod Liver Oil, Pumpkin Pie, Raw Oysters, Lobster, Fiddlehead Ferns Canada: Sugar Pie, Cod Tongues, Cod Cheeks, Pemmican, Cracklings, Seal Flipper Pie, Spruce Beer Mexico: Tequila Worms, Menudo, Habanero & Jalapeno Peppers, Mole, Chichirrones (Chitterlings), Ceviche, Grasshoppers Web Link 12.5 Ray’s List of Weird and Disgusting Foods Lecture Launcher 12.5: Is Food Addictive?

This is a highly controversial idea but it provides an excellent opportunity for a critical evaluation of experimental research and the conclusions that are drawn from it.

Before this question can be answered, addiction must be defined. Addiction is presented in later chapters, and is better discussed in detail then. Defining addiction is not trivial. The word “addiction” has very different meanings to the general public, practicing clinicians, and researchers studying the neurobiology of addiction. Food may be addictive by one definition, but not by another. This is an excellent opportunity to illustrate the importance of clear definitions and how difficult it can become to conduct scientific analysis when the definition of the phenomenon one is studying is unclear.

Does research provide evidence that junk food is addictive?

A number of studies have been carried out in rats to look at processed foods and addiction. One study found that a high-fat diet appears to alter the brain biochemistry in a similar way to drugs such as morphine.

A similar study was done on sugar addiction, where rats were gradually fed a diet with increasing amounts of sugar. The more sugar given, the quicker the rats ate it, and when it was suddenly withdrawn from their food, they experienced “addiction-type” reactions, such as chattering teeth, anxiety, and shaking.

Rats fed on a high-fat diet become more resistant to leptin—the hormone that stops eating. At the same time, levels of galanin—a brain peptide that stimulates eating and slows down energy expenditure— increases.

Recently, newspapers reported that Dr. Martin Yeomans claimed that “high-fat foods stimulate pleasure chemicals [opioids] in the brain.”

Hunger for fatty foods and alcohol share a chemical trigger.

A brain chemical that stokes hunger for food and fat also triggers thirst for alcohol and may play a role in chronic drinking. Rats injected with galanin, a natural signaling agent in the brain, chose to drink increasing quantities of alcohol even while consuming normal amounts of food and water. “Consumption of alcohol produces galanin, and galanin promotes the consumption of alcohol. That would perpetuate the behavior.”

When the animals were given a drug that blocked the effects of galanin, they maintained normal eating and drinking habits.

Web Links 12.9 Fat Addiction

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Chapter 12: Hunger, Eating, and Health

Lecture Launcher 12.6: Obesity Obesity is an increasing problem worldwide, as well as in the United States. It creates health problems, as well as social problems. Why do people maintain weight when there is considerable pressure to be thin?

This is an interesting question for students who have struggled to lose weight, as well as for those who don’t understand why people would remain obese.

An important outcome of the discussion in this chapter is to provide students with a better understanding of the limitations of human initiative in the face of biological imperative, as well as to help them better assess the viability of diets or weight-loss plans that they might consider.

Lecture Launcher 12.7: Athletics and Eating Disorders Many of your students may be involved in athletics of some form. Does this predispose them to eating disorders?

ABSTRACT: “This is a review article examining the relationship between involvement in athletics and disordered eating. According to research on risk factors in the general population, gender, race, and activities that encourage dieting or weight loss by emphasizing a thin shape play an important role in the prevalence of eating disturbance. Factors in the athletic environment that increase the athlete’s risk are addressed, such as the belief among athletes and coaches that a reduction in weight or body fat can enhance athletic performance. The authors propose a shift in emphasis from athletic performance to the health of the athlete. Practical educational recommendations to reduce the athlete’s risk of disordered eating are offered for athletes and sport management personnel. Additionally, preventative suggestions are offered for modifying aspects of the athletic environment.”

Thompson, R. A. & Sherman, R. T. (1999). “The Damage Is Done: Consequences of the Thinness Pursuit Athletes, Athletic Performance, and Eating Disorders: Healthier Alternatives.” Journal of Social Issues. 55 (2), 317.

Web Links 12.10 Anorexia Nervosa 12.11 Basic Biological Overview of Eating Disorders < Return to Table of Contents

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ACTIVITIES Activity 12.1: An Animated Tour through the Digestive Tract As a quick refresher for your students, you can take them through a very nice (albeit somewhat juvenile) and humorous animation of the digestive process. That animation can be found by placing “John Kitses Digestion” in the search bar of your browser. Select the matching link.

Activity 12.2: Weight Management Information Evaluation The ability to evaluate information on nutrition and weight management is an important outcome of this chapter. Ask students to bring printouts of Web pages, or other brochures, popular articles, or advertising, about weight control. Have the students discuss and/or prepare a critique of the materials based on the chapter’s information on eating and weight regulation. < Return to Table of Contents

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Chapter 12: Hunger, Eating, and Health

WEB LINKS Web Link 12.1: Prader-Willi Syndrome Go to http://www.med.umich.edu/ and place “Praders” in the search box. Select the link that leads you to Prader-Willi Syndrome.

Outline of characteristics. Illustration of “floppy baby.” University of Michigan Health System.

Web Link 12.2: Genes and Disease: Prader-Willi Syndrome Go to https://ghr.nlm.nih.gov/and place “Prader-Willi Syndrome” in the search bar. Select the link that matches that name.

Web Link 12.3: Normal Regulation of Blood Glucose Go to http://endocrineweb.com/ and place “Normal Regulation of Blood Glucose” in the search bar. Scroll down the page and select the link with the same name.

The important roles of insulin and glucagon: diabetes and hypoglycemia.

Web Link 12.4: The Real Deal on the Digestive System Go to http://kidshealth.org/ and select the link for “parents.” Once there, place “digestive system” in the search bar and select the link with the same name as prepared for parents.

Animated diagram of the digestive system clarifies the parts on a standard diagram.

Web Link 12.5: Ray’s List of Weird and Disgusting Foods Go to http://www.andreas.com and place “weird food” in the search bar. Follow the clickable links to the page dedicated to weird foods from around the world.

Just what you would imagine—with a useful glossary.

Web Link 12.6: The Genetics and Pathophysiology of Obesity Go to http://www.findarticles.com/ and place “genetics and pathophysiology of obesity” in the search bar.

Select the link with the matching name from the NIH website.

Web Link 12.7: Appetite-Related Gut Peptides in Obesity and Binge Eating Disorder Go to http://online.sagepub.com/ and place “Gut Peptides in Obesity” in the search bar. Select the first link that contains that search string in the link.

Web Link 12.8: Laboratory of Behavioral Neuroscience Go to http://www.rockefeller.edu/ and place “Leibowitz” in the search bar. Select the link that leads you to the Laboratory of Behavioral Neuroscience.

The Rockefeller University, Laboratory of Behavioral Neuroscience, Dr. Sarah F. Leibowitz.

Web Link 12.9: Fat Addiction Go to https://www.scientificamerican.com and place “addiction to fat” in the search bar. Click on the link presented to you as an option.

Web Link 12.10: Anorexia Nervosa Go to http://www.nationeatingdisorders.org and place “anorexia nervosa” in the search bar. Select the first link with the matching name.

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Biopsychology, Tenth Edition Web Link 12.11: Basic Biological Overview of Eating Disorders Go to http://www.acnp.org/ and place “psychopharmacology 4th Generation” in the search bar. Select the matching link and page down the resulting page until you reach the “eating disorders” section. Within that section, select the article “Basic Biological Overview of Eating Disorders” and click that link.

Halmi, K. A. Basic Biological Overview of Eating Disorders. Psychopharmacology—The Fourth Generation of Progress, American College of Neuropsychopharmacology.

Web Link 12.12: Gut Microbiome and Obesity Go to https://www.ncbi.nlm.nih.gov and place “PMC4443745” in the search bar.

Web Link 12.13: Genetics and Epigenetics of Obesity Go to https://www.ncbi.nlm.nih.gov and place “PMC3213306” in the search bar.

< Return to Table of Contents

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Chapter 12: Hunger, Eating, and Health

HANDOUTS Handout 12.1: Web Search on Weight Loss Name: ________________________________________ Section: ___________ Date: ___________ Many Americans believe that they are overweight, from a few pounds to a few hundred pounds. Because of this, weight loss systems are big business. This assignment asks you to evaluate one of these weight loss systems in terms of the information you have been exploring about the physiology of ingestive behavior.

Search the Internet for information on weight loss. Choose a Web site that proposes a mechanism for loss of excess weight. Document the key proposals in terms of the main proposals and reasons given for the effectiveness of the program. Then compare the proposal with what you have learned about the physiology of eating and drinking. Evaluate the proposal and suggest whether you would try this weight loss system or recommend it to someone else.

Here is an outline for the paper: Title The URL for the Web site that you are discussing. (10 percent of paper grade) The title or descriptive name of the weight loss plan proposed. (10 percent of paper grade) A list of the key components of the weight loss program. For example, restriction of fat, small portions, etc.

(20 percent of paper grade) The rationale for the effectiveness of the weight loss program. This should be a paragraph or more in length and should make the reasons for the components of the program clear to the reader. (20 percent of paper grade) Physiological components involved in the weight loss program. This should be several paragraphs long and should clearly express your understanding of the physiology of the process of hunger, satiation, eating, and drinking as is relevant for the weight loss method you have chosen to report on. For example, long periods between meals would be likely to reduce blood sugar levels. (20 percent of paper grade) An evaluation of the weight loss program. This section is your opinion about the potential effectiveness of the weight loss program and your sense of the difficulty in following the proposed plan. Would you try it or recommend it to someone else? (20 percent of paper grade) < Return to Table of Contents

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Biopsychology, Tenth Edition Handout 12.2: Comparing Regulatory Mechanisms Name: ________________________________________ Section: ___________ Date: ___________

Feature

Temperature

Eating

System variable— characteristic to be regulated

Set point—optimal value of the system variable

Detector—monitors the value of the system variable

Correctional mechanism—restores system variable to set point

< Return to Table of Contents

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Drinking

13 Hormones and Sex: What’s Wrong with the Mamawawa?

TABLE OF CONTENTS Chapter-at-a-Glance

2

Learning Objectives

3

Brief Chapter Outline

4

Teaching Outline

5

Lecture Launchers

16

Assignments

17

Web Links

18

Handouts

20

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Chapter 13: Hormones and Sex

CHAPTER-AT-A-GLANCE

Brief Outline Chapter Introduction (p. 332) 13.1 Neuroendocrine System (pp. 333– 338) 13.2 Hormones and Sexual Development of the Body (pp. 338–341) 13.3 Hormones and Sexual Development of the Brain and Behavior (pp. 341–345) 13.4 Three Cases of Exceptional Human Sexual Development (pp. 345– 348) 13.5 Effects of Gonadal Hormones on Adults (pp. 348–351) 13.6 Brain Mechanisms of Sexual Behavior (pp. 352–354) 13.7 Sexual Orientation and Sexual Identity (pp. 354–358)

Instructor’s Manual Resources Lecture Launcher 13.1 Lecture Launcher 13.2, Assignment 13.1 Lecture Launchers 13.4, 13.5 Assignment 13.2

Lecture Launcher 13.3

< Return to Table of Contents

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LEARNING OBJECTIVES After completion of this chapter, the student should be able to: LO 13.1 LO 13.2 LO 13.3

LO 13.4 LO 13.5 LO 13.6

LO 13.7 LO 13.8 LO 13.9 LO 13.10 LO 13.11 LO 13.12 LO 13.13 LO 13.14 LO 13.15 LO 13.16 LO 13.17 LO 13.18 LO 13.19 LO 13.20 LO 13.21

Explain the distinction between exocrine glands and endocrine glands, describe the functions of the gonads, and distinguish between the X chromosome and the Y chromosome.

Describe the three classes of hormones, and then describe three classes of gonadal hormones.

Explain why the pituitary is sometimes called the master gland, and describe its anatomy.

Discuss the female vs. male patterns of gonadal and gonadotropic hormone release, and explain the evidence that discounted a role for the anterior pituitary in those patterns of release.

Explain how the anterior and posterior pituitary are controlled.

Describe the research that led to the discovery of the hypothalamic releasing hormones.

Describe three different types of signals that regulate hormone release. Also, describe how hormones are released over time and the effect this pattern of release has on levels of circulating hormones.

Summarize the model of gonadal endocrine regulation.

Describe the development of the internal and external reproductive organs.

Describe the male and female secondary sex characteristics and the role of hormones in their development.

Describe the evolution of research and thinking about sex differences in the brain.

Describe the results of studies of sex differences in behavior in humans and nonhumans.

Explain what androgen insensitivity syndrome, androgenital syndrome, and ablation penis have taught us about human sexual development.

Describe the role of testosterone in male sexual behavior.

Describe the role of testosterone in female sexual behavior.

Describe the dangers associated with anabolic steroid use.

Describe the roles of the cortex, hypothalamus, amygdala, and ventral striatum in sexual activity.

Describe the results of the two studies on the genetics of sexual orientation by Bailey and Pillard (1991, 1993) and describe the fraternal birth order effect and why it is thought to occur.

Describe the hypothesized role of adrenal cortex steroids in the emergence of sexual attraction.

Describe the famous study of LeVay (1991) and the major problem with its finding.

Explain what transsexualism is, and describe the process of sexual reassignment.

Sexual attraction, gender identity, and body type are independent. Explain and give an example.

< Return to Table of Contents

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Chapter 13: Hormones and Sex

BRIEF CHAPTER OUTLINE Lecture Launcher 13.1: Differentiation Animation 1. Neuroendocrine System a. Glands b. Hormones c. The Pituitary d. Control of the Pituitary e. Discovery of Hypothalamic Releasing Hormones f. Regulation of Hormone Levels g. Summary Model of Gonadal Endocrine Regulation Lecture Launcher 13.2: Gender Testing of Female Athletes 2. Hormones and Sexual Development of the Body a. Sexual Differentiation b. Puberty: Hormones and Development of Secondary Sex Characteristics 3. Hormones and Sexual Development of Brain and Behavior a. Sex Differences in the Brain b. Development of Sex Differences in Behavior 4. Three Cases of Exceptional Human Sexual Development a. Exceptional Cases of Human Sexual Development Lecture Launcher 13.3: Estrogen and Synaptogenesis 5. Effects of Gonadal Hormones on Adults a. Male Sexual Behavior and Testosterone b. Female Sexual Behavior and Gonadal Hormones c. Anabolic Steroid Abuse 6. Brain Mechanisms of Sexual Behavior a. Four Brain Structures Associated with Sexual Activity

7. Sexual Orientation and Sexual Identity a. Sexual Orientation b. What Triggers the Development of Sexual Attraction? c. Is There a Difference in the Brains of Homosexuals and Heterosexuals? d. Gender Identity e. Independence of Sexual Orientation and Gender Identity < Return to Table of Contents

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Biopsychology, Tenth Edition

TEACHING OUTLINE 1. Neuroendocrine System (see Figures 13.1–13.5 in Biopsychology) a. Glands LO 13.1 Explain the distinction between exocrine glands and endocrine glands, describe the functions of the gonads, and distinguish between the X chromosome and the Y chromosome.

Exocrine glands release their chemicals into ducts; endocrine glands release hormones directly into the circulatory system.

Gonads • The gonads (the testes and the ovaries) are central to any discussion of hormones and sex.

• They produce sperm cells and ova.

• At conception, a sperm and ova combine to form a zygote, which then contains all of the genetic information needed for the development of a complete adult organism.

• The sex chromosomes contain the genetic programs that direct sexual development. Female cells contain two large X chromosomes; male cells contain one X chromosome and a small Y chromosome. b. Hormones LO 13.2 Describe the three classes of hormones, and then describe three classes of gonadal hormones.

• • •

There are three kinds of hormones: amino acid derivatives, peptides and proteins, and steroids.

Steroid hormones play the major role in sexual development and behavior.

Like other hormones, steroids can act as receptors in cell membranes; unlike other hormones, however, steroids are small and fat soluble and this allows them to cross the neural membrane to bind to receptors in the cytoplasm or the nucleus.

Sex Steroids • The gonads also produce and release the same steroid hormones: androgens, estrogens, and progestins.

• Testosterone is the most common androgen; estradiol is the most common estrogen.

• Progestins are released by ovaries and testes. The most common is progesterone, which in females prepares the uterus and the breast for pregnancy.

• The adrenal cortex also releases small amounts of all of the sex steroids. c. The Pituitary LO 13.3 Explain why the pituitary is sometimes called the master gland, and describe its anatomy. Discuss the female vs. male patterns of gonadal and gonadotropic hormone release, and explain the evidence that discounted a role for the anterior pituitary in those patterns of release.

•

The pituitary gland is often referred to as the “master gland” because it releases a variety of hormones, called tropic hormones, which travel through the blood to other glands and stimulate them to release hormones that have diverse, long-lasting effects.

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Chapter 13: Hormones and Sex • •

The pituitary is, in fact, two glands: the anterior pituitary and the posterior pituitary, which dangle together from the pituitary stalk and are attached to the hypothalamus.

Strictly speaking, it is the anterior pituitary that is the master gland; only it releases tropic hormones.

Female Gonadal Hormone Levels Are Cyclic; Male Gonadal Hormone Levels Are Steady • A major difference between men and women is that gonadotropin release from the anterior pituitary cycles approximately every 28 days in women, but its release varies little from day to day in men. The release pattern for both sexes is pulsatile; attempts to understand this malefemale difference led to an important discovery.

• First, it was assumed that male and female pituitaries are fundamentally different (steady versus cyclic), but female pituitaries implanted in males became “steady pituitaries,” and male pituitaries implanted in females became “cyclic pituitaries”; this suggested that the pattern of anterior pituitary release was being controlled by another organ. It suggested that “the master gland had its own master.” d. Control of the Pituitary LO 13.4 Explain how the anterior and posterior pituitary are controlled.

Attention turned to the hypothalamus, the neural structure to which the pituitary is connected; it was soon discovered that the hypothalamus controls the pituitary in two different ways: one way for the posterior pituitary and one for the anterior pituitary.

Control of the Anterior and Posterior Pituitary by the Hypothalamus • Axons of neurons in the paraventricular and supraoptic nuclei of the hypothalamus terminate in the posterior pituitary.

• Vasopressin and oxytocin are synthesized in the cell bodies of these neurons, they are transported down their axons, and they are released from the posterior pituitary into general circulation. Vasopressin facilitates reabsorption of water by the kidneys; oxytocin stimulates contractions of the uterus and ejection of milk in women.

• The release of tropic hormones from the anterior pituitary is controlled by other hormones called releasing hormones. They are released by the hypothalamus into the hypothalamopituitary portal system, which carries them to the anterior pituitary; gonadotropin-releasing hormone stimulates the release of the anterior pituitary’s two gonadotropins: follicle stimulating hormone and luteinizing hormone. e. Discovery of Hypothalamic Releasing Hormones LO 13.5 Describe the research that led to the discovery of the hypothalamic releasing hormones.

• • •

f.

The hypothalamic hormones that were thought to stimulate the release of an anterior pituitary hormone were referred to as releasing hormones. Those thought to inhibit the release are called release-inhibiting hormones.

In the 1960s, a discovery was made that thyrotropin-releasing hormone triggered the release of thyrotropin from the anterior pituitary, which in turn stimulates the release of hormones from the thyroid gland.

Gonadotropin-releasing hormone was soon discovered which stimulates the release of follicle-stimulating hormone and luteinizing hormone.

Regulation of Hormone Levels 6 ..

Biopsychology, Tenth Edition LO 13.6 Describe three different types of signals that regulate hormone release. Also, describe how hormones are released over time and the effect this pattern of release has on levels of circulating hormones.

Regulation by Neural Signals Endocrine glands located in the brain are regulated by cerebral neurons. Endocrine glands outside the CNS are innervated by the autonomic nervous system.

Regulation by Hormonal Signals Hormone release is regulated by other hormones and by feedback of the hormones themselves onto receptors in the same structures responsible for their release (this system maintains the blood levels of the hormones).

Regulation by Nonhormonal Chemicals Glucose, calcium and sodium levels in the blood all influence the release of particular hormones.

Pulsatile Hormone Release Hormones tend to be released in pulses; they are discharged several times a day in large surges, typically lasting no more than a few minutes. One consequence of this is that there are often minuteto-minute fluctuations in the levels of circulating hormones. g. Summary Model of Gonadal Endocrine Regulation LO 13.7 Summarize the model of gonadal endocrine regulation.

Figure 13.5 provides a summary of the regulation of gonadal hormones. According to this model, the brain controls the release of gonadotropin-releasing hormone from the hypothalamus into the hypothalamopituitary portal system, which carries it to the anterior pituitary. The anterior pituitary release gonadotropins to the gonads, which then release androgens, progestins, and estrogens.

These then feed back into the brain to regulate subsequent release.

2. Hormones and Sexual Development of the Body (see Figures 13.6–13.9 in Biopsychology) a. Sexual Differentiation LO 13.8 Describe the development of the internal and external reproductive organs.

Nature’s default is to femaleness. Only when the female system is shut down will a male develop.

Fetal Hormones and the Development of Reproductive Organs • The differentiation of male and female gonads occurs about six weeks after fertilization. At this time, males and females have identical primordial gonads, each with two parts: a medulla and a cortex.

• In males, the Sry gene on the Y chromosome triggers the manufacture of Sry protein. The presence of Sry protein causes the medulla (core) of the primordial gonads to develop into testes.

• If no H–Y antigen is present (as in normal genetic females), the cortex of the primordial gonads naturally develops into ovaries.

• Accordingly, genetic female fetuses injected with Sry protein develop testes, and genetic male fetuses injected with a drug that blocks Sry protein develop ovaries.

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Chapter 13: Hormones and Sex Internal Reproductive Ducts • Six weeks after fertilization, each fetus has two sets of undeveloped internal reproductive ducts, one male and one female: the undeveloped male system is called the Wolffian system; the undeveloped female system is called the Müllerian system.

• In normal genetic males, the testes release androgens in the third month, and this causes the Wolffian system to develop; the testes also release Müllerian-inhibiting substance, which causes the Müllerian system to degenerate and the testes to descend into the scrotum. All fetuses exposed to androgen in the third month, whether genetic male or female, develop male ducts.

• Any fetus not exposed to androgens in the third month after conception (e.g., a normal genetic female, an ovariectomized genetic female, or an orchidectomized genetic male) will develop female reproductive ducts.

• Ovariectomy refers specifically to removal of the ovaries, orchidectomy refers specifically to removal of the testes, and castration and gonadectomy refer generally to removal of gonads.

External Reproductive Organs • Every normal human fetus begins with the same bipotential precursor of external reproductive organs.

• There are four parts to the bipotential precursor: the glans, the urethral folds, the lateral bodies, and the labioscrotal swellings.

• In males, the glans become the head of the penis, the urethral folds simply fuse, the lateral bodies form the shaft of the penis, and the labioscrotal folds become the scrotum.

• In females, the glans become the clitoris, the urethral folds become the labia minora, the lateral bodies form the hood of the clitoris, and the labioscrotal folds become the labia majora.

• Like the internal reproductive organs, testosterone release at the right time in development causes this bipotential precursor to develop into male external genitals; in the absence of testosterone, it develops into female external genitals. b. Puberty: Hormones and the Development of Secondary Sex Characteristics LO 13.9 Describe the male and female secondary sex characteristics and the role of hormones in their development.

• • • •

Puberty is the transitional period between childhood and adulthood during which fertility is achieved, the adolescent growth spurt occurs, and secondary sexual characteristics develop.

Secondary sexual characteristics are those features other than the reproductive organs that distinguish males from females.

Puberty is associated with an increase in the release of growth hormones—the only anterior pituitary hormone that does not have a gland as its primary target.

An increase in the release of gonadotropic hormone and adrenocorticotropic hormone causes the gonads and adrenal cortex to increase their release of hormones, which in turn initiates the maturation of the genitals.

3. Hormones and Sexual Development of Brain and Behavior a. Sex Differences in the Brain LO 13.10 Describe the evolution of research and thinking about sex differences in the brain.

There is considerable evidence of differences between the brains of men and women in terms of overall brain size, the size of specific structures in the brain, and in patterns of brain activity.

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• • • •

•

• • •

•

• • • • •

First Discovery of a Sex Difference in Mammalian Brain Function The functional significance of these differences is currently the focus of intense study.

In the pioneering study in this area, Pfeiffer (1936) found that sexual differences in the brain appear to depend on exposure to high levels of androgens at developmentally crucial times.

Most early research on brain differentiation focused on the differentiation of the hypothalamuscontrolled pattern of gonadotropin release into the steady male pattern or the female cyclic pattern.

Consistent with what you have already learned about reproductive-system development, rats exposed to androgens in the perinatal period (e.g., intact genetic male rats, intact female or ovariectomized female rats that received testes transplants) develop the steady, male pattern of gonadotropin release.

In contrast, rats not exposed to androgen in the perinatal period (e.g., intact genetic female rats, ovariectomized genetic female rats, orchidectomized genetic male rats) develop the cyclic, female pattern of gonadotropin release.

Aromatization Hypothesis There is evidence to support the idea that in order to masculinize the brain, testosterone must be converted to estradiol—a process called aromatization.

The aromatization hypothesis suggests that testosterone released during the perinatal period enters the brain and is aromatized to estradiol, and that it is actually estradiol that masculinizes the brain.

Two lines of evidence support this theory, both coming from experiments on rats and mice: (1) findings demonstrating the masculinizing effects on the brain of early estradiol injections, and (2) findings showing that masculinizing the brain does not occur in response to testosterone that is administered with agents that block aromatization or in response to androgens that cannot be aromatized (dihydrotestosterone).

Estradiol masculinizes the brain of the male fetus because testosterone is immune to alpha fetoprotein; it can travel unaffected from the testes to brain cells.

Sex Differences in the Brain: The Modern Perspective The view that female brain development is the default program and is normally overridden in genetic males by prenatal exposure to testosterone aromatized to estradiol remained the main theory, as long as research focused on rats.

At this time, many of the sex differences observed in the brain cannot be linked to human behaviors.

It has recently become clear that sexual dimorphism in the brain is not simply a function of prenatal exposure to testosterone.

The sex chromosomes themselves contribute to differences in brain dimorphism. There is evidence that various dimorphisms appear at different points during development and are controlled by a variety of influences.

Estradiol may play a more active role in brain development than previously thought.

b. Development of Sex Differences in Behavior LO 13.11 Describe the results of studies of sex differences in behavior in humans and nonhumans.

Development of Reproductive Behaviors in Laboratory Animals • Considerable attention has been paid to the role of hormones on the development of sexual behavior.

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Chapter 13: Hormones and Sex •

• • • • • • • •

Phoenix and colleagues (1955) demonstrated that perinatal injections of testosterone masculinize and defeminize a genetic female’s copulatory behaviors; as adults, such females display male-like mounting behaviors when injected with testosterone and they display less lordosis when injected with progesterone and estradiol.

Alternatively, male rats that are not exposed to testosterone early in development are feminized and demasculinized.

Male rats castrated shortly after birth failed to display the typical male copulatory pattern of mounting, intromission, and ejaculation.

In addition, perinatal testosterone alters the proceptive behaviors displayed by rats; there is less hopping, darting, and ear wiggling by receptive female rats. Female rats tend to be more aggressive when they mature and their maternal behaviors are also altered.

In males, the surge in gonadotropic hormones increases the release of androgens from the testes.

This masculinizes the body. There is muscle development, body hair and pubic hair growth, lowering of the voice, the development of fertility, growth of sex organs, etc.

In females, the pubertal surge of gonadotropin release stimulates the release of estrogens from the ovaries.

This partially feminizes the body; estrogens stimulate breast growth, hip growth, onset of the menstrual cycle, fertility, etc.

Masculinization and defeminization are independent from feminization and demasculinization.

Development of Sex Differences in the Behavior of Humans • Maleness and femaleness are not discrete, mutually exclusive concepts. Some behaviors are sexually dimorphic (two distinct classes); other behaviors show substantial overlap between the two sexes.

• Most differences between the behavior of average human males and average human females are small and characterized by substantial overlap.

• There are often differences in the susceptibility of human males and females to behavioral disorders. (Ex: dyslexia, stuttering, autism spectrum disorders are more prevalent in males while depression, anxiety disorders and Alzheimer’s occur more in females.)

4. Three Cases of Exceptional Human Sexual Development (see Figure 13.10 in Biopsychology) a. Exceptional Cases of Human Sexual Development LO 13.12 Explain what androgen insensitivity syndrome, adrenogenital syndrome, and ablation penis have taught us about human sexual development Androgenic Insensitivity Syndrome • There are otherwise normal genetic males who suffer from the androgen insensitivity syndrome; they have normal levels of androgen, but their bodies lack the receptors to not respond to it.

• Genetic males with androgen insensitivity frequently come to the attention of a physician when they become concerned about their inability to get pregnant; they are ostensibly happily married women.

• A physical examination reveals: (1) sparse pubic and axillary hair, (2) they do not menstruate, (3) they have shallow vaginas, (4) they have internal testes and undeveloped male internal reproductive ducts, and (5) their cells are all of the normal male XY chromosome type.

• During development, individuals with androgen insensitivity syndrome develop along preprogrammed female lines, without the overriding effects of androgens.

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Biopsychology, Tenth Edition •

Money and Earhardt (1972) found that the childhood behaviors of these patients were those one would expect of a female; in spite of their genetic maleness, they looked like females, were raised like females, and they acted like females.

Androgenital Syndrome • Androgenital syndrome is caused by congenital adrenal hyperplasia and results from a deficiency in the release of cortisol from the adrenal cortex; this causes adrenal hyperactivity and excessive release of adrenal androgens.

• Males are generally unaffected; females are often born with an enlarged clitoris and partially fused labia, though the internal reproductive organs are usually normal.

• This disorder is usually detected at birth; administration of cortisol reduces the levels of the adrenal androgens.

• Females who receive early treatment still display a high degree of tomboyishness and little interest in maternity when they are teenagers; however, their behavior is still well within the normal range.

• In adulthood, females who receive early treatment show normal sexual preferences.

Ablatio Penis • As the name implies, this is a condition produced when the penis is removed.

• In the most famous case, a baby’s penis was accidentally destroyed during a circumcision; the child was castrated, an artificial vagina was created, and estrogen was administered to feminize the boy.

• As this case was originally reported by Money (1975), the boy developed into a “normal” female, supporting the idea that “Nurture can overcome Nature.”

• Long-term follow-ups tell a different story: The child acted in a masculine way, he suspected he was a boy beginning in the second grade, and he moved and talked in a masculine manner.

• By age fourteen, the boy had decided to be a male and was only then told of his early history.

He requested androgen treatments, had a mastectomy and phaloplasty (removal of breasts and surgical creation of a penis), married at 25 and became strictly heterosexual. He could ejaculate and experience orgasm, though the castration left him permanently sterile.

• This patient never fully came to terms with the emotional scars that this experience left and ultimately committed suicide. Clearly, irrevocable treatments that alter a person’s sexual identity should await puberty and the emergence of the person’s sexual identity and preferences.

Do the Exceptional Cases Prove the Rule?

The answer is yes, although current theories do not supply all of the answers when it comes to sexual dimorphisms and behavior, they have contributed greatly to the understanding of exceptional patterns of sexual differentiation of the body.

5. Effects of Gonadal Hormones on Adults (see Figure 13.11 in Biopsychology) Hormones not only influence the development of the body and brain along male or female lines, they play a role in activating the sexual behavior of men and women. a. Male Sexual Behavior and Testosterone LO 13.13 Describe the role of testosterone in male sexual behaviors.

•

The role of androgens in activating the sexual behavior of adult males is apparent following orchidectomy.

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Chapter 13: Hormones and Sex • • • •

•

In about half the cases, there is a complete loss of ability to achieve an erection and of sexual motivation within a week or two of the operation; however, in other cases, the decline is less complete and/or more gradual. The reason for this variability is not understood.

Castrated men also exhibit a variety of physical changes, e.g., reduction of body hair, deposition of fat on hips and chest, softening of the skin, a marked reduction of strength.

Testosterone replacement injections restore sexual motivation, sexual potency, and remasculinize the bodies of orchidectomized males; but they remain sterile.

The fact that testosterone injections restore the sexuality of orchidectomized males has led to the view that the sexual motivation and performance of a male is determined by his level of testosterone, and thus that sexual motivation and performance can be increased in healthy intact males by testosterone injections.

This is NOT the case. In healthy intact males, there is no correlation between testosterone levels and sexuality, and substantial increases (e.g., by injection) or decreases (e.g., by hemiorchidectomy) in testosterone levels have no effect on sexual motivation or performance.

b. Female Sexual Behavior and Gonadal Hormones LO 13.14 Describe the role of testosterone in female sexual behavior.

• • • • • •

In female rodents, the four- or five-day menstrual cycle is correlated with a cycle of sexual receptivity (i.e., with an estrous cycle).

In the day or two prior to ovulation, there is a gradual increase in estrogens, and a sudden surge in progesterone just as the mature egg is being released from its follicle.

During the next twelve to eighteen hours, the female is said to be in estrus—or that she is fertile, receptive, proceptive, and sexually attractive to male rats.

Ovariectomy abolishes the estrous cycle in rodents; but ovariectomized female rodents can be readily brought into estrus by an injection of estradiol, followed a day and a half later by an injection of progesterone.

Human females are different; there is no clear-cut cycle of sexual receptivity associated with the menstrual cycle. Ovariectomy eliminates vaginal lubrication, the menstrual cycle, and fertility, but it has no effect on sexual motivation.

The jury is still out as to whether estradiol or testosterone is responsible for a female’s sexual drive.

c. Anabolic Steroid Abuse LO 13.15 Describe the dangers associated with anabolic steroid use.

• • • •

•

Testosterone has anabolic (growth promoting) effects, but it is not a particularly effective anabolic agent because it is quickly broken down in the body.

Chemists have synthesized over 100 similar chemicals belonging to the same class (steroids) that are not broken down so quickly; these are the so-called anabolic steroids.

There is currently an epidemic of anabolic steroid abuse among athletes and the general public who use them for cosmetic purposes.

However, there are a number of devastating side-effects: testicular atrophy and gynecomastia (breast growth) have been reported in men; amenorrhea, sterility, hirsutism (excessive growth of body hair), growth of the clitoris, masculine body shape, baldness, and deepening of the voice have been reported in women.

In both men and women, there have been reports of muscle pain, muscle spasms, excessive water retention, acne, nausea, vomiting, bleeding of the tongue, fits of anger, aggression, or depression, cardiovascular problems and premature death.

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Biopsychology, Tenth Edition 6. Brain Mechanisms of Sexual Behavior (see Figures 13.12–13.14 in Biopsychology) a. Four Brain Structures Associated with Sexual Activity LO 13.16 Describe the roles of the cortex, hypothalamus, amygdala, and ventral striatum in sexual activity.

Cortex and Sexual Activity • In both men and women, many cortical regions are activated by sexually-arousing stimuli.

Hypothalamus and Sexual Activity • The role of the hypothalamus in the control of the pituitary gland led to an examination of sex differences in the hypothalamus.

• Notably, the sexually dimorphic nucleus in the medial preoptic area in rats was found to be several times larger in males than in females.

• At birth, the sexually dimorphic nucleus is the same size in both sexes; however, within the first few days postnatal, this area grows rapidly in males, but not females. This growth is stimulated by estradiol, aromatized from testosterone. Castration at day-1 postnatal reduces the size of the medial preoptic in adult rats.

• The size of the sexually dimorphic nucleus has been correlated with testosterone levels and some aspects of sexual behavior. However, bilateral lesions of the nucleus have only slight effects on male rat sexual behavior and its function remains unclear.

• In males, the medial preoptic area plays a key role in sexual behavior; lesions abolish sexual behavior in all areas studied, and stimulation in the area elicits copulatory behavior.

• Interestingly, lesions to the medial preoptic area do not diminish the desire for sexual behavior, just copulatory behavior.

• The medial preoptic area seems to influence copulatory behavior via the lateral tegmental fields; lesions here also eliminate copulatory behavior in rodents.

• Recent research on the role of the medial preoptic area in male sexual behavior has shown that dopamine increases in this area before and during copulation; that androgen receptors decrease after copulation and that endogenous opioids increase in the area during copulation.

• Dopamine agonists microinjected to the medial preoptic area facilitate male sexual behavior, whereas, dopamine antagonists block it.

• In female rats, the ventromedial nucleus of the thalamus contains circuits critical to sexual behavior; stimulation elicits these behaviors, and lesions there reduce it.

• The ventromedial thalamic nucleus is critical to the onset of estrus in female rats, as microinjections of estrogen and progesterone there will bring on estrus.

• The ventromedial thalamic nucleus appears to act via a projection to the periaqueductal gray.

Amygdala and Sexual Activity • The amygdala processes visual and olfactory signals that help identify possible mating partners.

• Bilateral destruction of the amygdala can produce Kluver-Bucy syndrome, which is characterized by hypersexuality and inability to limit advances to appropriate partners.

• Males are more likely to be aroused by erotic images than females. This is evidenced by activation of the amygdala.

Ventral Striatum and Sexual Activity • The ventral striatum can be activated in anticipation of sexual or pleasurable activities.

7. Sexual Orientation and Gender Identity

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Chapter 13: Hormones and Sex Many humans are not heterosexual; they are sexually attracted to members of the same bodily sex (homosexual), or to members of both bodily sexes (bisexual). a. Sexual Orientation LO 13.17 Describe the results of the two studies on the genetics of sexual orientation by Bailey and Pillard (1991, 1993), and describe the fraternal birth order effect and why it is thought to occur.

Sexual Orientation and Genes • Sexual orientation appears to have a genetic basis. For example, monozygotic twins of homosexuals have a concordance rate of about 50%.

Sexual Orientation and Early Hormones • There are no differences in circulating sex hormones between homosexuals and heterosexuals.

• People discover their sexual preferences early in life, suggesting perinatal hormones might play a role.

• In animals, perinatal castration of males or testosterone treatment of females induces same-sex preferences.

• The relevance of these data to humans are unclear; the experiments necessary to test the idea that early hormone exposure has a role in sexual orientation cannot be ethically performed on humans, and homosexuality and bisexuality are difficult to model in nonhumans.

• One promising line of research on sexual orientation focuses on the fraternal birth order effect. This states that the probability of a male being gay increases as a function of the number of older brothers he has. It is proposed that the mother becomes progressively more immune to masculinizing hormones with each male fetus. Therefore, younger sons might be affected by the mother deactivating the masculinizing hormones (maternal immune hypothesis).

• Research by Ehrhardt concluded that perinatal estrogen exposure does encourage lesbianism and bisexuality in females but its effect is very weak. b. What Triggers the Development of Sexual Attraction?

LO 13.18 Describe the hypothesized role of adrenal cortex steroids in the emergence of sexual attraction.

•

Sexual attraction emerges at around the age of ten and appears to be due to adrenal androgens.

c. Is There a Difference in the Brains of Homosexuals and Heterosexuals?

LO 13.19 Describe the famous study of LeVay (1991) and the major problem with its finding.

• •

LeVay (1991) found that the third interstitial nucleus of the hypothalamus is more than twice as large in heterosexual males as it is in heterosexual females and homosexual males.

However, this study has not been consistently replicated.

d. Gender Identity LO 13.20 Explain what transsexualism is, and describe the process of sexual reassignment.

• • •

Gender identity is the gender, male or female, that a person believes himself or herself to be.

Usually, sexual identity coincides with a person’s anatomical sex, but not always.

Transsexualism exists when a person believes that they are trapped in the body of a member of the opposite sex; they often seek surgical sexual reassignment.

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Biopsychology, Tenth Edition • •

Sexual reassignment surgery requires that a full psychiatric assessment to determine if the person is a good candidate for surgery. Counseling follows to help with coping strategies for after the surgery. Then, estrogen administration is begun and the surgery performed.

The causes of transsexualism are unknown.

e. Independence of Sexual Orientation and Gender Identity LO 13.21 Sexual attraction, gender identity, and body type are independent. Explain and give an example.

• • • •

A powerful test of any theory is its ability to explain exceptional cases.

Men and women are similar, yet they are different in many ways. They are not opposites!

Consider the case of transsexuals, having the body type of one sex, and the sexual identity of the other sex, but the orientation of their sexual attraction is an independent matter.

Clearly, femaleness or maleness is a combination of many different attributes, each of which can develop independently.

< Return to Table of Contents

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Chapter 13: Hormones and Sex

LECTURE LAUNCHERS Lecture Launcher 13.1: Differentiation Animation To help your students understand how male and female genitalia develop from a bipotential precursor, you can use the following video in your lecture. Go to http://www.youtube.com and search “Sex Differentiation” and click on the matching link.

Lecture Launcher 13.2: Gender Testing of Female Athletes Here’s an old twist on the MAMAWAWA theme: Since the 1960s, gender testing has been common among world-class female athletes to ensure that they are, in fact, females. To help you discuss this issue in class, use the Web-based Gender-Testing forum presented by the Howard Hughes Medical Institute at http://www.hhmi.org/ and place “the meaning of sex: genes and gender” in the search bar. You probably won’t want to complete the whole discussion in class, but simply completing the first assessment will stimulate a class discussion.

Lecture Launcher 13.3: Estrogen and Synaptogenesis Students generally have no problem discussing the implications of recent research demonstrating estrogen’s neuroprotectant effects and the resulting differences between males and females.

Lecture Launcher 13.4: What Is Your “Sex”?

Understanding that “sex” is not just male or female may be one of the most important lessons in this chapter.

A brief lecture on the basic biology of reproductive combination is paradigm refining for most students.

Lecture Launcher 13.5: Effect of Environmental Estrogens The popular press and many scientific sources have expressed concern that estrogen-like compounds in the environment may be changing how human beings mature. The jury is still out. Here are two sources, one on each side of the issue, with some good information.

Web Links 13.12 Environmental Estrogens 13.13 Endocrine Disruptors < Return to Table of Contents

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Biopsychology, Tenth Edition

ASSIGNMENTS Assignment 13.1: Organizing Effects and Activating Effects of Hormones Students create a table that differentiates between the organizing effects and activating effects of hormones.

Based on the table, the following questions are answered: I. Do hormones have the same organizing effects in males and females?

(List the hormones and describe the same or different effects.)

II. Describe the two times during development that activating effects of sex hormones are most important.

Handout 13.1 Organizing Effects and Activating Effects of Hormones Assignment 13.2: How Can You Tell If Someone Is Male or Female?

Handout 13.2 How Can You Tell If Someone Is Male or Female? < Return to Table of Contents

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Chapter 13: Hormones and Sex

WEB LINKS Web Link 13.1: Society for Human Sexuality http://www.sexuality.org/ This site provides a variety of links to sexuality resources and Internet sites.

Web Link 13.2: Human Behavior and Evolution Society http://www.hbes.com/ This is an interdisciplinary international society of researchers from social and natural sciences who use evolutionary theory and studies of animal behavior to better understand human nature, behavior, and sexuality. Includes Debate (available on streaming video, audio, or transcript), Pinker vs. Spelke: The Science of Gender and Science. Go to http://www.edge.org/ and place “Pinker Debate” in the search bar.

Select the debate between Pinker and Spelke.

Web Link 13.3: The Kinsey Institute Go to http://www.indiana.edu/ and place “Kinsey” in the search bar. Click on the “Kinsey Institute” link.

Housed at IU in Bloomington, this is one of the top research groups on sexual behavior.

Web Link 13.4: Afraid to Ask http://www.afraidtoask.com/ Basic anatomy associated with reproduction and puberty.

Web Link 13.5: Handbook of Andrology Go to http://andrologysociety.com/ and place “andrology handbook” in the search bar. Select the link with the matching name.

Determinants of normal male and female sex differentiation in the human.

Web Link 13.6: Human Menstrual Cycle Go to http://www.merckmanuals.com and place “Menstrual Cycle” in the search bar. Click on the matching link. Note: This is the consumer version. There is a more in depth professional version also available from the same site.

Good explanation of human menstrual cycle hormones and events.

Web Link 13.7: Intersex Society of North America http://www.isna.org/ Presents information about intersexuality, ambiguous genitalia, etc.

Web Link 13.8: What Is Congenital Adrenal Hyperplasia?

Go to http://www.mayoclinic.org and place “Congenital Adrenal Hyperplasia” in the search bar. Select the matching link.

Web Link 13.9: Gender Testing of Female Athletes Go to http://www.hhmi.org/ and click on the link for “Educational Resources” found at the top of the page.

Select “Biointeractive” from that link. Once there, place “gender testing female athletes” in the search bar.

Interactive tutorial/problem solving activity.

Web Link 13.10: Is Chemical Castration an Acceptable Punishment for Male Sex Offenders?

Place “Sex Crimes, Punishment, and Therapy” in the search bar of your browser. Look for a result from “csun.edu” and click that link. This will take you to a page that contains resources that have been used to 18 ..

Biopsychology, Tenth Edition defend using or not using chemical castration. Once there, you can use the link at the bottom of the page titled “Back to Index” to go back to a full listing of the links available on this site and access the resources for the opposite argument than the one you clicked on originally.

Web Link 13.11: Anabolic Steroids: Side Effects Go to http://www.sportsci.org/ and scroll down the left side of the page and click on the link that allows you to search “this site.” Place “Anabolic Steroids: Side Effects” in the search bar and select the matching link.

Harm Kuipers, M.D., Ph.D. Department of Physiology, University of Limburgt, The Netherlands.

Web Link 13.12: Environmental Estrogens Go to http://www.enhs.umn.edu and place “environmental estrogens in men’s health” in the search bar.

Select the matching link.

The effect of environmental estrogens on men’s health.

Web Link 13.13: Endocrine Disruptors Go to http://www.niehs.nih.gov and place “endocrine disruptors” in the search bar. Select the link that leads to the detailed page dedicated to this topic (do not access the fact sheet). A good summary of compounds, sources, and concerns. < Return to Table of Contents

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Chapter 13: Hormones and Sex

HANDOUTS Handout 13.1: Organizing Effects and Activating Effects of Hormones Name: ________________________________________ Section: ___________ Date: ___________ Create a table that differentiates between organizing effects and activating effects of hormones. Based on your table, answer the following questions.

Do hormones have the same organizing effects in males and females?

List the hormones and describe the same or different effects.

Describe the two times during development that activating effects of sex hormones are most important.

HORMONE

ORGANIZING Female

ORGANIZING Male

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ACTIVATION Female

ACTIVATION Male

Biopsychology, Tenth Edition Handout 13.2: How Can You Tell If Someone Is Male or Female?

You will have an opportunity to conduct the gender testing of a female athlete.

Go to http://www.hhmi.org/ and click on the link for “Educational Materials” found at the top of the page.

Select “Biointeractive” from that link. Once there, place “gender testing female athletes” in the search bar.

This will take you to an interactive site that will allow you to explore the phenotypic and genotypic aspects of gender. When you have completed the activity, answer the questions below: 1. Did you decide that the athlete should be qualified to compete or be disqualified?

2. What reasons can you give for your decision?

< Return to Table of Contents

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14 Sleep, Dreaming, and Circadian Rhythms: How Much Do You Need to Sleep?

TABLE OF CONTENTS Chapter-at-a-Glance

2

Learning Objectives

3

Brief Chapter Outline

5

Teaching Outline

7

Lecture Launchers

18

Activities

23

Assignments

24

Web Links

26

Handouts

29

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Chapter 14: Sleep, Dreaming, and Circadian Rhythms

CHAPTER-AT-A-GLANCE

Brief Outline Chapter Introduction (p. 361) 14.1 Stages of Sleep (pp. 362–364)

14.2 Why Do We Sleep, and Why Do We Sleep When We Do? (pp. 365–366) 14.3 Effects of Sleep Deprivation (pp. 366–371) 14.4 Circadian Sleep Cycles (pp. 372– 375)

14.5 Four Areas of the Brain Involved in Sleep (pp. 375–379) 14.6 Drugs That Affect Sleep (pp. 379– 381) 14.7 Sleep Disorders (pp. 381–384)

14.8 Effects of Long-Term Sleep Reduction (pp. 384–387)

Instructor’s Manual Resources Lecture Launcher 14.1, Activity 14.1 Lecture Launcher 14.6, Assignment 14.2 Lecture Launchers 14.2, 14.7, 14.10 Lecture Launchers 14.11, 14.12, Assignments 14.1, 14.3, 14.4, 14.5

Lecture Launchers 14.3, 14.5, 14.8,14.9 Lecture Launcher 14.4

< Return to Table of Contents

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Biopsychology, Tenth Edition

LEARNING OBJECTIVES After completion of this chapter, the student should be able to: LO 14.1 LO 14.2 LO 14.3

LO 14.4 LO 14.5 LO 14.6 LO 14.7 LO 14.8 LO 14.9 LO 14.10 LO 14.11 LO 14.12 LO 14.13 LO 14.14 LO 14.15 LO 14.16 LO 14.17 LO 14.18 LO 14.19 LO 14.20 LO 14.21 LO 14.22 LO 14.23 LO 14.24 LO 14.25 LO 14.26 LO 14.27 LO 14.28

Describe the three standard physiological measures of sleep.

Describe the three stages of sleep EEG, and explain the difference between REM and nonREM sleep.

Describe the relationship between REM sleep and dreaming. Also, describe five common beliefs about dreaming and assess their validity. Finally, describe the activation-synthesis theory of dreams.

Describe the two kinds of theories of sleep.

Explain four conclusions that have resulted from the comparative analysis of sleep.

Explain how stress can often be a confounding variable when considering the effects of sleep deprivation.

List the three predications that recuperation theories make about the effects of sleep deprivation.

Describe two classic sleep-deprivation case studies.

Describe the major effects of sleep deprivation in humans.

Describe the key studies of sleep deprivation in laboratory animals. Provide a critique of the carousel apparatus as a method of sleep deprivation.

Describe the effects of REM-sleep deprivation.

Describe six pieces of evidence that indicate that less sleep is associated with more efficient sleep.

Describe the circadian sleep-wake cycle and the role of zeitgebers in maintaining circadian rhythms.

Describe free-running rhythms and internal desynchronization, and explain why they are incompatible with recuperation theories of sleep.

Describe the disruptive effects of jet lag and shift work on circadian clock in the suprachiasmatic nucleus (SCN) of the hypothalamus.

Describe the research that led to the discovery of a circadian clock in the suprachiasmatic nucleus (SCN) of the hypothalamus.

Explain the mechanism by which SCN neurons are entrained by the 24-hour light-dark cycles.

Understand the genetics of circadian rhythms and the important discoveries that have resulted from the discovery of circadian genes.

Describe the research that led to the identification of the anterior and posterior hypothalamus as brain regions involved in the regulation of sleep and wakefulness.

Describe the research that led to the identification of the reticular formation as a brain region involved in the regulation of sleep and wakefulness.

Discuss how REM sleep is controlled by the reticular formation and what implications this has for understanding the neural mechanisms of behavior.

Describe three classes of hypnotic drugs. Compare and contrast them in terms of their efficacy and side effects.

Describe three classes of antihypnotic drugs.

Recognize the relationship between the pineal gland and melatonin and how melatonin affects sleep.

Describe four causes of insomnia.

Describe the symptoms of narcolepsy and the role of orexin (hypocretin) in this disorder.

Describe one REM-sleep-related disorder and its presumed neural mechanisms.

List the main differences between short and long sleepers.

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Chapter 14: Sleep, Dreaming, and Circadian Rhythms LO 14.29 LO 14.30 LO 14.31

Describe the results of studies of long-term reduction of nightly sleep.

Describe the results of studies of long-term reduction of sleep by napping.

Recognize how shorter sleep times relate to longevity.

< Return to Table of Contents

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Biopsychology, Tenth Edition

BRIEF CHAPTER OUTLINE Lecture Launcher 14.1: Sleep in the News 1. Stages of Sleep a. Three Standard Psychophysiological Measures of Sleep b. Three Stages of Sleep EEG c. Dreaming 2. Why Do We Sleep, and Why Do We Sleep When We Do? a. Two Kinds of Theories of Sleep b. Comparative Analyses of Sleep Lecture Launcher 14.2: Sleep across Species 3. Effects of Sleep Deprivation a. Interpretation of the Effects of Sleep Deprivation: The Stress Problem b. Predictions of Recuperation Theories about Sleep Deprivation c. Two Classic Sleep-Deprivation Case Studies d. Experimental Studies of Sleep Deprivation in Humans e. Sleep-Deprivation Studies with Laboratory Animals f. REM-Sleep Deprivation g. Sleep Deprivation Increases the Efficiency of Sleep 4. Circadian Sleep Cycles a. Circadian Rhythms b. Free-Running Circadian Sleep-Wake Cycles c. Jet Lag and Shift Work d. A Circadian Clock in the Suprachiasmatic Nuclei e. Neural Mechanisms of Entrainment f. Genetics of Circadian Rhythms 5. Four Areas of the Brain Involved in Sleep a. Two Areas in the Hypothalamus Involved in Sleep b. Reticular Formation and Sleep c. Reticular REM-Sleep Nuclei 6. Drugs that Affect Sleep a. Hypnotic Drugs b. Antihypnotic Drugs c. Melatonin Lecture Launcher: 14.3: Your Sleep Habits 7. Sleep Disorders a. Insomnia b. Hypersomnia c. REM Sleep-Related Disorders Lecture Launcher: 14.4: Amazing Feats of Sleep 5 ..

Chapter 14: Sleep, Dreaming, and Circadian Rhythms 8. Effects of Long-Term Sleep Reduction a. Differences between Short and Long Sleepers b. Long-Term Reduction of Nightly Sleep c. Long-Term Sleep Reduction by Napping d. Effects of Shorter Sleep Times on Health e. Long-Term Sleep Reduction: A Personal Case Study < Return to Table of Contents

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Biopsychology, Tenth Edition

TEACHING OUTLINE 1. Stages of Sleep a. Three Standard Psychophysiological Measures of Sleep (see Figure 14.1 Biopsychology) LO 14.1 Describe the three standard physiological measures of sleep.

• • • •

It was discovered that although EEG waves are generally high-voltage and slow during sleep, there are periods during sleep when they are similar to the low-voltage fast waves of wakefulness.

In the 1950s, it was discovered that rapid eye movements (REMs) occurred under the eyelids of sleeping subjects during the periods of low-voltage fast EEG activity.

In 1962, Berger and Oswald found that there was a dramatic decline of EMG (electromyogram) activity in the muscles of the body core during these same sleep periods.

Since these three discoveries, EEG, EOG (electrooculogram), and EMG have been monitored in most sleep experiments.

b. Three Stages of Sleep EEG (see Figures 14.2 and 14.3 in Biopsychology) LO 14.2 Describe the three stages of the sleep EEG, and explain the difference between REM and non-REM sleep.

• •

• • • • •

Just before a subject falls asleep, the EEG is typically punctuated by bursts of alpha waves (large-amplitude, regular, 8-to-12-Hz waves indicative of relaxed wakefulness).

When the subject falls asleep, the EEG progresses in sequence through initial stage 1, stage 2, stage 3, and stage 4.

– Initial stage 1 sleep EEG is low-voltage, fast activity similar to, but slightly slower than, that of wakefulness.

– Stage 2 sleep EEG is of higher voltage and slower than stage 1; its most obvious characteristics are K complexes (a single large negative wave followed by a single large positive wave) and sleep spindles (1-to-2-second waxing-and-waning bursts of 12-to-15-Hz waves).

– Stage 3 sleep EEG is defined by the predominance of delta waves, the largest and slowest EEG waves (1 to 2 Hz).

Once the sleeping subject has gone through initial stage 1 to stage 3, he or she goes back through the stages to stage 1 EEG. When the subject returns to stage 1 EEG, it is referred to as emergent stage 1 EEG because it emerges from the other stages. The rest of the night is spent going between emergent stage 1 through to stage 3 sleep, and then back again.

It is important to distinguish between initial stage 1 EEG and emergent stage 1 EEG because only emergent stage 1 EEG is associated with REMs and low levels of muscle tonus in core muscles.

The stage during which emergent stage 1 occurs is often called REM sleep or paradoxical sleep (it was initially considered a paradox that subjects slept, while their EEGs suggested that they were awake).

The progression of EEG stages changes during a typical night’s sleep: Each cycle is about 90 minutes long; as the night progresses, less time is spent in stage 2 and 3 more is spent in REM sleep, and there are brief periods of wakefulness, which are normally forgotten in the morning.

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Chapter 14: Sleep, Dreaming, and Circadian Rhythms

c. Dreaming LO 14.3 Describe the relationship between REM sleep and dreaming. Also, describe five common beliefs about dreaming and assess their validity. Finally, describe the activationsynthesis theory of dreams.

REM Sleep and Dreaming • The discovery of REM in 1953 by Kleitman and his colleagues led to the obvious hypothesis that REM-sleep periods were periods of dreaming. This hypothesis was confirmed by waking subjects up during various stages of sleep and asking them if they had been dreaming; about 80 percent of awakenings from REM sleep led to dream reports, and only 7 percent of awakenings from non-REM-sleep stages led to dream reports.

• In the years since this discovery, it has become apparent that dreaming during non-REM is more common than previously believed.

• Antidepressant drugs can reduce REM sleep without affecting dream recall and cortical lesions can abolish dreaming without affecting REM sleep.

Testing Common Beliefs about Dreaming • Are external stimuli incorporated into dream sequences? (Yes. Dripping water onto subjects occurred in 14 out of 33 dream cases.)

• Do dreams run on “real time”? (Yes. Subjects awakened five or fifteen minutes after the beginning of a dream could guess the correct interval on the basis of the contents of their dreams.)

• Does everybody dream? (Yes. Even people who claimed that they did not dream had normal amounts of REM, and they reported dreams if they were awakened during REM— although less frequently.)

• Are penile erections indicative of dreams with sexual content? (No. Penile and clitoral tumescence occur during all dreams, regardless of sexual content.)

• Are somnambulism and sleep talking the acting out of dreams? (No. Sleep talking can occur during any stage, and sleep walking usually occurs during slow-wave sleep.)

Interpretation of Dreams • The Freudian theory of dreams holds that dreams represent unacceptable (often sexual) wishes, and was based on the science and beliefs of the 1890s. It has no support today.

• Hobson has proposed an activation-synthesis theory of dreaming, based upon the idea that the information passed on to the cortex during REM is random, and dreams are the cortex’s effort to make sense of these random signals.

2. Why Do We Sleep, and Why Do We Sleep When We Do? a. Two Kinds of Theories of Sleep LO 14.4 Describe the two kinds of theories of sleep.

• • • •

Two types of theories have developed to account for why we sleep: recuperation theories and adaptive theories.

The essence of various recuperation theories of sleep is that being awake disrupts homeostasis in some way and that sleep is required to restore it.

This is the way that most people think about sleep.

According to the adaptive theory of sleep, sleep is not a response to an internal imbalance; sleep is an adaptive response that evolved to conserve energy and to protect organisms 8 ..

Biopsychology, Tenth Edition

•

b.

from mishap and predation. The urge to sleep evolved to be greatest during the night for animals that do not see well in dim illumination.

The circadian theory of sleep considers sleep to be like sexual behavior; it is adaptive and there is a strong drive to engage in it, but its purpose is not to correct an inner deficiency.

Comparative Analyses of Sleep (see Figure 14.4 and Table 14.2 in Biopsychology) LO 14.5 Explain four conclusions that have resulted from the comparative analysis of sleep.

• • • • •

All mammals and birds sleep in a fashion similar to humans; fish, reptiles, amphibians, and insects also go through periods of inactivity similar to sleep.

The fact that most mammals and birds sleep suggests that the primary function of sleep is not some special, higher-order human function.

The fact that all animals sleep suggests that sleep in not uniquely human, but has evolved for some sort of important physiologic reason.

Differences in sleep duration suggest that it is not needed in large amounts; many animals sleep only two to three hours per night.

Sleep duration seems to be correlated with how vulnerable a species is when it sleeps; predators tend to sleep longer, whereas prey species sleep for shorter periods of time.

3. Effects of Sleep Deprivation (see Figures 14.5 and 14.6 in Biopsychology) a. Interpretation of the Effects of Sleep Deprivation: The Stress Problem LO 14.6 Explain how stress can often be a confounding variable when considering the effects of sleep deprivation.

• • •

One way to identify the function of sleep is to determine what happens when a person is deprived of sleep.

You need to be cautious about interpreting sleep deprivation studies, since when most people are deprived they do so because they are under stress.

Therefore, it is difficult to separate the effects of sleep loss from the effects of the stressful conditions.

b. Predictions of Recuperation Theories about Sleep Deprivation LO 14.7 List the three predication that recuperation theories make about the effects of sleep deprivation.

•

The recuperation theory predicts: 1) that long periods of wakefulness will result in debilitating physiological deficits; 2) that these deficits will grow steadily worse as the sleep deprivation continues; and 3) that after the sleep deprivation has ended, much of the lost sleep will be regained.

c. Two Classic Sleep-Deprivation Case Studies LO 14.8 Describe two classic sleep-deprivation case studies.

• •

A group of sleep-deprived students exhibited the following features: during the first night, subjects felt very tired and usually felt an attack of sleep drowsiness between 3 and 6 A.M. Those subjects that continued in the study continued to exhibit a wavelike increase and decrease in sleep around the same time every night.

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Chapter 14: Sleep, Dreaming, and Circadian Rhythms • •

In a separate case, Randy Gardner wanted to break the world record of 260 hours of conscious wakefulness.

He managed to stay awake for 11 days. When he finally went to sleep, the first night he slept 14 hours; thereafter, he returned to his normal pattern of 8 hours.

d. Experimental Studies of Sleep Deprivation in Humans LO 14.9 Describe the major effects of sleep deprivation in humans.

• • • • • •

There are many studies in which subjects have been totally deprived of sleep for several days; these studies have not confirmed the predictions of the recuperation theory.

No marked physiological disturbances other than increased sleepiness have been discovered in sleep-deprived subjects.

Sleep-deprived subjects often display mood disturbances and problems maintaining vigilance.

After two to three days of sleep deprivation, subjects experience microsleeps (two-orthree-second periods during which subjects remain sitting or standing, but their eyelids droop and they are unresponsive to external stimuli).

Sleep-deprived subjects appear to perform poorer on cognitive abilities that require the executive function (of the prefrontal cortex).

Adverse effects on physical performance have surprisingly been inconsistent.

e. Sleep-Deprivation Studies with Laboratory Animals LO 14.10 Describe the key studies of sleep deprivation in laboratory animals. Provide a critique of the carousel apparatus as a method of sleep deprivation.

Sleep deprivation in lab animals has suggested that sleep plays a critical role in the well-being of an organism, as several days of total sleep deprivation has led to subject mortality. However, these data should be interpreted with caution as the sleep-deprivation paradigms used in these studies appeared to severely stress the animals involved. f.

REM-Sleep Deprivation LO 14.11 Describe the effects of REM-sleep deprivation.

• •

•

•

Because REM sleep is associated with dreaming, there has been much interest in the effects of the selective deprivation of REM sleep.

There are two major effects of REM sleep deprivation: − REM deprivation is enforced by waking subjects up each time that REMs begin to occur; as a period of REM deprivation progresses, subjects must be awakened more and more frequently to prevent them from having periods of REM sleep. − After REM deprivation is curtailed, REM rebound is often seen; subjects get more than their normal amount of REM sleep for the next two or three nights.

One of the main challenges for anyone suggesting that REM sleep is critical to normal functioning must explain why tricyclic antidepressants, which block REM sleep at common therapeutic doses, have produced none of the adverse psychological side effects attributable to REM deprivation in patients who have taken them regularly for years.

One current theory posits that REM exists simply because it is difficult to maintain a nonREM state; when an organism has bodily needs like hunger or thirst, it wakes up. But when these needs do not exist, the organism maintains a wake-like REM state rather than struggle to maintain a non-REM state.

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Biopsychology, Tenth Edition g. Sleep Deprivation Increases the Efficiency of Sleep LO 14.12 Describe six pieces of evidence that indicate that less sleep is associated with more efficient sleep.

• •

A key feature of much of the work on sleep deprivation is that it increases the efficiency of sleep; for example, deprived subjects display more slow-wave sleep stages.

This stage seems to play a restorative function.

3. Circadian Sleep Cycles (see Figures 14.7-14.9 Biopsychology) a. Circadian Rhythms LO 14.13 Describe the circadian sleep-wake cycle and the role of zeitgebers in maintaining circadian rhythms.

• •

Almost every physiological function in surface-dwelling animals displays some kind of circadian rhythmicity; the sleep-wake cycle is the most obvious.

The light-dark cycle is an important factor in the timing of most circadian rhythms; environmental cues (such as the light-dark cycle) that entrain circadian rhythms are called zeitgebers.

b. Free-Running Circadian Sleep-Wake Cycles LO 14.14 Describe free-running rhythms and internal desynchronization, and explain why they are incompatible with recuperation theories of sleep.

• • • • • •

Circadian rhythms in constant environments are said to be free-running rhythms. The duration of a free-running cycle is its free-running period.

Even animals raised from birth in unchanging laboratory environments display highly regular free-running cycles; circadian cycles thus do not appear to be learned.

Sometimes sleep-wake cycles and body temperature cycles can break away from one another so that they are out of phase; this is called internal desynchronization, and suggests that there is more than one circadian timing mechanism in the brain.

The fact that such regularity is precisely maintained despite large day-to-day variations in physical and mental activity is strong support for circadian theories of sleep.

Several studies have found a negative correlation between the length of a period of wakefulness and the length of the following period of sleep, even under free-running conditions; this is the opposite of what the recuperation theory would predict.

It seems that we are programmed to go to sleep every 24 hours or so; if we stay awake longer than usual during a particular 24-hour cycle, there is less time left for sleep in that cycle.

c. Jet Lag and Shift Work LO 14.15 Describe the disruptive effects of jet lag and shift work on circadian rhythmicity and how one can minimize such effects.

•

Alternating shift work and jet lag are situations where zeitgebers are phase advanced (moving to an earlier shift or flying east) or phase delayed (moving to a later shift or flying west); people must adjust their natural sleep-wake cycles or endure problems, such as sleep disturbances, fatigue, and performance decrements. Phase advances are more difficult adjustments than are phase delays.

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What can be done to reduce the disruptive effects of jet lag and shift work? Two behavioral approaches seem to work. − One is to gradually shift one’s sleep-wake cycle in the days prior to the flight. − The other is to expose oneself to bright light in the early morning, resetting the biological clock.

d. A Circadian Clock in the Suprachiasmatic Nuclei LO 14.16 Describe the research that led to the discovery of a circadian clock in the suprachiasmatic nucleus (SCN) of the hypothalamus.

• • • • •

The fact that circadian sleep-wake cycles persist in the absence of environmental cues indicates the physiological need for an internal timing mechanism—the circadian clock.

This clock is located in the suprachiasmatic nuclei (SCN) of the medial hypothalamus.

Richter (1967) discovered that lesions to the SCN disrupts various circadian cycles.

Ralph and others (1990) removed the SCN from the fetuses of a strain of mutant hamster (free-running 20 hour periods) and transplanted them into normal hamsters. Recipient hamsters’ circadian rhythms were restored but were only 20 hours long.

Research in the 1980s and 1990s showed the existence of other circadian timing mechanisms. Bilateral SCN lesions have been shown to leave some circadian rhythms unaffected while abolishing others. Bilateral SCN lesions do not abolish the ability of environmental stimuli to entrain circadian rhythms. Further, cells from other parts of the body display free-running cycles when maintained in culture.

e. Neural Mechanisms of Entrainment LO 14.17 Explain the mechanisms by which SCN neurons are entrained by the 24-hour light-dark cycles.

•

f.

24-hour light-dark cycle entrains various circadian cycles via direct axonal connections between the retina and the SCN (these are the retinohypothalamic tracts). Amazingly, rods and cones do NOT appear to be necessary for this entrainment to occur; instead, a special type of retinal ganglion cell is responsible for this entrainment. Their photopigment is melanopsin.

Genetics of Circadian Rhythms LO 14.18 Understand the genetics of circadian rhythms and the important discoveries that have resulted from the discovery of circadian genes.

•

• •

Several circadian genes that have been identified to date, including tau and clock; these have been found in various types of tissue, and they appear to be conserved in a wide variety of organisms (ranging from bacteria to humans), suggesting that they appeared early in evolutionary history.

Once the circadian genes were discovered, the fundamental molecular mechanism of circadian rhythms was quickly clarified.

Surprisingly, these genes are found in most cells of the body.

4. Four Areas of the Brain Involved in Sleep (see Figures 14.10–14.12 in Biopsychology) a. Two Areas of the Hypothalamus Involved in Sleep LO 14.19 Describe the research that led to the identification of the anterior and posterior hypothalamus on brain regions involved in the regulation of sleep and wakefulness.

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Biopsychology, Tenth Edition

Von Economo discovered the first two brain regions known to be involved in sleep; he found that patients who died during a flu epidemic in which many victims slept almost continuously had suffered damage to the posterior hypothalamus. By contrast, patients who had been unable to sleep all had damage to the anterior portion of the hypothalamus. b. Reticular Formation and Sleep LO 14.20 Describe the research that led to the identification of the reticular formation as a brain region involved in the regulation of sleep and wakefulness.

•

•

• •

Bremer proposed the first major theory of sleep physiology—a passive theory of sleep in which sleep occurs because of a reduction of sensory input to the forebrain. In support of this idea, he found that cutting the brainstem between the superior and inferior colliculi (a cerveau isolé preparation) produced a state of almost continuous slow-wave sleep.

This idea was replaced by an active theory of sleep based around the idea of a reticular activating system. Three findings contributed to this new theory: − Cutting the brainstem at the caudal end (an encephalé isolé preparation) did not affect sleep, although such surgery damaged most of the same sensory pathways as the cerveau isolé preparation. − The cerveau isolé preparation only impaired sleep when it transected the reticular activating system core of the brainstem. − Electrical stimulation of the reticular activating system in sleeping cats awakened them.

The research generated by this hypothesis led to the discovery that sleep is NOT a passive process; the brain is still very active, and in some areas, neurons are more active during sleep than they are during waking hours.

Moruzzi and Magoun proposed that low levels of activity in the reticular formation produce sleep and high levels produce wakefulness.

c. Reticular REM-Sleep Nuclei LO 14.21 Discuss how REM sleep is controlled by the reticular formation and what implications this has for understanding the neural mechanisms of behavior.

• • •

Several brain regions have been implicated in regulation of sleep. These sites include a site for the reduction of core-muscle tone, a site for EEG desynchronization, a site for rapid eye movements, etc.

The brain is organized along different principles, and REM sleep occurs only when a network of independent structures becomes active together.

REM sleep, slow-wave sleep, and wakefulness all result from the interaction of several mechanisms that are capable under certain conditions independently of one another.

5. Drugs That Affect Sleep (see Figure 14.13 in Biopsychology) a. Hypnotic Drugs LO 14.22 Describe three classes of hypnotic drugs. Compare and contrast them in terms of their efficacy and side effects.

• Hypnotic drugs are drugs that increase sleep; the most common hypnotic drugs are the benzodiazepines (e.g., Valium). They increase drowsiness, decrease the time it takes to fall asleep, reduce the number of awakenings, and increase total sleep time.

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Chapter 14: Sleep, Dreaming, and Circadian Rhythms •

• •

They should not be prescribed for long-term sleep problems, as they all suffer from the development of tolerance to their hypnotic effects, they produce insomnia as part of their withdrawal syndrome, they are addictive, and they distort the normal sleep pattern.

They can lead to next-day drowsiness and increase the incidence of traffic accidents. Most troubling is that chronic use of benzodiazepines substantially reduces life expectancy.

Imidazopyridines (Zolpidem), a GABAA agonist has been shown to be no safer or more effective than benzodiazepines.

Serotonergic agonists like 5-hydroxytryptophan (the precursor for serotonin) have proven ineffective in the treatment of insomnia.

b. Antihypnotic Drugs LO 14.23 Describe three classes of antihypnotic drugs.

• • •

These drugs decrease sleep; the most common antihypnotic drugs are the cocaine-derived stimulants, amphetamine-derived stimulants, and tricyclic antidepressants.

These types of drugs increase the activity of neurons releasing catecholamine (dopamine; norepinephrine) neurotransmitters.

These drugs have many unwanted side effects: they are addictive, they suppress appetite, they increase anxiety and tremors, and they may interfere with normal sleep patterns.

c. Melatonin LO 14.24 Recognize the relationship between the pineal gland and melatonin, and how melatonin affects sleep.

• • • •

Melatonin is a hormone synthesized from serotonin in the pineal gland.

This gland has inherent timing properties and is important in some species in the regulation of circadian cycles and seasonal changes in reproductive behavior.

The role of the pineal gland in humans is not clear; though it produces circadian rhythms in melatonin release and is believed to play a role in promoting sleep, pinealectomy has little effect on a person’s behavior.

Melatonin has a slight, but statistically significant sleep-promoting effect. It has also been shown to shift timing of mammalian circadian cycles leaving many to call it a chronobiotic.

6. Sleep Disorders a. Insomnia LO 14.25 Describe four causes of insomnia.

•

•

• •

There are two categories of sleep disorders: insomnia and hypersomnia. Insomnia includes all disorders of initiating and maintaining sleep; whereas hypersomnia includes disorders of excessive sleep. A third major class of disorders is specifically related to REM sleep.

Insomnia is often iatrogenic (physician-created), due to the prescription of hypnotic drugs like benzodiazepines (valium). At first these drugs are effective; however, some patients develop a tolerance and experience withdrawal when they are stopped (see the case of Mr. B.).

Insomniacs take on average one hour to fall asleep and sleep only 4.5 hours per night.

However, in sleep laboratories, the sleep latency is only 15 minutes, and on average they sleep 6.5 hours.

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Biopsychology, Tenth Edition • • • • •

• •

• •

Insomnia, therefore, appears to be a problem of too little undisturbed sleep.

Sleep restriction is an effective treatment; a person’s sleep is greatly restricted, and then slowly increased in duration.

Some cases of insomnia have a specific medical cause such as sleep apnea. Here the patient stops breathing while they are sleeping many times throughout the night.

Frequently the patient is unaware of the multiple awakenings and instead complains of excessive sleep, getting a diagnosis of hypersomnia.

There are two types of apnea: 1) obstructive and 2) central sleep apnea. − Obstructive apnea results from the obstruction of the respiratory passages by muscle spasms or atonia (lack of muscle tone). − Central sleep apnea results from failure of the CNS to stimulate respiration.

Apnea is more common in males, in people who are overweight, and the elderly.

Two other causes of insomnia are related to the legs: periodic limb movement syndrome and restless leg syndrome. − Periodic limb movement syndrome is characterized by movements of the limbs, often twitches during sleep. The patient complains of poor sleep and is often unaware of the movements. − In contrast, in restless leg syndrome, the patient is aware of the problem and complains of a tension in their legs that keeps them awake.

More research needs to be done, although dopamine agonists can be effective.

Therefore, the four causes of insomnia are iatrogenic, sleep apnea, restless legs syndrome and periodic limb movement syndrome.

b. Hypersomnia LO 14.26 Describe the symptoms of narcolepsy and the role of orexin (hypocretin) in this disorder.

• • • • • • • • • •

Hypersomnia can be one of numerous problems of excessive or inappropriate sleep; sleep promoting conditions are called soporific.

The most studied disorder of hypersomnia is narcolepsy, where one in 2000 people suffer.

Narcoleptics tend to fall asleep in totally inappropriate situations (while having conversations, eating, or scuba diving). They usually sleep for 10 or 15 minutes and then reawaken.

Narcolepsy results in an abnormality in the mechanism that triggers REM sleep. Patients typically go immediately into REM. Cataplexy is another symptom of narcolepsy; patients lose muscle tone during wakefulness, often falling to the ground as though they were shot.

Narcoleptics also often display sleep paralysis (inability to move when falling asleep) and hypnagogic hallucinations (dreamlike experiences during wakefulness).

Narcoleptics go directly into REM sleep, rather than going through other sleep stages, thus narcolepsy is often categorized with REM-sleep-related disorders.

Occasionally patients will suffer from brain damage that prevents REM sleep; these patients appear to suffer few negative consequences.

Some patients experience REM sleep without core muscle atonia. These people are able to act out their dreams; it is believed this is due to damage to the nucleus magnocellularis.

Research in narcoleptic dogs has also revealed a gene that causes the disorder; the gene codes for a receptor that binds a protein called orexin (sometimes called hyocretin) that is reduced in the brains of narcoleptics.

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Chapter 14: Sleep, Dreaming, and Circadian Rhythms • •

Orexin is synthesized in the posterior hypothalamus—the same region implicated in the promotion of wakefulness. Neurons there have diffuse projections, most notably to the brainstem reticular activating system.

Typically, narcoleptics are prescribed stimulants (amphetamines), which have side effects.

There exists a new drug, modafinil, which is shown to be effective. Sometimes they are given antidepressants for the cataplexy.

c. REM Sleep-Related Disorders LO 14.27 Describe one REM-sleep-related disorder and its presumed neural mechanisms.

Several sleep disorders are specific to REM, even narcolepsy can be classified as an REM disorder. Occasionally, patients are discovered who have very little or no REM. One such patient experienced no ill effects. Some patients experience REM without atonia (REM-sleep behavior disorder) and “act out” their dreams. This is due to damage to the nucleus magnocelluaris (a structure in the reticular formation) or to an interruption of its output.

7. Effects of Long-Term Sleep Reduction (see Figures 14.14 and 14.15 in Biopsychology) Because they are so time-consuming, few studies of long-term sleep patterns have been conducted. a. Differences between Short and Long Sleepers LO 14.28 List the main differences between short and long sleepers.

• •

Numerous studies have compared short sleepers (6 hours or less) to long sleepers (8 hours or more).

Reports from a large (239 people) study found that no physical or emotional differences existed between the groups.

b. Long-Term Reduction of Nightly Sleep LO 14.29 Describe the results of studies of long-term reduction of nightly sleep.

• • • •

Two studies have been conducted.

Eight volunteers reduced their nightly sleep by 30 minutes every two weeks until they reached 6.5 hours per night, then gradually to five hours, and then by 30 minutes thereafter.

The minimum duration of nightly sleep averaged five hours after a year.

In each participant, a reduction in sleep time was associated with an increase in sleep efficiency: a decrease in the amount of time it took to fall asleep after going to bed, a decrease in the number of nighttime awakenings, and an increase in the proportion of slowwave sleep.

c. Long-Term Sleep Reduction by Napping LO 14.30 Describe the results of studies of long-term reduction of sleep by napping.

• Most mammals and human infants display polyphasic sleep cycles; that is, they regularly sleep more than once a day.

• In contrast, adults display monophasic sleep cycles; that is, they sleep once a day. Which sleep pattern is most efficient?

• Studies have shown the following: 1) subjects required a long time to adapt to polyphasic sleep; 2) once adapted, participants were content and displayed no deficits on performance tests; 3) four-hour sleep schedule worked well in some unstructured cases; 4) most people display a strong preference for particular durations and refrain from sleeping too little or

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Biopsychology, Tenth Edition too much; and 5) most of the sleep is in slow-wave sleep initially, but eventually returns to a mix of REM and slow-wave. d. Effects of Shorter Sleep Times on Health LO 14.31 Recognize how shorter sleep times relate to longevity.

• • •

Two studies have maintained subjects on programs of sleep reduction.

In general, there appear to be few negative consequences to sleep reduction.

Sleep eight hours is not the healthy ideal. Five to seven hours seems to be optimum for longevity.

e. Long-Term Sleep Reduction: A Personal Case Study The case of the author, who reduced his sleep to 5.5 hours per night with no ill effects. < Return to Table of Contents

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Chapter 14: Sleep, Dreaming, and Circadian Rhythms

LECTURE LAUNCHERS Lecture Launcher 14.1: Sleep in the News One way to stimulate some potentially heated class discussion is to open your lecture with the presentation of any one of many news articles that report that we are all suffering from sleep deprivation or a lack of sleep (e.g., just type “sleep” into Google News: http://news.google.com/). Then, tell the class what is wrong with that news report or the research it is based upon. Don’t give them too many details about what exactly is wrong; just end by saying something to the effect that: “In the following lecture(s) we will examine what is wrong with this news report.”

Lecture Launcher 14.2: Sleep Across Species To convey to your class the tremendous variation in sleep/wake cycles across the animal kingdom, spend a few minutes with this cross-species sleep chart, provided by Dr. Eric Chudler and his Neuroscience for Kids site at http://faculty.washington.edu/ and place “Chudler Animal Sleep” in the search bar. Select the link for “Neuroscience for Kids – Animal Sleep.” Don’t neglect the interesting tidbit about the dolphin’s peculiar sleep habits found at the bottom of the page.

Lecture Launcher 14.3: Your Sleep Habits If your class is small enough, ask each student to keep a sleep log for seven days and then return the completed log to you. Before one of your sleep lectures, analyze the sleep logs for things like average sleep time, average sleep time for each day of the week, sleep problems, caffeine intake, etc., and then present the results to illustrate some of the points that Pinel makes in this chapter. You can access a simple, easy-to-complete sleep log at http://sleepfoundation.org and place “sleep diary” in the search bar. Scroll down the page to the link entitled “NSF Official Sleep Diary.”

Lecture Launcher 14.4: Amazing Feats of Sleep Most students are surprised at how mild the effects are of long-term sleep deprivation/reduction. You can provide some dramatic case studies of self-induced sleep deprivation: (1) Randy Gardner, the longtime holder of the world record for the longest period of having no sleep (e.g., see http://www.gelfmagazine.com/ and place “sleeping in” in the search bar, select the 2nd article), and (2) Tony Wright, who beat Randy’s record in 2007 (e.g., see http://news.bbc.co.uk/ and place “man claims sleepless record” in the search bar. Select the matching link.). The latter case is quite interesting to discuss, since Tony Wright kept an ongoing blog of his period of sleep deprivation. Place “Cornwall Sleep Deprivation Diary” in your favorite browser. Select the BBC website with the matching name.

Lecture Launcher 14.5: Applications of Sleep Research Psychology has provided many suggestions to improve sleep quality in people who are not able to sleep eight hours every night. Students are often encouraged to find that changing when or where one sleeps may influence how rested one feels. This is also a great example of how psychology can be used in a career.

Web Link 14.2 Sleep Psychology in Practice: Sleep Psychologist Paul Saskin Helps Las Vegans Sleep More Soundly, Day and Night Lecture Launcher 14.6: Napping “Evidence is mounting that sleep—even a nap—appears to enhance information processing and learning. New experiments by NIMH grantee Alan Hobson, M.D., Robert Stickgold, Ph.D., and colleagues at Harvard University show that a midday snooze reverses information overload and that a 20 percent overnight improvement in learning a motor skill is largely traceable to a late stage of sleep 18 ..

Biopsychology, Tenth Edition that some early risers might be missing. Overall, their studies suggest that the brain uses a night’s sleep to consolidate the memories of habits, actions, and skills learned during the day.”

Web Link 14.3 “Power Nap” Prevents Burnout; Morning Sleep Perfects a Skill Lecture Launcher 14.7: Sleep Deprivation in Children You may have students who have children and who are interested in education. Other students may have recent experience caring for a child. You may wish to have your students take both sides in a debate over whether or not sleep deprivation is really that important in children or adults.

Web Links 14.13 Sleep Problems in Children and Teens 14.14 Adolescent Sleep Lecture Launcher 14.8: Sleep Disorders Sleep disorders are a good topic to get students interested in the topic of sleep. Many will have personal experience and can vouch for the difficulties of living with these problems.

Web Links 14.15 SleepNet 14.16 The Open Directory Project: Sleep Disorders 14.17 Medline Plus—Sleep Disorders Lecture Launcher 14.9: Cause of Narcolepsy Scientists Pinpoint Possible Cause for Debilitating Sleep Disorder Narcolepsy: Tuesday, August 29, 2000 “Scientists believe they may have identified the cause of the debilitating sleep disorder narcolepsy in humans. A new study shows a dramatic reduction—up to 95 percent—in the number of neurons containing a substance called hypocretin in the brains of people with narcolepsy compared to control brains. Hypocretin peptides are neurotransmitters that play an important role in regulating sleep and appetite. The researchers hypothesize that the pronounced loss of these neurons could be caused either by a neurodegenerative process or an autoimmune response.”

Web Link 14.18 Scientists Pinpoint Possible Cause for Debilitating Sleep Disorder Narcolepsy Lecture Launcher 14.10: Nightshift Since pre-Roman times, work has been done during the night as well as during daylight hours. While workers have always complained about being tired when working at night, it has not been until relatively recently that the degree of impairment has been researched and documented. Diminished performance is only one of the problems caused by being out of phase with one’s environment. Worker and public safety also can be compromised. Although other factors may have been involved, fatigue should not be ruled out as a contributor to the following much publicized disasters: Chernobyl Bhopal Three-Mile Island

1:23 A.M. 12:40 A.M. 4:00 A.M.

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Chapter 14: Sleep, Dreaming, and Circadian Rhythms Fatigue may also be involved in other types of accidents. The National Transportation and Safety Board carefully studies accident reports and statistics and attempts to determine common factors in accidents.

This information is then used to inform the enactment of new laws and to educate the public on risks associated with transportation.

For example, here is a summary of a report: Title: Evaluation of U.S. Department of Transportation Efforts in the 1990s to Address Operator Fatigue NTSB Report Number: SR-99-01, adopted on 5/11/1999: You can access the full article by placing “Evaluation of U.S. Department of Transportation Efforts in the 1990s to Address Operator Fatigue” in the search bar of your favorite browser. Select the PDF file that comes up matching the name of your search.

Synopsis: During the 1980s, the National Transportation Safety Board investigated several aviation, highway, and marine accidents that involved operator fatigue. Following completion of these accident investigations, the Safety Board in 1989 issued three recommendations to the U.S. Department of Transportation (DOT) addressing needed research, education, and revisions to hours-of-service regulations.

Ten years have passed since these safety recommendations were issued. In the interim, the Safety Board has issued more than 70 additional recommendations to the DOT, states, industry, and industry associations to reduce the incidence of fatigue-related accidents. In response to the three 1989 recommendations, the DOT and the modal administrations have, in general, acted and responded positively to the recommendations addressing research and education; little action, however, has occurred with respect to revising the hours-of-service regulations. Nevertheless, the Safety Board believes that support has grown in recent years to make substantive changes to these regulations.

This report provides an update on the activities and efforts by the DOT and the modal administrations to address operator fatigue and, consequently, the progress that has been made in the past 10 years to implement the actions called for in the three intermodal recommendations and other fatigue-related recommendations. The report also provides some background information on current hours-of-service regulations, fatigue, and the effects of fatigue on transportation safety.

As a result of this safety report, the National Transportation Safety Board issued new safety recommendations to the U.S. Department of Transportation, the Federal Aviation Administration, the Federal Highway Administration, the Federal Railroad Administration, the Research and Special Programs Administration, and the United States Coast Guard. The Safety Board also reiterated two recommendations to the Federal Aviation Administration.

Transportation Accidents 1982 and 1992

Avg. # of Passenger Deaths/Year

Average Rate/Year (Deaths per 100 Million Passenger Miles)

Airplanes

119.1

.033

Trains

6.5

.055

Buses

36.3

.030

Cars

23,585

1.040 20

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Biopsychology, Tenth Edition

Researchers have found that “the neural processes controlling alertness and sleep produce an increased sleep tendency and diminished capacity to function during certain early morning hours (circa 2–7 A.M.) and, to a lesser degree, during a period in the mid-afternoon (circa 2–5 P.M.), whether or not we have slept. Several studies of single-vehicle car accidents that have been judged to be fatigue-related have shown two peak times for accidents—a major one between midnight and 7 A.M., and a secondary peak between 1 and 4 P.M.” What kinds of changes could be made to improve worker performance and/or prevent accidents due to circadian limitations?

The NTSB has made several recommendations to improve truck safety. (See: National Transportation Safety Board. Fatigue, Alcohol, Other Drugs, and Medical Factors in Fatal-to-the-Driver Heavy Truck Crashes. Vol. I. PB90–917002. NTSB/SS–90/01. Washington, D.C.: National Transportation Safety Board, 1990, 181 pp.) These include education on the effects of fatigue, on-board recording devices that keep track of driver hours, a review of trucking operations that might create incentives for drivers to violate hours of service regulations, and revision of certain parts of the Code of Federal Regulations to prohibit employers from scheduling shipments which would require drivers to exceed the hours of service regulations. Certainly, the other transportation industries could adopt similar strategies to reduce the likelihood of catastrophic accidents caused by fatigue and circadian desynchrony.

Web Link 14.19 Evaluation of U.S. Department of Transportation Efforts in the 1990s to Address Operator Fatigue Lecture Launcher 14.11: Medical Treatment and Circadian Rhythms Circadian physiologic processes do more than change body temperature and cause jet lag. There is evidence that drug absorption, distribution, metabolism, and excretion differ based on circadian rhythms. As a result, researchers suggest that drug doses need to be adjusted to meet the differing needs of target organs or tissue at various times of day.

Taking prescription medication at regular intervals throughout the day may not only be ineffective, but counterproductive, or even harmful. Some medical illnesses whose symptoms show a circadian rhythm respond better when drugs take that rhythm into account. Medications for asthma, epilepsy, cancer, cardiovascular disease, and allergies all have shown better results with minimum side effects when given at particular times.

For example, Dr. Hrushesky at Albany Medical College gave patients with advanced ovarian cancer two different drugs at 6 A.M. and 6 P.M. The second group received the same drugs at the same time but in reverse order. After five years, 50 percent of one group was still alive, but only 10 percent of the second group had survived. Chemotherapy drugs are toxic to both the cancer cells and the host cells, but there may be a time when the body is more resistant or tolerant to the drugs and the cancer cells more sensitive.

Another study timed breast cancer surgery with respect to the patient’s menstrual cycle. The study found that women whose surgery was performed mid-cycle or near ovulation, when estrogen is highest, had fewer and later recurrences when evaluated five to twelve years after surgery than women who had surgery during menstruation.

Lamberg, L. (1991). Chronotherapeutics: Implications for Drug Therapy. American Pharmacy. N831 (11): 20–23.

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Chapter 14: Sleep, Dreaming, and Circadian Rhythms

Lecture Launcher 14.12: Jet Lag Travel across time zones can result in fatigue, gastrointestinal complaints, and shortened attention span.

This discomfort is greater than can be accounted for by sleep loss and the resulting interrupted circadian rhythms alone. The timing of meals, activities, and sleep are shifted as are environmental cues, especially light.

According to the Office of Technology Assessment (OTA), “...conflict between the traveler’s own circadian clock and external rhythms in a new time zone is the primary agent of jet lag. Furthermore, promote synchronization between circadian rhythms and the new time zone. Since different circadian rhythms may adjust to the new time zone at different rates, the traveler experiences a period when internally generated rhythms are no longer in synchrony with each other.” (U.S. Congress, Office of Technology Assessment. Biological Rhythms: Implications for the Worker. OTA-BA-463.

Washington, D.C.: U.S. Government Printing Office, September 1991, 249 pp.)

The temperature cycle is in one time zone, and the sleep-wake cycle quickly catches up to the new time zone; but all the other human systems are scattered somewhere else. Furthermore, many factors influence the degree to which a traveler feels jet lag: age, direction of travel (going west is better than going east), number of time zones crossed, and factors specific to the individual. < Return to Table of Contents

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Biopsychology, Tenth Edition

ACTIVITIES Activity 14.1: EEG Data: Learning to Focus on Relevant Characteristics If you know someone who works in a hospital or sleep laboratory, you may be able to get samples of real EEG tracings of sleeping patients. Hand these out to pairs of students. Ask them to sort the segments into stages 1 through 4, awake, or REM sleep. The goal of this exercise is to encourage the students to ask themselves how they might describe any differences that they see and/or notice patterns in the tracings.

How difficult is it to determine sleep stage from an EEG? < Return to Table of Contents

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Chapter 14: Sleep, Dreaming, and Circadian Rhythms

ASSIGNMENTS Assignment 14.1: Vocabulary Crossword Puzzle Part of the assignment will require that the students know the terminology used in describing the nervous system. I have created a crossword puzzle for this assignment. Crosswords provide cues in the length of the words and in letters determined from easier clues.

This can be used as an assignment, a test, or an in-class activity done in small groups of two to five students.

ACROSS 2. EMG – An abbreviation for the electrical potential recorded from and electrode placed on a muscle 6. PINEAL – A gland attached to the dorsal tectum; produces melatonin and plays a role in seasonal and circadian rhythms 8. NON-REM – All stages of sleep except REM sleep 9. CIRCADIAN – A daily rhythmical change in behavior or physiological processes 10. NARCOLEPSY – A sleep disorder characterized by periods of irresistible sleep, attacks of cataplexy, sleep paralysis, and hypnagogic hallucinations 12. ZEITGEBER – A stimulus that resets the biological clock DOWN 1. LOCUS COERULEUS – A dark-colored group of noradrenergic cell bodies located in the pons and involved in arousal and vigilance 3. MELATONIN – A hormone secreted during the night by the pineal body; plays a role in circadian and seasonal rhythms 4. CATAPLEXY – A symptom of narcolepsy; or complete paralysis that occurs during waking 5. SLEEP-PARALYSIS – A symptom of narcolepsy; or paralysis occurring just before a person falls asleep 7. SLOW-WAVE – Non-REM sleep; characterized by synchronized EEG activity during its deeper stages 11. REM – A period of desynchronized EEG activity during sleep, at which time dreaming, rapid eye movements, and muscular paralysis appear Handout 14.2 Vocabulary Crossword Puzzle Assignment 14.2: Theories of Sleep: Energy Conservation Theory This handout includes a table with average sleep durations for human beings at different ages and for a variety of animals. Students are asked to make comparisons that will provide support for an energy conservation theory of sleep.

Handout 14.3 Theories of Sleep: Energy Conservation Theory

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Biopsychology, Tenth Edition Assignment 14:3: Body Temperature and Reaction Time Laboratory The Effect of Circadian Rhythms on Body Temperature Students can monitor an internal human circadian rhythm by keeping track of their own body temperatures over the course of two days. The student should try to take a measurement every four hours over a two-day period. The key to the readings is being consistent in the time of day from day to day. Be sure that the student understands that the changes in temperature may only be a few tenths of a degree. A regular fever thermometer will not be adequate for accurate readings. Basal thermometers, sold for measuring temperature changes during the menstrual cycle to estimate ovulation and fertility, are easier to read for these purposes.

After students have submitted their data, you can see if some of the observations can be combined to form a better estimate. Encourage students to discuss confounding factors that might have affected scores or temperature more than circadian rhythms.

Handout 14.4 Body Temperature and Reaction Time Laboratory Assignment 14.4: Jet Lag, Circadian Rhythms, and Athletic Performance Read this article on the effect that changing time zones might have on athletic performance: Jehue, R., et al. (1993). Effect of Time Zone and Game Time Changes on Team Performance: National Football League. Medicine and Science in Sports and Exercise. 25(1), 127–131.

Choose a sports team that travels to play other teams. Use a sports almanac or other source of game records to examine performance in home games compared to away games, and note time zone shifts as well as the direction of the shift.

Assignment 14.5: Application Exercise on Shiftwork and Circadian Issues Manny Workman, Luna Nightshift, and Raydawn Summerson have come to you, the owner of a consulting firm, Shiftwork Express. They are having trouble with their social and family lives, their health, their sleep, and their jobs.

Assign your consultants (students) to these individuals and have them report on the recommendations that they would make. You may also give them a resource sheet that includes Web sites and brief recommendations on improving performance in night and shift workers. < Return to Table of Contents

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Chapter 14: Sleep, Dreaming, and Circadian Rhythms

WEB LINKS Web Link 14.1: Papers on Sleep http://www.sleep.org contains a search bar where you can input anything you want to know about sleep and past articles that have been written about that topic.

This site provides a searchable archive for papers and abstracts relating to sleep.

Web Link 14.2: Sleep Psychology in Practice: Sleep Psychologist Paul Saskin Helps Las Vegans Sleep More Soundly, Day and Night Go to http://www.apa.org/ and place “sleep psychology in practice Paul Saskin” in the search bar. Select the matching link.

Smith, D. (October 2001) Monitor on Psychology. 32(9).

Web Link 14.3: “Power Nap” Prevents Burnout; Morning Sleep Perfects a Skill Go to http://www.medicalnewsservice.com/ and place “power nap” in the search bar. Select the link that is presented on power napping.

Web Link 14.4: Sleep Paralysis Page Place “Sleep paralysis acheyne” in your browser search bar. Select the link to the “Sleep Paralysis Page” from the University of Waterloo.

This site provides students with access to an online questionnaire on sleep paralysis.

Web Link 14.5: Sleepnet.com http://www.sleepnet.com/ Web Link 14.6: Sleep Tight Animated Game http://www.sleeptight.ca/ Comprehensively covers various aspects of sleep. Includes information about sleep problems, dreams, how to sleep well, and sleep studies.

Web Link 14.7: Sleep Medicine Home Page Search “sleep medicine home page” from your favorite browser. Select the Web site offered to you from Cloud 9 Internet.

This comprehensive site on sleep offers links to newsgroups on sleep, sleep journals, sleep disorders, drugs, and transmitters that influence sleep, and sleep research sites.

Web Link 14.8: Articles from Scientific American http://www.scientificamerican.com/ There are many good articles on sleep available. The Web site has abstracts. Files can be downloaded for a fee. The “Ask the Expert” section has several brief articles on useful topics.

Web Link 14.9: American Academy of Sleep Medicine http://www.aasmnet.org/ Includes a Sleep Quiz.

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Biopsychology, Tenth Edition Web Link 14.10: SleepQuest http://www.sleepquest.com/ William C. Dement, M.D., Ph.D., is one of the foremost researchers on sleep. This site tells about his work while also providing information on sleep and sleep disorders.

Web Link 14.11: A New Neurocognitive Theory of Dreams Visit http://ucsc.edu/ and place “Neurocognitive Theory of Dreams” in the search bar. Select the link containing your search string.

G. William Domhoff, University of California, Santa Cruz.

Web Link 14.12: The Quantitative Study of Dreams http://Dreamresearch.net Research using content analysis of dreams.

Web Link 14.13: Sleep Problems Go to http://www.athealth.com/ and place “sleep issues” in the search bar.

Web Link 14.14: Adolescent Sleep Go to http://www.stanford.edu/ and search for “adolescent sleep” and click on the matching link.

A good overview of concerns about sleep deprivation in adolescents.

Web Link 14.15: SleepNet Go to http://www.sleepnet.com/ and click on the link to “sleep disorders.”

This site provides a comprehensive treatment of sleep disorders. A variety of links are provided to give students access to on-line tests of sleep disorders with rapid feedback. The site also provides links to sites dealing with dreaming, sleep deprivation, and sleep research laboratories.

Web Link 14.16: The Open Directory Project: Sleep Disorders Go to http://dmoz.org/ and click on the “Health” link. From there select the link for “Conditions and Diseases” and select “Sleep Disorders” from that page.

Web Link 14.17: Medline Plus—Sleep Disorders Go to https://medlineplus.gov/ and search for “Sleep Disorders” and utilize this wealth of information available to you.

Web Link 14.18: Narcolepsy Go to http://www.ninds.nih.gov/and place “Narcolepsy” in the search box. Click on the information page for Narcolepsy.

Web Link 14.19: Evaluation of U.S. Department of Transportation Efforts in the 1990s to Address Operator Fatigue Using your favorite browser, place “Evaluation of U.S. Department of Transportation Efforts in the 1990s to Address Operator Fatigue” in your search bar. Select the matching pdf file.

NTSB Report Number: SR-99-01, adopted on 5/11/1999.

Web Link 14.20: Nonvisual Responses to Light Exposure in the Human Brain during the Circadian Night Go to https;//www.ncbi.nlm.nih.gov and select “PubMed” from the dropdown menu of options for where to search. Search “Nonvisual responses to light exposure in the human brain during the circadian night” from the search bar.

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Chapter 14: Sleep, Dreaming, and Circadian Rhythms

Web Link 14.21: The Open Directory Project: Shift Work Go to http://dmoz.org/ and click on the “Society” link. From there select the link for “Work” from that page and click on “Shift work” on the final page.

Web Link 14.22: National Traffic and Safety Board http://www.ntsb.gov/ A good source of reports and data on factors affecting safety, including fatigue. NTSB hires many psychologists to investigate accidents.

Web Link 14.23: Biotiming Tutorial Go to http://millar.bio.ed.ac.uk/ and scroll down the page to the link titled “Web Tutorials on Biological Clocks.” Once there, pick any link to find out further information on our biological clock. < Return to Table of Contents

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Biopsychology, Tenth Edition

HANDOUTS Handout 14.1: Concept Maps

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Chapter 14: Sleep, Dreaming, and Circadian Rhythms

Commented [N1]: “Antinflamitories” – should this be “Anti-inflammatories”?

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Biopsychology, Tenth Edition

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Chapter 14: Sleep, Dreaming, and Circadian Rhythms Handout 14.2: Vocabulary Crossword Puzzle Name:________________________________________ Section: ___________ Date: ________

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Biopsychology, Tenth Edition ACROSS 2.

6.

An abbreviation for the electrical potential recorded from an electrode placed on a muscle A gland attached to the dorsal tectum; produces melatonin and plays a role in seasonal and circadian rhythms 8. All stages of sleep except REM sleep 9. A daily rhythmical change in behavior or physiological processes 10. A sleep disorder characterized by periods of irresistible sleep, attacks of cataplexy, sleep paralysis, and hypnagogic hallucinations 12. A stimulus that resets the biological clock DOWN 1.

A dark-colored group of noradrenergic cell bodies located in the pons and involved in arousal and vigilance 3. A hormone secreted during the night by the pineal body; plays a role in circadian and seasonal rhythms 4. A symptom of narcolepsy; or complete paralysis that occurs during waking 5. A symptom of narcolepsy; or paralysis occurring just before a person falls asleep 7. Non-REM sleep; characterized by synchronized EEG activity during its deeper stages 11. A period of desynchronized EEG activity during sleep, at which time, dreaming, rapid eye movements, and muscular paralysis appear Puzzle created with Puzzlemaker at DiscoverySchool.com

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Chapter 14: Sleep, Dreaming, and Circadian Rhythms Handout 14.3: Theories of Sleep Name:________________________________________ Section: ___________ Date: ________ ENERGY CONSERVATION THEORY Fast-moving animals with high metabolic rates sleep more than those that burn calories more slowly, and thereby conserve their energy.

Given the table of animal sleep durations, do you find any support for the Energy Conservation Theory?

A. Most animals have a daily pattern of rest and activity. Some animals are more active during the day (diurnal) and some are more active during the night (nocturnal).

B. Compare animals that are similar in size and activity. Do they seem to need the same amount of sleep?

C. Compare human beings at different ages. How might age play a part in energy needs and sleep?

D. Compare small animals with large animals. Do larger animals need to rest more to conserve energy?

E. Compare animals that are herbivores (plant eaters) with those that are carnivores (meat eaters) or omnivores (anything eaters). Meat is a more concentrated food. Can carnivores sleep more?

Species Brown Bat Giant Armadillo North American Opossum Python Owl Monkey Human (Infant) Tiger Squirrel Western Toad Ferret Three-toed Sloth Golden Hamster Platypus Lion Gerbil Rat Cat Cheetah Mouse Rhesus Monkey Rabbit

Average Total Sleep Time ( Percentage of 24 Hours) 82.9 percent 75.4 percent 75 percent 75 percent 70.8 percent 66.7 percent 65.8 percent 62 percent 60.8 percent 60.4 percent 60 percent 59.6 percent 58.3 percent 56.3 percent 54.4 percent 52.4 percent 50.6 percent 50.6 percent 50.3 percent 49.2 percent 47.5 percent

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Average Total Sleep Time (Hours/Day) 19.9 hr 18.1 hr 18 hr 18 hr 17.0 hr 16 hr 15.8 hr 14.9 hr 14.6 hr 14.5 hr 14.4 hr 14.3 hr 14.0 hr 13.5 hr 13.1 hr 12.6 hr 12.1 hr 12.1 hr 12.1 hr 11.8 hr 11.4 hr

Biopsychology, Tenth Edition

Species Jaguar Duck Dog Bottle-nosed Dolphin Star-nosed Mole Baboon European Hedgehog Squirrel Monkey Chimpanzee Guinea Pig Human (Adult) Pig Guppy (Fish) Gray Seal Human (Elderly) Goat Cow Asiatic Elephant Sheep African Elephant Donkey Horse Giraffe

Average Total Sleep Time ( percent of 24 Hours) 45 percent 45 percent 44.3 percent 43.3 percent 42.9 percent 42.9 percent 42.2 percent 41.3 percent 40.4 percent 39.2 percent 33.3 percent 32.6 percent 29.1 percent 25.8 percent 22.9 percent 22.1 percent 16.4 percent 16.4 percent 16 percent 13.8 percent 13.0 percent 12.0 percent 7.9 percent

Average Total Sleep Time (Hours/Day) 10.8 hr 10.8 hr 10.6 hr 10.4 hr 10.3 hr 10.3 hr 10.1 hr 9.9 hr 9.7 hr 9.4 hr 8 hr 7.8 hr 7 hr 6.2 hr 5.5 hr 5.3 hr 3.9 hr 3.9 hr 3.8 hr 3.3 hr 3.1 hr 2.9 hr 1.9 hr

References: The table was adapted from four sources: Aserinsky, E. (1999). Eyelid condition at birth: relationship to adult mammalian sleep-waking patterns, In Rapid Eye Movement Sleep, edited by B.N. Mallick and S. Inoue, Narosa Publishing, New Delhi, p.

7.

Campbell, S. S. & Tobler, I., (1984). Animal sleep: a review of sleep duration across phylogeny.

Neuroscience and Biobehavioral Rev., 8:269–300.

Kryger, M. H., Roth, T. & Dement, W. C. (1989). Principles and Practice of Sleep Medicine, W. B. Saunders Co., Philadelphia, pp. 39–41.

Tobler, I. (1989). Napping and polyphasic sleep in mammals, In Sleep and Alertness: Chronobiological, Behavioral and Medical Aspects of Napping, edited by D. F. Dinges and R. J. Broughton, Raven Press, New York, pp. 9–31.

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Chapter 14: Sleep, Dreaming, and Circadian Rhythms Handout 14.4: Body Temperature and Reaction Time Laboratory

You will need a basal thermometer and a timed or scored video game, or some other brief task that can be scored.

You will be monitoring an internal human circadian rhythm by keeping track of your own body temperatures over the course of two days. The key to the readings is being consistent in the time of day from day to day.

Please be aware that the changes in temperature may only be a few tenths of a degree. A regular fever thermometer will not be adequate for accurate readings. Basal thermometers, sold for measuring temperature changes during the menstrual cycle to estimate ovulation and fertility, are easier to read for these purposes.

Choose a 48-hour period when you are not planning any unusual activity. (No all-night cramming sessions, trips, etc.)

Begin taking your temperature and playing three rounds of the game when you get up in the morning (such as 8:00 A.M.). Continue taking your temperature and playing the game every 4 hours, even while you are sleeping. (Set your alarm!)

Also, record the times and general level of your activity (eating, sleeping, exercise, sitting quietly, etc.).

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Biopsychology, Tenth Edition Figure 2. Sample plot with two variables, each plotted on a single axis.

Score

Temperature

Circadian Rhythms

8:00 12:00 4:00 AM PM AM

8:00 12:00 4:00 AM PM AM

8:00 12:00 4:00 AM PM AM

8:00 12:00 4:00 AM PM AM

Temperature Score Time

Plot the results of your data, using the mean of the three game scores. Write a brief report summarizing your data and drawing any conclusions you find reasonable based on the data that you have collected.

Answer at least one of the following questions in your report.

Circadian Rhythms

100

1.

How could you determine whether these rhythms are controlled endogenously or exogenously?

700

600 99

Temperature

500

400

Score

98

2.

What confounding variables might be affecting these measurements, and how could they be eliminated experimentally?

300 97

200 96 100

95

8:00 AM

12:00 AM

4:00 PM

8:00 PM

12:00 PM

4:00 AM

8:00 AM

12:00 AM

4:00 PM

8:00 PM

12:00 PM

4:00 AM

Temperature

98

98.7

98.6

98.4

97.9

97.4

98.2

98.8

98.5

98.4

98.2

98

Average Score (3)

523

527

591

540

510

407

488

529

578

502

420

320

3.

How might the changes in reaction time and motor coordination affect people who work at night (e.g., police, medical personnel)?

0

Time

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Chapter 14: Sleep, Dreaming, and Circadian Rhythms Handout 14.5: Jet Lag, Circadian Rhythms, and Athletic Performance

Date of Game

Home or Away

Location

Time Zone Difference in Hours Winner

Score

Relative Point Difference

Read this article on the effect that changing time zones might have on athletic performance.

Jehue, R., Street, D., & Huizenga, R. (1993). Effect of Time Zone and Game Time Changes on Team Performance: National Football League. Medicine and Science in Sports and Exercise. 25(1), 127–131.

Choose a sports team that travels to play other teams. Use a sports almanac or other source of game records to examine performance in home games compared to away games. Note time zone shifts as well as the direction of the shift.

DATA COLLECTION TABLE You might also look at the time of day that the game was played, the weather, or other conditions that might be unusual for the players on one team, and therefore determine whether any imbalance occurred in the effect on performance.

Calculate the average score for Home and Away games.

Calculate the average score for Home and Away games, keeping separate the games one, two, and three time zones away, etc., and record movement to the east or west.

Calculate the above for score differences instead of just win versus loss or total points.

Write a brief paper in APA style summarizing your data and commenting on the implications related to the physiology of circadian rhythms and sleep.

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Biopsychology, Tenth Edition Handout 14.6: Application of Knowledge Name:________________________________________ Section: ___________ Date: ________

SHIFTWORK EXPRESS REQUEST FOR CONSULTATION Client Name: Manny Workman Consultant Name: Client Age: 47 Client Gender: Male Client Occupation: Night Foreman in a Factory CLIENT BACKGROUND Mr. Workman is responsible for making sure that work is completed in a safe and efficient manner, filling in when workers are ill or absent, and keeping track of employee attendance and performance.

On a typical evening, he gets to the plant at 10:00 P.M. and checks to see if any workers have called in sick. He calls replacements in, if possible, or makes plans to cover essential operations. He tours the plant floor to see if there are problems with the earlier shift and then heads to his office to look at the day’s orders, grabbing a cup of coffee from the machine on his way.

During the evening, Mr. Workman takes hourly tours of the plant floor. If there are no problems, he returns to his office to do paperwork. At about 2:00 A.M. he stops by the vending machines for a coke, a cheese sandwich, and a bag of chips. He then goes down to the shop floor and fills in for people taking breaks, or steps in if a part of the line is having trouble keeping up. Usually there are three or four moderately difficult problems to solve in an evening. About once a week, a major problem requires rapid response and clear thinking. These problems are unpredictable and can occur at any time during the shift. Some are a threat to the equipment or to the wellbeing of the workers. Mr. Workman is responsible for calling in assistance and making sure the problem is solved quickly.

Mr. Workman leaves the plant about 7:30 in the morning. He drives east on the interstate about 20 minutes and then another 10 minutes on winding country roads on his way home. When he gets home, his kids are getting ready for school. His wife has already left for work. Sometimes the kids are not ready and miss the bus, so he has to drive them to school.

CURRENT PROBLEMS REPORTED When Mr. Workman gets home, he is too tired to eat anything, so he goes to bed. He can usually sleep about four hours before his elderly mother calls, asking him to come over and help her. Sometimes he gets a nap in the afternoon, but by the time the kids are home from school, he cannot sleep any more.

He can be very irritable and often yells at the kids for trivial behaviors.

Mr. Workman has complained to his doctor about stomachaches and indigestion. He also reports feeling tired all the time, but being unable to get to sleep. Last week, when there was an emergency at the plant, he cut his hand on a piece of machinery.

Questions to be considered: 1. How would you describe Manny’s sleep patterns?

2. What do you see as factors that would disrupt his sleep?

3. What in his life suggests that he is not sleeping appropriately?

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Chapter 14: Sleep, Dreaming, and Circadian Rhythms Name:________________________________________ Section: ___________ Date: ________

SHIFTWORK EXPRESS REQUEST FOR CONSULTATION Client Name: Luna Nightshift Consultant Name: Client Age: 25 Client Gender: Female Client Occupation: Emergency Room Nurse CLIENT BACKGROUND Ms. Nightshift typically works a 12-hour shift at the local small-town hospital. The current rotation is three days on and one day off. Last week, she worked Sunday through Tuesday nights, had Wednesday night off, and then worked Thursday through Saturday evenings with Sunday evening off.

The hospital is chronically short staffed and Ms. Nightshift frequently works double shifts, staying at the hospital for 24 hours at a time. Ms. Nightshift is frequently the nurse asked to take the double shift, as she is unmarried and does not have childcare responsibilities.

Ms. Nightshift manages to spend time with her friends on the evenings that she is off, but she finds that there are many social activities that she has had to give up, due to her irregular schedule. She often is free during weekdays when her friends are at work.

CURRENT PROBLEMS REPORTED Ms. Nightshift complains of fatigue, but when she gets tired, she tries to sleep longer on her days off.

If she is off on a weekend and she is spending time with her friends, she may not sleep for 48 hours at a time. She then has difficulty staying awake at work and has asked her doctor to prescribe some stimulant drugs to get her through some of the long shifts.

She is also having trouble with mild depression and she feels isolated and lonely.

Questions to be considered: 1. While in the short term, Ms. Nightshift does not have too many sleep problems, what problems do you predict could occur as she continues on this schedule?

2. What types of things might Ms. Nightshift do to improve her social life without causing sleep deprivation?

3. Could you suggest a different schedule for the hospital that would be better for their nursing staff?

4. The hospital has been having trouble finding night staff and has decided to rotate all staff from eight days on day shift to eight days on night shift. Will this be better for Ms. Nightshift, or would you predict either more or different problems?

Recommendations: 1. What recommendation would you make to Ms. Nightshift to improve her sleep and her waking performance?

2. Why would you make these specific recommendations? Please provide reasons based on your text or other cited resource.

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Biopsychology, Tenth Edition Name:________________________________________ Section: ___________ Date: ________

SHIFTWORK EXPRESS REQUEST FOR CONSULTATION Client Name: Raydawn Summerson Consultant Name: Client Age: 32 Gender: Female Client Occupation: Manager of a Fast Food Restaurant CLIENT BACKGROUND Ms. Summerson has a brief history of insomnia. She has always taken a while to get to sleep, but since moving to her new job as a manager of a fast food restaurant, she has had increasing trouble sleeping.

She sometimes cannot get to sleep until 5 or 6 in the morning, and when she does get to sleep, she may awaken in the early morning and not be able to get back to sleep. This has resulted in fatigue during the day while she is at work.

Ms. Summerson has resorted to taking a 10-minute nap in her car in the middle of the afternoon during a break. She finds that she can fall asleep easily in this environment, and wakes easily to the sound of her watch alarm.

Ms. Summerson has tried going to bed earlier to have more time to get to sleep, or exercising for an hour before bedtime in hope that fatigue will make her sleepy. She has also tried lavender aromatherapy candles, but she finds that she worries that the house will catch fire if she falls asleep.

Questions to be considered: 1. While in the short term, Ms. Summerson does not have too many sleep problems, what problems do you predict could occur as she continues on this schedule?

2. What types of things might Ms. Summerson do to improve her ability to get to sleep and to stay asleep?

Recommendations: 1. Describe a therapeutic program for Ms. Summerson to enhance her ability to get sleep and improve her waking performance.

2. Why would you make these specific recommendations? Please provide reasons based on your text or other cited resource.

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Chapter 14: Sleep, Dreaming, and Circadian Rhythms RESOURCES DO: • • •

•

• •

Exercise regularly, but not within 4 to 6 hours of going to bed.

Take a short nap during the day if you’re tired, but keep it brief. In addition, do it early in the day.

Take a rest break if you feel tired while driving. Fresh air or loud music won’t keep you alert, but a short nap may do the trick, especially if you combine it with caffeine, says Dr. James Kiley of the National Center on Sleep Disorders Research.

Try to relax and let nature take its course. If that doesn’t help you fall asleep, get up and move around. Go to another room and read, watch television or listen to music. Don’t take sleeplessness lying down.

Go to sleep and get up at the same time each day, even on weekends and holidays.

See a doctor for any medical conditions affecting your quality or quantity of sleep, such as arthritis, bronchitis, asthma, certain heart problems, hormone disorders such as hyperthyroidism, and sleep-related disorders like RLS and sleep apnea.

DON’T: • Use alcohol for at least 2 hours before bedtime. It may make your drowsy at first, but after a few hours it can disrupt sleep.

• Overdo your consumption of caffeinated beverages or over-the-counter medicines during the day. Some painrelieving medications contain caffeine—check the labels. Be aware that certain prescription medicines, such as those for asthma, some antidepressants, and anti-anxiety drugs, may cause insomnia.

• Use the bedroom to pay bills, watch television, or discuss the problems of the day. The bedroom should be used only for sex and sleep.

• Rely on over-the-counter herbs, or other sleep-promoting substances whose safety and effectiveness have not been determined.

• Smoke, especially before bedtime.

Nicotine can disrupt sleep and reduce total hours slept. Smokers report far greater sleepiness and minor accidents than do nonsmokers.

• Think that sleep problems cannot be treated. In most instances, there are effective treatments, even for older men and women or those with health problems.

From: Sleep Strategies for Shift Workers http://www.sleepfoundation.org/ A Word to the Wise There is no surefire method that guarantees a good night’s sleep—not even a warm bath or a warm glass of milk. However, experts now recognize that there are some factors that may either help promote or discourage a peaceful night’s sleep. If your sleep problems persist, be sure to see your family physician or a sleep expert. Most problems can be treated with good results.

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15 Drug Addiction and the Brain’s Reward Circuits: Chemicals That Harm with Pleasure TABLE OF CONTENTS Chapter-at-a-Glance

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Learning Objectives

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Brief Chapter Outline

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Teaching Outline

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Lecture Launchers

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Web Links

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Handouts

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Chapter 15: Drug Addiction and the Brain’s Reward Circuits

CHAPTER-AT-A-GLANCE

Brief Outline Chapter Introduction (p. 390) 15.1 Basic Principles of Drug Action (pp. 391–394) 15.2 Role of Learning in Drug Tolerance (pp. 394–396) 15.3 Five Commonly Abused Drugs (pp. 396–404) 15.4 Comparing the Health Hazards of Commonly Used Drugs (pp. 404–406) 15.5 Early Biopsychological Research on Addiction (pp. 406–409) 15.6 Current Approaches to the Mechanisms of Addiction (pp. 409–414)

Instructor’s Manual Resources Lecture Launcher 15.1

Lecture Launchers 15.2, 15.5

Lecture Launcher 15.3 Lecture Launcher 15.4

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LEARNING OBJECTIVES After completion of this chapter, the student should be able to:

LO 15.1 LO 15.2

Compare the various routes of drug administration.

Explain the ways in which drugs can influence the nervous system and how they are eliminated from the body.

LO 15.3 Describe how the body becomes tolerant to drugs and the process of drug withdrawal. Explain what it means to be physically dependent on a drug.

LO 15.4 Define drug addiction.

LO 15.5 Explain contingent drug tolerance.

LO 15.6 Describe conditioned drug tolerance and conditioned compensatory responses.

LO 15.7 Describe the health hazards associated with smoking tobacco.

LO 15.8 Describe the health hazards associated with alcohol consumption and the various stages of the full-blown alcohol withdrawal syndrome.

LO 15.9 Explain the health effects of marijuana and the mechanism of action of THC. LO 15.10 Describe the health hazards associated with the consumption of cocaine and other stimulants.

LO 15.11 Describe the health hazards associated with the consumption of opioids and the opioid withdrawal syndrome.

LO 15.12 Explain why it is difficult to determine causality in studies of the health hazards of drugs.

LO 15.13 Compare the direct health hazards of alcohol, tobacco, marijuana, heroin, and cocaine.

LO 15.14 Explain the physical-dependence and positive-incentive perspectives of addiction.

LO 15.15 Describe the intracranial self-stimulation (ICSS) paradigm.

LO 15.16 Describe two methods for measuring the rewarding effects of drugs.

LO 15.17 Explain the role of the nucleus accumbens in drug addiction.

LO 15.18 Describe the three stages in the development of drug addiction.

LO 15.19 Describe two sets of findings that have challenged the relevance of drug self-administration studies.

LO 15.20 Explain the significance of the case of Sigmund Freud. < Return to Table of Contents

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Chapter 15: Drug Addiction and the Brain’s Reward Circuits

BRIEF CHAPTER OUTLINE Lecture Launcher 15.1: Drug Use in America 1. Basic Principles of Drug Action a. Drug Administration and Absorption, and Penetration of the Central Nervous System b. Drug Action, Metabolism, and Elimination c. Drug Tolerance, Drug Withdrawal Effects, and Physical Dependence d. Drug Addiction: What Is It? 2. Role of Learning in Drug Tolerance a. Contingent Drug Tolerance b. Conditioned Drug Tolerance Lecture Launcher 15.2: On the Legalization of Marijuana 3. Five Commonly Abused Drugs a. Tobacco b. Alcohol c. Marijuana d. Cocaine and Other Stimulants e. The Opioids: Heroin and Morphine 4. Comparing the Health Hazards of Commonly Used Drugs a. Interpreting Studies of the Health Hazards of Drugs b. Comparison of Hazards of Tobacco, Alcohol, Marijuana, Cocaine, and Heroin Lecture Launcher 15.3: The Case of Sigmund Freud 5. Early Biopsychological Research on Addiction a. Physical-Dependence and Positive-Incentive Perspectives of Addiction b. Intracranial Self-Stimulation and the Mesotelencephalic Dopamine System c. Early Evidence of the Involvement of Dopamine in Drug Addiction d. Nucleus Accumbens and Drug Addiction Lecture Launcher 15.4: Watching the Brain on Drugs 6. Current Approaches to the Mechanisms of Addiction a. Three Stages in the Development of an Addiction b. Current Concerns about the Drug Self-Administration Paradigm c. A Noteworthy Case of Addiction < Return to Table of Contents

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TEACHING OUTLINE 1. Basic Principles of Drug Action • More than 1 billion people are addicted to nicotine worldwide. Many millions more are addicted to alcohol, illegal drugs, and prescription drugs.

• It is important to note at the outset that the legal status of a drug says nothing about its safety or the health risks associated with it. For the most part, a drug’s legal status was determined before we knew much about the risks associated with it. a. Drug Administration and Absorption LO 15.1 Compare the various routes of drug administration.

Drugs are usually consumed in the following ways: • Ingestion, or oral administration, is the preferred route of administration for many drugs. It is convenient, but several major drawbacks include the unpredictability of absorption from the stomach or small intestine (absorption can be greatly influenced by food in the stomach) and the fact that some drugs are deactivated before they can be absorbed from the digestive tract; most drugs are absorbed from the small intestine, but some (e.g., alcohol) can be absorbed through the stomach wall, and thus act more rapidly.

• Injection, whether SC, IM, or IV, is the favored route in medical practice because the effects of injected drugs are strong, fast, and predictable; in particular, addicts favor the IV route, but it is particularly dangerous as there is an increased risk of death from overdose, impure drugs, or allergic reactions. There are only a few sites on the body appropriate for IV injection, thus addicts frequently develop infections and scar tissue at these sites.

• Inhalation allows many chemicals to be absorbed directly into the bloodstream from the lungs (e.g., chemicals in tobacco and marijuana smoke); shortcomings include fact that dose is hard to regulate and lung damage is a serious risk from the repeated inhalation of chemicals.

• Absorption through mucous membranes allows some drugs (e.g., cocaine) to be readily absorbed through the mucous membranes of the nose, mouth, or rectum; this method of administration is problematic as these membranes can be easily damaged. b. Drug Action, Metabolism, and Elimination LO 15.2 Explain the ways in which drugs can influence the nervous system and how they are eliminated from the body.

Drug Penetration of the Central Nervous System The blood-brain barrier makes it difficult for many drugs to enter the CNS. Mechanisms of Drug Action Once a psychoactive drug has penetrated the CNS, it can influence neural activity in numerous ways; e.g., it can act diffusely on neural membranes or interact specifically with particular classes of neurotransmitters and receptors.

Drug Metabolism and Elimination The effects of most psychoactive drugs are terminated by their metabolism (i.e., by their conversion to nonactive metabolites); liver enzymes metabolize most drugs. In general, only small amounts of unmetabolized active drugs are eliminated in sweat, breath, urine, etc.

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Chapter 15: Drug Addiction and the Brain’s Reward Circuits c. Drug Tolerance, Drug Withdrawal Effects, and Physical Dependence (see Figure 15.1 in Biopsychology) LO 15.3 Describe how the body becomes tolerant to drugs and the process of drug withdrawal. Explain what it means to be physically dependent on a drug.

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Drug tolerance is a state of decreased sensitivity to a drug’s effect that results from prior exposure to the drug.

Tolerance can be measured in two ways: (1) by measuring the decrease in the response elicited by the same dose of the drug, or (2) by measuring the increase in the amount of drug required to produce the same effect; in effect, drug tolerance is a shift in the dose-response curve to the right.

Exposure to one drug can lead to the development of tolerance to another drug’s effects (cross tolerance).

Tolerance does not develop equally to all of the effects of a drug; indeed, sensitization can develop to some drug effects at the same time that tolerance can develop to other drug effects.

While there are multiple physiological mechanisms that can underlie a given form to drug tolerance, it is common to think of tolerance effects as being of two different types: − Metabolic tolerance (any tolerance effect that results from a decrease in the amount of drug reaching the target cells); or − Functional tolerance (any tolerance that results from a decrease in the ability of the drug to influence the target cells).

Tolerance to most psychoactive drugs is primarily functional; it may be due to several types of neural changes, including changes in the number of receptors it binds to or the way it interacts with those receptors.

Drug Withdrawal Effects and Physical Dependence After significant amounts of a drug have been in the body for a period of time, its sudden elimination can trigger an illness called a drug withdrawal syndrome; these are usually opposite to the initial effects of the drug. When someone suffers from withdrawal symptoms if they stop taking a drug, they are said to be physically dependent on the drug.

Tolerance and withdrawal are thought to be different manifestations of the same underlying physiological change. When the drug is removed, the physiological changes that compensate for a drug’s effects on the nervous system that are the basis of tolerance are no longer held in check by the drug, and withdrawal symptoms opposite to the original effects of the drug are the result.

In general, longer drug exposure and more rapid elimination of a drug lead to greater withdrawal effects.

d. Drug Addiction: What Is It? LO 15.4 Define drug addiction.

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Addicts are habitual drug users who continue to use a drug despite its adverse effects on their health and social life, and despite repeated attempts to stop using it.

Addiction does not equal physical dependence; avoidance of withdrawal is rarely the primary motivating force behind addictive behaviors. Addicts often renew their addictive behaviors after months, or years, of abstinence when simple physical withdrawal symptoms are unlikely to be severe.

Drug addiction involves more than periodic drug use. Addicted people continue to use drugs despite the adverse effects on their health and social life.

Addicts use drugs for many reasons besides simply alleviating withdrawal symptoms.

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Addiction is not restricted to drugs. It can also occur to things like gambling, food, and the Internet.

2. Role of Learning in Drug Tolerance (see Figures 15.2, 15.3, and 15.4 in Biopsychology) Three lines of research have shown that learning can influence the development of tolerance or withdrawal to a drug’s effects: demonstrations of contingent drug tolerance, conditioned drug tolerance, and conditioned drug withdrawal. a. Contingent Drug Tolerance LO 15.5 Explain contingent drug tolerance.

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Contingent drug tolerance is tolerance that develops only to drug effects that are actually experienced.

It is usually demonstrated by before-and-after experiments.

In before-and-after experiments, the subjects in one condition (the drug-before-test condition) are tested after each injection, so that they repeatedly experience the effect of the drug on the test behavior.

The subjects in the other condition (the drug-after-test condition) are tested before each injection, so that they do not repeatedly experience the drug’s effect on the test behavior.

The typical finding in such experiments is that the development of tolerance is substantially greater in the drug-before-test condition than in the drug-after-test condition.

For example, Pinel et al. demonstrated contingent tolerance to the anticonvulsant effect of ethanol.

During the tolerance-development phase of this experiment, the rats in the ethanol-before group received an ethanol injection once every 48 hours, one hour before a convulsive amygdala stimulation, thus they repeatedly experienced ethanol’s anticonvulsant effect.

The rats in the ethanol-after group received ethanol injections on the same bi-daily schedule, but one hour after each convulsive stimulation, thus never experiencing ethanol’s anticonvulsant effect.

On the test day, only the rats in the ethanol-before-stimulation group were tolerant to alcohol’s anticonvulsant effect.

b. Conditioned Drug Tolerance LO 15.6 Describe conditioned drug tolerance and conditioned compensatory responses.

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Conditioned drug tolerance refers to tolerance that is maximally expressed in the presence of drug-predictive stimuli.

For example, Crowell, Hinson, and Siegel (1981) demonstrated conditioned tolerance to the hypothermic effect of alcohol. In this study, two groups of rats received 20 alcohol injections and 20 saline injections in alternating sequence, one every 48 hours.

The only difference between the two groups was that the rats in one group always received their alcohol in a distinctive test room and their saline in their colony room, whereas the rats in the other group received their saline in the test room and their alcohol in the colony room.

Remarkably, tolerance to the hypothermic effect of alcohol was revealed only when the subjects were tested in the same environment in which they had previously received alcohol.

According to Siegel and his colleagues, addicts develop tolerance to drug effects that are repeatedly experienced in the same environment and, consequently, they must start taking larger doses of the drug to maintain the effects that they see. However, when they take the elevated dose in a novel environment in which they are not tolerant, they run the risk of a drug overdose.

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In support of this hypothesis, Siegel et al. showed that rats were more susceptible to the lethal effects of a heroin overdose if they received the injection in an environment different from that in which they had experienced the effects of previous drug injections.

One theory of the situational specificity of tolerance is Siegel’s conditioned compensatory response theory.

Siegel proposed that each incidence of drug administration is like a Pavlovian conditioning trial. The drug effect is the UCS, which is preceded on each trial by the drug-predictive environment that serves as the CS. As conditioning occurs, the drug-predictive environmental CS begins to elicit CRs that are opposite to the effects of the drug. These conditioned compensatory responses—as Siegel termed them—offset the effects of the drug, and tolerance is the consequence.

It is also possible for conditioned sensitization to develop to a drug’s effects. For example, the administration of amphetamine every three to four days, for a total of ten injections, greatly increases the sensitivity of rats to subsequent amphetamine injections, but only if those injections are administered in the same environment in which they had experienced the previous amphetamine injections.

Most demonstrations of conditioned drug tolerance have employed exteroceptive stimuli (external, public stimuli) as the conditioned stimuli. However, interoceptive stimuli (internal, private stimuli) were just as effective for conditioning.

Conditioned-withdrawal effects can be elicited by the drug environment or other drugassociated cues in the absence of the drug itself.

Thinking about Drug Conditioning Conditioned drug effects are inevitable in any situation in which drugs are repeatedly administered; however, it is difficult to predict whether the conditioned response will complement the drug’s effects (and produce conditioned sensitization) or oppose the drug’s effects (and produce conditioned tolerance).

This unpredictability may reflect confusion on the part of researchers about the nature of the US and the UR; Ramsay and Woods (1997) have argued that the drug’s effects on the nervous system are the US (not the drug per se), and the UR reflects the response of the nervous system to the drug’s effects.

In most cases, the UR opposes the drug’s effects and thus the development of a CR leads conditioned tolerance.

In some cases, however, the UR complements the drug’s effects and thus the development of a CR leads conditioned sensitization.

3. Five Commonly Used Drugs (see Figure 15.5 in Biopsychology) a. Tobacco LO 15.7 Describe the health hazards associated with smoking tobacco.

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Nicotine is the major psychoactive ingredient; 4,000 other known chemicals are in tobacco.

Tobacco is highly addictive; for example, about 70% of people who try tobacco products end up addicted (as opposed to 10% for ethanol or 30% for heroin).

Tobacco is a leading cause of preventable death.

Nicotine acts on nicotinic cholinergic receptors.

Typically nicotine addiction develops very quickly, within a few weeks. Compulsive drug craving (an affective state in which there is a strong desire for the drug) occurs with smoking.

Nicotine addiction has a major genetic component with a heritability estimate of 55%.

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Addictive properties are highlighted by the behavior of patients with Buerger’s disease; they will still smoke, even after their limbs are amputated because of smoking-related vasoconstriction and gangrene.

Effects of tobacco range from nausea, vomiting, and diarrhea in new tobacco users to feelings of relaxation and alertness in experienced smokers.

Consequences of smoking include smoker’s syndrome, which results in chest pain, coughing, failure of the cardiorespiratory system, and cancer. This can also apply to victims of secondhand smoke.

Even the unborn are vulnerable to nicotine since it is a teratogen. Smoking during pregnancy increases the likelihood of miscarriage, stillbirth, and early death of a child.

Treatments for nicotine addiction are only marginally effective, although those who do stop smoking generally receive great health benefits.

b. Alcohol LO 15.8 Describe the health hazards associated with alcohol consumption and the various stages of the full-blown alcohol withdrawal syndrome.

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Alcohol is involved in at least 2 million deaths per year worldwide.

It is widely distributed within the body, as it is both fat and water-soluble.

It is classified as a depressant, though at low doses it can actually stimulate neural activity.

At moderate doses, alcohol impairs cognitive, perceptual, verbal, and motor skills, as well as a loss of control that can lead to a variety of socially unacceptable behaviors.

High doses result in a lack of consciousness, and very high doses can be lethal due to respiratory depression.

Tolerance and physical dependence can be produced; heavy drinkers are able to metabolize more alcohol than nondrinkers, though most tolerance is functional.

The withdrawal syndrome can range from the headache and nausea of a hangover to severe tremors, nausea, hallucinations, convulsions, and delirium tremens (DTs); the last two withdrawal symptoms can be severe enough to be fatal.

Alcohol attacks all body tissues, including the brain (e.g., Korsakoff’s syndrome); severe scarring or cirrhosis of the liver can result from long-term alcohol abuse.

Low to moderate regular drinking is associated with elevated levels of many cancers.

Alcohol also crosses the placenta and can result in birth defects such as Fetal Alcohol Syndrome; there is no time during a pregnancy at which ethanol consumption is risk-free.

Alcohol consumption demonstrates transgenerational epigenetic effects such that offspring of male drinkers can show symptoms of FAS. One of the most widely publicized erroneous findings about alcohol is that moderate drinking is good for the heart. This is based on correlational data and should be interpreted with caution.

c. Marijuana LO 15.9 Explain the health effects of marijuana and the mechanism of action of THC. • • • • •

Marijuana is derived from the cannabis plant.

Marijuana use is high with over 124 million users across the globe in the past year.

Marijuana elicits psychoactive responses largely due to THC (delta-9-tetrahydrocannabinol), however, it contains more than 80 other cannabinoids that can be psychoactive.

It may be inhaled or ingested orally (usually baked into an oil-rich substrate to aid absorption).

Marijuana use has a long history.

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At social doses, marijuana has subtle effects that range from an increased sense of well-being, craving sweets, and enhanced sensations; higher doses can lead to impaired judgment and short-term memory impairment.

Addiction potential is low and while tolerance may occur, withdrawal symptoms are rare.

Marijuana is associated with tachycardia, however, there is no convincing evidence that it causes brain damage and there is evidence it may be neuroprotective.

Marijuana binds to receptors associated with an endogenous substance known as anandamide.

Clinically, marijuana has been shown to block the nausea of cancer drugs, stimulate appetite, decrease the severity of glaucoma, and reduce some forms of pain.

New forms of administration such as a mouth spray have been developed to treat multiple sclerosis.

d. Cocaine and Other Stimulants LO 15.10 Describe the health hazards associated with the consumption of cocaine and other stimulants.

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These drugs all have the same general effect (to stimulate the brain), but differ greatly in their potency.

Cocaine is a commonly abused stimulant; it may be inhaled, absorbed across mucosal membranes, or injected. Cocaine can be converted to its base form, crack.

Cocaine is very addictive; however, its withdrawal syndrome is relatively mild.

Cocaine acts by blocking catecholamine reuptake; its euphoria-inducing properties seem to be due to its effects on dopaminergic neurotransmission.

Cocaine is a general stimulant, producing feelings of energy, well-being, and self-confidence.

Individuals who are addicted to cocaine tend to go on so-called cocaine sprees, binges in which extremely high levels of intake are maintained for periods of a day or two.

The effects of cocaine sprees include sleeplessness, tremors, nausea, hyperthermia, and cocaine psychosis.

Although tolerance develops, sensitization can be seen to the motor effects and withdrawal is generally mild (negative mood swing and insomnia).

Clinically, cocaine derivatives are effective as local anesthetics.

Amphetamine and related compounds like methamphetamine are the most commonly abused stimulants; currently, favored amphetamine-like drugs of abuse include methamphetamine and ecstasy.

The primary mechanism by which cocaine exerts its effects is the blockade of dopamine transporters, molecules in the presynaptic membrane that normally remove dopamine from the synapses and transfer it back in to presynaptic neurons.

Research shows negative long-term effects with stimulant use including cognitive impairments and heart pathology.

e. The Opioids: Heroin and Morphine LO 15.11 Describe the health hazards associated with the consumption of opioids and the opioid withdrawal syndrome.

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This family of drugs includes morphine, codeine, and heroin.

These are unmatched as analgesics and are very addictive; approximately 507,000 Americans currently use heroin.

Opioids have a long history dating back to 4000 B.C.

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Key addictive effects seem to be a rush of pleasure and drowsy euphoria; tolerance develops to these effects, meaning that addicts must administer very high doses to get the desired effect.

A withdrawal syndrome appears within hours of the last dose. Although the symptoms are not trivial, they are not as bad as the popular press would have us believe and seem to be similar to a bad case of the flu.

Undesirable side effects include constipation, pupil constriction, and reduced libido.

Opiates elicit their effects on the CNS by acting as receptors in the brain that normally bind endogenous opiates (also called endorphins).

While deaths from opiate abuse are reported, they often do not take into account multi-drug use as a potential contributor.

The increase in heroin is almost entirely due to misuse of legal synthetic opioid analgesics (such as Oxycontin and Lorcet).

Methadone replacement therapy involves substituting methadone for heroin to reduce the euphoria and prevent withdrawal.

Buprenorphine has fewer side-effects than methadone but is less effective.

Several European countries have successfully implemented programs that provide safe, inexpensive heroin administered under supervision and combined with counseling.

4. Comparing the Health Hazards of Commonly Used Drugs a. Interpreting Studies of the Health Hazards of Drugs LO 15.12 Explain why it is difficult to determine causality in studies of the health hazards of drugs.

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Interpretation is complicated by studies being primarily correlational and by studies using the most addicted people as their comparison group.

b. Comparison of the Hazards of Tobacco, Alcohol, Marijuana, Cocaine, and Heroin LO 15.13 Compare the direct health hazards of alcohol, tobacco, marijuana, heroin, and cocaine.

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In terms of the prevalence in society, tobacco and alcohol have a greater negative impact than marijuana, cocaine, and heroin.

Another method of comparison is based on global death rates. Tobacco has the highest death rate (5 million per year), then alcohol (2 million per year), then all other drugs combined (250,000 per year).

5. Early Biopsychological Theories on Addiction Are addicts driven to drugs by an internal need, or are they drawn by the anticipated positive effects? a. Physical-Dependence and Positive-Incentive Perspectives of Addiction LO 15.14 Explain the physical-dependence and positive-incentive perspectives of addiction.

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Early attempts to explain addiction attributed it to physical dependence; addicts take drugs to curtail the withdrawal symptoms that they otherwise would face.

From this perspective, treating addiction meant withdrawal from the drug in a hospital setting until the symptoms subsided.

Unfortunately, addicts almost always return to drug taking after they have been released from the hospital.

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Chapter 15: Drug Addiction and the Brain’s Reward Circuits − − •

Some highly addictive drugs produce little withdrawal distress (e.g., cocaine).

The pattern of drug taking in many addicts typically involves self-imposed cycles of binges and detoxification.

The failings of physical-dependence theories have lent support to positive-incentive theories; according to positive-incentive theories of addiction, most addicts take drugs to obtain their pleasurable effects, rather than to escape their aversive aftereffects.

b. Intracranial Self-Stimulation and the Mesotelencephalic Dopamine System (see Figures 15.6– 15.8 in Biopsychology) LO 15.15 Describe the intracranial self-stimulation (ICSS) paradigm.

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ICSS was discovered in the early 1950s by Olds and Milner.

Although animals self-stimulate a variety of brain structures, most early studies focused on the septum and lateral hypothalamus because the self-stimulation rates at these sites are impressively high.

Olds and Milner argued that animals self-stimulate sites that activate natural reward circuits (e.g., circuits that normally mediate the rewarding effects of food, water, sex, etc.).

The natural reward circuit consists of a portion of the mesotelencephalic dopamine system known as the mesocorticolimbic pathway.

The dopamine cell bodies of the mesocorticolimbic pathway reside in the substantia nigra and ventral tegmental area and a major projection target is the nucleus accumbens.

The mesocorticolimbic pathway plays an important role in mediating intracranial selfstimulation as evidenced by: 1) Many of the brain sites at which self-stimulation occurs are part of the mesocorticolimbic pathway; 2) Intracranial self-stimulation is often associated with an increase in dopamine release in the mesocorticolimbic pathway; 3) Dopamine agonists tend to increase intracranial self-stimulation, and dopamine antagonists tend to decrease it; and, 4) Lesions of the mesocorticolimbic pathway tend to disrupt intracranial self-stimulation.

c. Early Evidence of the Involvement of Dopamine in Drug Addiction LO 15.16 Describe two methods for measuring the rewarding effects of drugs.

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One animal model of human addiction that implicated the dopamine system is the drug selfadministration paradigm; animals will self-administer many addictive drugs, often mimicking many of the drug-taking behaviors characteristic of human addicts.

The conditioned place-preference paradigm is also used to examine the rewarding effects of drugs.

During the conditioning phase, rats repeatedly receive a drug in the drug compartment of a two-compartment box.

During testing, drug-free rats are placed in the box, and the proportion of time spent in the compartment where it used to receive the drug is compared to time spent in the control compartment.

During drug-free testing, rats spend more time in the drug compartment.

Both models implicated dopamine playing an important role in the rewarding effects of drug administration.

d. Nucleus Accumbens and Drug Addiction LO 15.17 Explain the role of the nucleus accumbens in drug addiction.

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Dopaminergic input to the nucleus accumbens is critical to the experience of reward and pleasure.

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Laboratory animals self-administer microinjections of addictive drugs into the nucleus accumbens.

Microinjections of drugs into the nucleus accumbens lead to the development of conditioned place-preferences.

Destruction of the VTA or the nucleus accumbens has been shown to block self-administration or the development of conditioned place preferences.

Self-administration of addictive drugs or natural reinforcers are both associated with increased dopamine release in the nucleus accumbens.

6. Current Approaches to the Mechanisms of Addiction (see Figures 15.9–15.11 in Biopsychology) a. Three Stages in the Development of Addiction LO 15.18 Describe the three stages in the development of a drug addiction.

Initial Drug Taking • There are a variety of environmental factors that facilitate (drug availability, social pressures, novelty-seeking traits) or protect from (access to non-drug reinforcers) initial drug use.

• Drugs can also come to be viewed as tools to achieve arousal or stress/anxiety relief.

• Drugs may also be used to self-medicate.

Habitual Drug Taking • Although the reduction of withdrawal symptoms undoubtedly plays a role in drug-taking behavior, most modern theorists believe that positive-incentive factors are primary in addictive behaviors.

• The positive incentive value of a drug is linked to the user’s want of a drug, whereas the hedonic value is linked to the user’s liking of the drug’s effect.

• The expectation of the pleasurable effects of drugs may become sensitized in addicts; a key point of this incentive-sensitization theory is that addicts don’t receive more hedonic value from the drug. It is the anticipated pleasure that motivates their behavior; thus, in drug addicts, the craving for a drug may be out of proportion with the pleasure that they actually derive from taking it.

• Research suggests that dopamine release in the nucleus accumbens plays a key role in the wanting of reward, rather than in the liking of reward itself. For example, dopamine is released in the nucleus accumbens following a signal that predicts reward, rather than when the reward itself is presented.

• Several changes in the brain’s responses appear to mediate the transition from incidental drug use to habitual drug taking. First, there are changes in how the striatum responds to drugs and drug-related cues. Second, the role of the prefrontal cortex in mediating drug-related behaviors seems to decline.

• Addiction might be one manifestation of a larger problem. Compared to healthy controls, drug addicts are poorer at making decisions, they engage in more risk-taking behavior, and they tend to have deficits in self-control. Such psychological differences must be taken into account when developing theories about addiction and when developing treatments.

• Addiction is not just limited to drugs: Many other conditions also involve the inability to refrain from a behavior that is damaging—for example, overeating.

Drug Craving and Addiction Relapse • Most addicts relapse at some point after they stop taking drugs. Three different causes have been identified: stress, drug priming, and conditioned environmental cues.

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Conditioned cues presented shortly after drug withdrawal are less likely to illicit craving than cues presented later. This incubation of drug craving can explain why addicts might relapse even after years of abstinence.

Animal literature on drug self-administration has suggested two additional factors that may play a role in drug craving and relapse. First, environmental enrichment after drug withdrawal has reduced cue-and stress-induced, but not drug-priming-induced, relapse of drug selfadministration. Second, even a few brief exposures to nondrug reinforcers can reliably reduce relapse of cocaine self-administration.

b. Current Concerns about the Drug Self-Administration Paradigm LO 15.19 Describe two sets of findings that have challenged the relevance of drug selfadministration studies.

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Two lines of study have challenged the relevance of drug self-administration: – When rats are housed in more naturalistic (enriched) environments, they are less likely to administer drugs.

Excessive focus on stimulants: − Most drug self-administration studies have focused on dopaminergic stimulants rather than examining other drugs (i.e. opioids) that manipulate different receptor systems.

c. A Noteworthy Case of Addiction LO 15.20 Explain the significance of the case of Sigmund Freud.

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Sigmund Freud’s case illustrates the powerful effects of drug addiction.

Freud took cocaine for three years, extolling its wonderful effects.

When he was 38, his physician told him to stop taking the drug because it was creating heart arrhythmias. In spite of this, he kept taking the drug.

At 67, he developed sores in his mouth that were found to be cancerous, yet he could not stop taking the drug. His addiction took hold of him. In total, he had to have 33 operations to deal with his oral cancer.

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Biopsychology, Tenth Edition

LECTURE LAUNCHERS Lecture Launcher 15.1: Drug Use in America It is often useful to spend a few minutes at the start of these lectures to describe patterns of drug use and abuse in the United States. A good place to look for data and figures to stimulate this kind of conversation can be found at the Web site supported by the Office of Applied Studies of SAMHSA (the Substance Abuse and Mental Health Services Administration: Go to http://www.samhsa.gov and browse around for whatever data you want to use in your discussion. They have data for both legal (alcohol, nicotine) and illegal drug use; some of their comparisons go as far back as the 1960s.

Lecture Launcher 15.2: On the Legalization of Marijuana Unless your students have been on another planet (more realistically, in another country), they will be aware of the ongoing debate in the United States about the legalization of marijuana. As more and more states vote to legalize marijuana, pitting them against federal law, it’s important to discuss the potential effect on Americans. You can stimulate some educated debate about this topic, by presenting some current data and support available at http://www.legalizationofmarijuana.com and place “Arguments for and against” in the search bar. Select the matching link to obtain information on the common arguments for and against legalizing marijuana.

Lecture Launcher 15.3: The Case of Sigmund Freud This case study, which is located at the end of this chapter, provides a good summary comparison between the addictive properties of cocaine versus nicotine. Most students know Freud for his various theories, and are usually surprised to hear that he was once a proponent of cocaine use.

Lecture Launcher 15.4: Imaging the Addicted Human Brain Go to https://www.ncbi.nlm.nih.gov/ and click on the dropdown box that currently says “All Databases” and scroll down to “PMC.” Type in “Imaging the Addicted Human Brain” into the search box and select the link that matches your search. These resources can be used to either complement your lecture material on human brain imaging studies or when you discuss the effects of particular drugs.

Lecture Launcher 15.5: Animations There are several nice animations online that represent the normal transmission of the nervous system and then represent the effects of some of the psychoactive drugs. These can be very useful to supplement a lecture, and the links to the animations can be made available for students to review after class. The National Institute on Drug Abuse (NIDA) has many resources for instructors available for download. < Return to Table of Contents

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Chapter 15: Drug Addiction and the Brain’s Reward Circuits

WEB LINKS Web Link 15.1: Why Do Some People Drink Too Much? The Role of Genetic and Psychosocial Influences Place the full title of the article listed above in your favorite browser. Select the pdf file from NIAAA. Abstract: “A sizable minority of the population abuses alcohol. Research has found that some vulnerability to developing alcohol-related problems is conveyed genetically, and animal research has indicated that inheritance can take many forms. Studies in mice have demonstrated that various individual genes or groups of genes can shape very distinct responses to alcohol. By identifying the proteins these genes encode and the mechanisms by which the genes influence an animal’s biochemical response to alcohol, scientists can gain insight into the features of human alcoholism and provide a basis for developing pharmaceuticals that short-circuit these genetically defined processes.”

Web Link 15.2: From Genes to Geography: The Cutting Edge of Alcohol Research Place the full title of the article listed above in your favorite browser. Select the pdf file from NIAAA. National Institute on Alcohol Abuse and Alcoholism, No. 48, July 2000. Brief research summary with citations.

Web Link 15.3: Close to Home: Moyers on Addiction Go to http://www.pbs.org/ and place “addiction” in the search bar. You will be able to explore numerous links associated with specific drugs.This PBS site provides facts and information relating to addiction and contains a series of links to animations of the effects of addictive drugs within the synapse.

Web Link 15.4: Drug Fact Sheets Go to http://www.dea.gov/. Once there, insert “drug fact sheet” in the search bar. From there you can just select whatever drug is of interest to you. Fact sheet links relating to specific illicit drugs such as alcohol and cocaine are provided within this site.

Web Link 15.5 EMCDDA: Drug Addiction Data Bases (European Monitoring Center for Drugs and Drug Addiction) Go to http://www.emcdda.eu.int/ and select the databases you need to find the data that you have interest in. This site provides access to three databases relating to drug use and addiction, as well as to links on drug abuse.

Web Link 15.6: National Institute on Drug Abuse http://www.drugabuse.gov This is the home page for the National Institute on Drug Abuse. The page contains links to research projects currently funded by NIDA. From here you can search for whatever drug you are interested in studying.

Web Link 15.7: Novelty Seekers and Drug Abusers Tap Same Brain Reward System, Animal Studies Show Go to http://archives.drugabuse.gov/ and type ”novelty seekers and drug abusers” in the search bar. Select the article with the same name.

Web Link 15.8: Cocaine and the Concept of Addiction: Environmental Factors in Drug Compulsions In your favorite browser, type “Cocaine and the Concept of Addiction” in the search bar. Select the link with the same name that leads you to the Web page for “speele.”

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Biopsychology, Tenth Edition A research classic: “Stanton and Richard DeGrandpre review human and animal research against the claim that cocaine is such a powerful reinforcer that it invariably causes the organism with unlimited access to self-administer the drug to the exclusion of all other activity and reward, often until death. In place of this model, Stanton and Rich apply behavioral economic research and models which show that animals balance the opportunities for available rewards, among which cocaine appears to be a strong but far from overwhelming or unique example. They contrast their view with that of Nobel prize-winning economist Gary Becker, who rather than suggesting an economic model of behavior instead imagines that drugs create a biologically compelling state that drives the addict’s behavior.” Published in Addiction Research, 6:235– 263, 1998.

Web Link 15.9: Pathology of Drug Abuse Go to http://www-medlib.med.utah.edu/ and place “Pathology of Drug Abuse Tutorial” in the search bar.

Select the matching link.

This site contains a collection of slides related to the pathologies in brain and peripheral tissues engendered by smoking, alcohol consumption, and cocaine abuse.

Handout 15.1 Drug Information Table < Return to Table of Contents

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Chapter 15: Drug Addiction and the Brain’s Reward Circuits

HANDOUTS Handout 15.1: Drug Information Table Please use your textbook, the Internet, and the library to answer the following questions about the drug you have been assigned.

Be sure that you keep track of the sources for each piece of information, and that you evaluate the quality of the source and the accuracy of the information based on the source’s credibility.

Question What is the chemical name of the drug?

Information

What other names are associated with it?

What kind of chemical is the drug? (mineral, amino acid, etc.)

Is it similar to a neurotransmitter?

How does the drug appear to act in the nervous system?

What locations in the nervous system are affected by the drug?

Does it act as an antagonist or agonist?

How much of the drug is necessary for its effects to be perceived?

How much of the drug would be a toxic dose?

What happens to a person who gets too much of this drug?

How is the drug typically administered?

Does its form of administration make overdose more or less likely?

Could a different form of administration make the drug safer?

Would it then lose its effectiveness?

Does the drug have any known potential side effects?

Where in the body is the drug acting to create these side effects? < Return to Table of Contents

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Source

16 Lateralization, Language, and the Split Brain: The Left Brain and Right Brain TABLE OF CONTENTS Chapter-at-a-Glance

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Learning Objectives

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Brief Chapter Outline

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Teaching Outline

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Lecture Launchers

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Activities

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Assignments

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Web Links

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Handouts

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Chapter 16: Lateralization, Language, and the Split Brain

CHAPTER-AT-A-GLANCE Brief Outline Chapter Introduction (p. 418) 16.1 Cerebral Lateralization of Function: Introduction (pp. 419–421) 16.2 The Split Brain (pp. 421–428) 16.3 Differences between Left and Right Hemispheres (pp. 428–432) 16.4 Evolutionary Perspective of Cerebral Lateralization and Language (pp. 432–436) 16.5 Cortical Localization of Language: Wernicke-Geschwind Model (pp. 436–438) 16.6 Wernicke-Geschwind Model: The Evidence (pp. 438–442) 16.7 Cognitive Neuroscience of Language (pp. 442–445) 16.8 Cognitive Neuroscience of Dyslexia (pp. 445–447)

Instructor’s Manual Resources Lecture Launcher 16.1, Assignment 16.1 Lecture Launcher 16.2 Lecture Launchers 16.4, 16.5

Lecture Launcher 16.3, Activity 16.1

< Return to Table of Contents

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Biopsychology, Tenth Edition

LEARNING OBJECTIVES After completion of this chapter, the student should be able to: LO 16.1 LO 16.2 LO 16.3 LO 16.4 LO 16.5 LO 16.6 LO 16.7 LO 16.8 LO 16.9 LO 16.10 LO 16.11 LO 16.12 LO 16.13 LO 16.14 LO 16.15 LO 16.16 LO 16.17 LO 16.18 LO 16.19 LO 16.20

LO 16.21 LO 16.22 LO 16.23 LO 16.24 LO 16.25 LO 16.26 LO 16.27 LO 16.28

Summarize early studies of the cerebral lateralization of function.

Describe three techniques for assessing cerebral lateralization of function.

Outline the discovery of the relationship between speech laterality and handedness.

Describe and evaluate the hypothesis that male brains are more lateralized than female brains.

Outline the groundbreaking experiment of Myers and Sperry on split-brain cats.

Describe the method used to demonstrate the hemispheric independence of visual experience in human split-brain patients.

Describe the evidence that indicates that the hemispheres of split-brain patients can function independently.

Outline the process of cross-cuing in split-brain patients.

Describe the helping-hand phenomenon and the use of the chimeric figures test in experiments on split-brain patients.

Explain the Z lens and how it was used to study split-brain patients.

Describe a case where the right hemisphere tried to take control of a split-brain patient’s everyday behavior.

Explain how complete hemispheric independence is not an inevitable consequence of splitbrain surgery.

Describe five examples of abilities that have been found to be lateralized, and explain what is meant by the “left hemisphere interpreter.”

Discuss how we’ve come to understand that the lateralization of function is better understood in terms of individual cognitive processes rather than clusters of abilities.

Describe three anatomical asymmetries in the human brain.

Describe and evaluate three theoretical explanations for why cerebral lateralization of function evolved.

Outline how cerebral lateralization evolved.

List two survival advantages of cerebral lateralization.

Describe what the study of nonhuman primates has suggested about the evolution of human language.

Describe the historical antecedents of the Wernicke-Geschwind model. Include descriptions of the following disorders: Broca’s and Wernicke’s aphasia, conduction aphasia, agraphia, and alexia.

Describe the Wernicke-Geschwind model.

Identify the effects of cortical damage and brain stimulation on language abilities, and evaluate the Wernicke-Geschwind model in light of these findings.

Summarize the current status of the Wernicke-Geschwind model.

Describe the three premises that define the cognitive neuroscience approach to language, and compare them with the premises on which the Wernicke-Geschwind model is based.

Describe two influential functional imaging studies of the localization of language, and explain what their findings indicate.

Describe the causes and neural mechanisms of developmental dyslexia.

Describe research that helped discredit the notion that dyslexia could not be a brain disorder because it is influenced by culture.

Describe the difference between the lexical procedure and the phonetic procedure for reading aloud. Then describe the difference between surface dyslexia and deep dyslexia.

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Chapter 16: Lateralization, Language, and the Split Brain

BRIEF CHAPTER OUTLINE Lecture Launcher 16.1: The Dichotic Listening Test 1. Cerebral Lateralization of Function: Introduction a. Discovery of the Specific Contributions of Left Hemisphere Damage to Aphasia and Apraxia b. Tests of Cerebral Lateralization c. Discovery of the Relation Between Speech Laterality and Handedness d. Sex Differences in Brain Lateralization Lecture Launcher 16.2: What’s It Like to Have a Split Brain?

2. The Split-Brain a. Groundbreaking Experiment of Myers and Sperry b. Commissurotomy in Humans with Epilepsy c. Evidence that the Hemispheres of Split-Brain Patients Can Function Independently d. Cross-Cuing e. Doing Two Things at Once f. The Z Lens g. Dual Mental Functioning and Conflict in Split-Brain Patients h. Independence of Split Hemispheres: Current Perspective 3. Differences Between Left and Right Hemispheres a. Examples of Cerebral Lateralization of Function b. What Is Lateralized—Broad Clusters of Abilities or Individual Cognitive Processes? c. Anatomical Asymmetries of the Brain 4. Evolutionary Perspective of Cerebral Lateralization and Language a. Theories of the Evolution of Cerebral Lateralization b. When Did Cerebral Lateralization Evolve? c. What Are the Survival Advantages of Cerebral Lateralization? d. Evolution of Human Language 5. Cortical Localization of Language: Wernicke-Geschwind Model a. Historical Antecedents of the Wernicke-Geschwind Model b. The Wernicke-Geschwind Model 6. Wernicke-Geschwind Model: The Evidence a. Effects of Cortical Damage and Brain Stimulation on Language Abilities b. Current Status of the Wernicke-Geschwind Model 7. Cognitive Neuroscience of Language a. Three Premises That Define the Cognitive Neuroscience Approach to Language b. Functional Brain Imaging and the Localization of Language Lecture Launcher 16.3: Living with Dyslexia

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Biopsychology, Tenth Edition 8. Cognitive Neuroscience of Dyslexia a. Developmental Dyslexia: Causes and Neural Mechanisms b. Developmental Dyslexia and Culture c. Cognitive Neuroscience of Deep and Surface Dyslexia < Return to Table of Contents

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Chapter 16: Lateralization, Language, and the Split Brain

TEACHING OUTLINE 1. Cerebral Lateralization of Function: Introduction (see Figure 16.2 in Biopsychology) In 1836, Dax, an unknown country doctor, reported that not one of his forty or so patients with speech problems had displayed damage restricted to the right hemisphere; his report attracted no interest. a. Discovery of the Specific Contributions of Left-Hemisphere Damage to Aphasia and Apraxia LO 16.1 Summarize early studies of the cerebral lateralization of function.

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Twenty-five years later, Broca reported the results of the postmortem examination of two aphasic patients (patients with deficits in the use of language that are not attributable to general sensory, motor, or intellectual dysfunction); both had diffuse left hemisphere damage that seemed to be centered in an area of the inferior left prefrontal lobe, just in front of the primary motor face area.

In the next few years, Broca examined seven more brains of deceased aphasic patients; all had damage that included the same left frontal area, which became known as Broca’s area.

Subsequently, Liepmann discovered that apraxia (difficulty performing movements with either side of the body when asked to do so, but not when performing them spontaneously) was almost always associated with left hemisphere damage.

This led to the view that the left hemisphere performed all complex activities; the left and right hemispheres thus became known as the dominant and minor hemispheres, respectively.

b. Tests of Cerebral Lateralization LO 16.2 Describe three techniques for assessing cerebral lateralization of function.

The first evidence of language laterality came from comparisons of the effects of left and right unilateral lesions; today, the sodium amytal test and the dichotic listening test are commonly used to assess language laterality.

Sodium Amytal Test • The sodium amytal test is administered to patients prior to neurosurgery, so that the surgeon knows the side of speech lateralization and can take special care to avoid damaging the language areas.

• A small amount of sodium amytal is injected into one carotid artery; this anesthetizes the ipsilateral hemisphere and allows the abilities of the contralateral hemisphere to be assessed.

• When the injection is made on the side of the dominant speech hemisphere (usually the left), the patient is totally mute for a minute or two, and as the ability to talk returns, the patient makes speech errors (e.g., errors of naming and serial order).

• When the injection is on the side of the nondominant speech hemisphere (usually the right), there is no mutism and only a few speech errors.

Dichotic Listening Test • In the conventional form of the dichotic listening test, a sequence of three pairs of digits is presented through earphones; the two digits of each pair are presented simultaneously, one digit to each ear.

• When the subject is asked to report the six digits that she or he has heard, there is a slight, but consistent, tendency to report more of the digits presented to the ear contralateral to the dominant language hemisphere (usually the right ear).

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Biopsychology, Tenth Edition Functional Brain Imaging PET or fMRI techniques have revealed that there is typically more activity in the left hemisphere than the right during language-related activities. c. Discovery of the Relation Between Speech Laterality and Handedness LO 16.3 Outline the discovery of the relationship between speech laterality and handedness.

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In individuals with brain damage about 60% of dextrals (right-handers with left-hemisphere lesions) and 2% of those with right-hemisphere lesions were diagnosed with aphasia. Sinestrals (left-handers) were about 30% and 24% respectively. This indicates that the left-hemisphere is dominant for language.

Many studies have reported a relationship between speech laterality and handedness; the following general conclusions have been reached: • Nearly all (about 92%) right-handed subjects are left-hemisphere dominant for speech; • Most left-handed or ambidextrous subjects (about 69%) are also left-hemisphere dominant for speech; and • Early left-hemisphere damage can cause the right hemisphere to become dominant for speech and the left hand to be preferred. d. Sex Differences in Brain Lateralization LO 16.4 Describe and evaluate the hypothesis that male brains are more lateralized than female brains.

There is some evidence (from studies of unilateral strokes) that the brain is more lateralized in males than in females, although the data are hardly unequivocal.

2. The Split-Brain (see Figures 16.1, 16.3–16.7 in Biopsychology) a. Groundbreaking Experiment of Myers and Sperry LO 16.5 Outline the ground-breaking experiment of Myers and Sperry on split-brain cats.

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In 1953, Myers and Sperry performed an experiment on cats that changed the way that we think about the brain, and it provided a means of comparing the functions of the two hemispheres.

It was an experiment designed to reveal the function of the brain’s largest commissure, the corpus callosum.

The corpus callosum is the largest tract in the human brain, contains approximately 200 million axons, and is the highest level at which the two cerebral hemispheres are connected.

On the basis of its size and location, one would think that severing it would have devastating consequences; however, many earlier studies had failed to reveal any deficits in laboratory animals following callosal transection, and people born without a corpus callosum had been reported to be perfectly normal (leading some neuroscientists to joke that its job was to keep the cortex out of the ventricles). Sperry was intrigued by the paradox.

In 1953, Myers and Sperry published a groundbreaking paper that solved this apparent paradox.

In their experiment, there were four groups of cats: (1) corpus callosum severed, (2) optic chiasm severed, (3) corpus callosum and optic chiasm severed, and (4) intact controls.

In Phase 1 of the experiment, all cats learned a lever-press pattern discrimination task with a patch over one eye; all four groups readily learned this simple task.

In Phase 2, the patch was switched to the other eye; the cats in the optic-chiasm-severed group, in the corpus-callosum-severed group, and in the control group kept performing at close to 7 ..

Chapter 16: Lateralization, Language, and the Split Brain

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100% when the patch was shifted; in contrast, the cats with both their optic chiasms and corpus callosums severed, acted as if the task were completely new to them—they had to learn it again with no savings.

Myers and Sperry concluded: – The cat forebrain has the capacity to act as two separate forebrains, each capable of independent learning and of storing its own memories; – The function of the corpus callosum is to carry information between hemispheres; and – The best strategy for studying corpus callosum function is to use a method to limit information to a single hemisphere (e.g., by cutting the optic chiasm and blindfolding one eye).

b. Commissurotomy in Humans with Epilepsy LO 16.6 Describe the method used to demonstrate the hemispheric independence of visual experience in human split-brain patients.

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Commissurotomy is performed on patients with life-threatening cases of epilepsy to reduce the severity of convulsions by restricting epileptic discharges to half the brain.

The operation is remarkably effective; many commissurotomized epileptic patients never experience another major convulsion. More remarkably, they experience few obvious side effects in their daily lives.

The controlled neuropsychological testing of these split-brain patients has revealed some amazing things about the human brain; Sperry and Gazzaniga conducted the testing of the initial series of patients.

To test split-brain patients, visual stimuli were flashed (to eliminate the effect of eye movement) on a screen to the left or right of a fixation point for 0.1 seconds (contrast this method of limiting visual input to one hemisphere with the method used by Myers and Sperry in cats).

Tactual information was presented to one hand under a ledge or in a bag to prevent visual scanning of the objects; responses were either verbal responses or manual responses performed by one hand or the other under a ledge.

Amazingly, these tests confirmed the provocative conclusions of the experiments on split-brain laboratory animals in showing that the commissurotomized patients had two independent streams of consciousness; however, unlike split-brain laboratory animals, the two hemispheres of commissurotomized patients were not equal; e.g., the left hemisphere could speak, but the right could not.

If you are having difficulty understanding these results because you are used to thinking of yourself as an indivisible entity, think of each person as two subjects: (1) Mr. or Ms. Right Hemisphere who understands a few simple instructions but cannot speak, who receives sensory information from the left visual field and left hand, and who controls the fine motor responses of the left hand; and (2) Mr. or Ms. Left Hemisphere who understands complex speech and can speak, who receives sensory information from the right-visual field and right hand, and who controls the fine motor responses of the right hand.

c. Evidence That the Hemispheres of Split-Brain Patients Can Function Independently LO 16.7 Describe the evidence that indicates that the hemispheres of split-brain patients can function independently.

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When an object was presented to the left hemisphere, either by touching with the right hand or by viewing something in the right visual field, the subject: 1) could pick out the correct 8 ..

Biopsychology, Tenth Edition

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object with the right hand; 2) could not pick out the correct object with the left hand; and 3) could name the correct object.

When an object was presented to the right hemisphere, either by touching with the left hand or by viewing something in the left visual field, the subject: 1) could pick out the correct object with the left hand, 2) could not pick out the correct object with the right hand, 3) claimed nothing had been presented.

d. Cross-Cuing LO 16.8 Outline the process of cross-cuing in split-brain patients.

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Cross-cuing represents communication between hemispheres via a nonneural route.

For example, in one test, a red or a green light was flashed in the left visual field; the split-brain patient was then asked to name the color: red or green.

Most split-brain patients get 50% correct on this task; however, one patient eventually developed the ability to perform almost perfectly.

When the performance of this subject was carefully observed, it was noticed that on the trials when the patient initially said (the left hemisphere) the incorrect color, his head shook, and the patient then changed his guess to the other, correct color; apparently, the right hemisphere (which knew the correct answer) heard the incorrect guess of the left hemisphere, and signaled to the left hemisphere that it was wrong by shaking the person’s head; when only first guesses were counted, performance immediately fell to 50%.

e. Doing Two Things at Once LO 16.9 Describe the helping-hand phenomenon and the use of the chimeric figures test in experiments on split-brain patients.

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Split-brain patients are capable of learning two things at once.

If a split-brain patient is visually presented with two objects at the same time—let’s say a pencil in the left visual field and an apple in the right—she or he can reach into two different bags at the same time, one with each hand, and pull out the two objects—a pencil in the left hand and an apple in the right.

What would a split-brain subject say in this example if she were asked what she had in her hands before withdrawing them from the bags? (“Two apples.”)

An interesting phenomenon, called the helping-hand phenomenon, occurs when the two hemispheres are presented with different information about the correct choice and then are asked to reach out and pick up the correct object from a collection in full view.

Usually the right hand will reach out to pick out what the left hemisphere saw (i.e., the apple in our previous example), but the right hemisphere, seeing what it thinks is an error being made, causes the left hand to grab the right hand and pull it over to the other object (i.e., the pencil in our previous example).

Another example of the split-brain’s ability to do two things at once involves the phenomenon of visual completion.

The ability of the hemispheres of split-brain patients to engage simultaneously and independently engage in completion has been demonstrated in studies using the chimeric figures test—named after chimera, a mythical monster composed of parts of different animals.

Levy, Trevarthen, and Sperry flashed photographs composed of fused-together half-faces of two different people onto the center of a screen in front of split-brain patients (see Figure 16.6).

The patients were asked to describe what they saw or to indicate by pointing to it a series of photographs of intact faces.

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Chapter 16: Lateralization, Language, and the Split Brain • •

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Each patient reported seeing a compete, bilaterally symmetrical face, even when asked such leading questions as “Did you notice anything peculiar about what you just saw?”

When the patient was asked to describe what they saw, they usually described a completed version of the half that had been presented to the right visual field (the left hemisphere).

The Z Lens LO 16.10 Explain the Z lens and how it was used to study split-brain patients.

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Early studies of lateralization of function were limited by the fact that visual stimuli requiring more than .1 second to perceive could not be studied using the conventional methods.

Zaidel eliminated this methodological barrier by developing a lens, called the z lens, that limits visual input to one hemisphere of split-brain patients while they scan complex visual material.

It is a contact lens that is opaque on one side; it moves with the eye, permitting visual input to enter only one hemisphere, irrespective of eye movement.

g. Dual Mental Functioning and Conflict in Split-Brain Patients LO 16.11 Describe a case where the right hemisphere tried to take control of a split-brain patient’s everyday behavior.

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In most split-brain patients, the left hemisphere seems to control activities.

However, in a few cases there can be serious conflicts between the left and right hemispheres, when the right hemisphere takes on a more active role.

One such patient, Peter, unlike most other split-brain patients, was not able to respond with the left side of his body to verbal input.

Apparently, his left hemisphere could not control the left side of his body via ipsilateral fibers.

In the lab, his left hemisphere sometimes became angry with his left hand, trying to force it with his right hand to do what his left hemisphere wanted.

h. Independence of Split Hemispheres: Current Perspective LO 16.12 Explain how complete hemispheric independence is not an inevitable consequence of split-brain surgery.

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Interestingly, the emotional content of images presented to the right hemisphere was reflected in patients’ speech, as well as in their nonverbal behavior.

Emotional information is somehow passed from the right hemisphere to the left.

Also, as tasks become more difficult, they are more likely to involve both hemispheres of splitbrain patients.

This finding is important for two reasons: It complicates the interpretation of brain-imaging studies of lateralization of function—if tasks are difficult, both hemispheres show activity, even though one hemisphere is specialized for that task. Second, it explains why the elderly often display less lateralization of function; with aging, neural responses decline, and both hemispheres become involved in a task.

3. Differences Between Left and Right Hemispheres (see Table 16.1 and Figures 16.8 and 16.9 in Biopsychology) a. Examples of Cerebral Lateralization of Function LO 16.13 Describe five examples of abilities that have been found to be lateralized, and explain what is meant by the “left hemisphere interpreter.”

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Language is the most lateralized of all abilities. The left hemisphere is better than the right at all language-related tasks; however, the right hemisphere proved to be able to understand written and spoken words and simple grammatical principles. The various language abilities of the right hemisphere proved to be comparable to those of a normal preschool-aged child.

Table 16.1 lists some abilities that are often found to be lateralized.

Superiority of Left Hemisphere in Controlling Ipsilateral Movement • The left hemisphere has also proven to be better at controlling ipsilateral body movements.

• Left-hemisphere lesions are more likely to produce ipsilateral motor problems.

Superiority of Right Hemisphere in Spatial Ability The right hemisphere proved better than the left at tasks involving spatial ability (e.g., block designs subtest of the WAIS; stereognosis).

Specialization of the Right Hemisphere for Emotion The right hemisphere is also superior in processing emotional stimuli—for example, in accurately identifying facial expressions of emotion.

Superior Musical Ability of Right Hemisphere • The right hemisphere is specialized for musical tasks (the perception of melodies).

• This is consistent with the findings that right temporal lobe lesions are more likely to disrupt musical discriminations than are left temporal lobe lesions.

Hemispheric Differences in Memory • Finally, the two hemispheres seem to engage different types of memory processing; the left hemisphere plays a greater role in verbal memory, while the right hemisphere plays the greater role in nonverbal memory.

• Thus, the right hemisphere should not be regarded as the minor hemisphere; it has different abilities, not less important ones.

• It is critical to keep in mind the idea that complex clusters of cognitive abilities (e.g., language) are NOT lateralized; instead, the constituent cognitive processes that underlie complex cognitive functions seem to be lateralized to one or the other hemisphere of the brain.

The Left-Hemisphere Interpreter • The left and right hemisphere approach tasks in different ways.

• The left hemisphere is referred to as the interpreter—a hypothetical neuronal mechanism that continuously assesses patterns of events and tries to make sense of them. b. What Is Lateralized—Broad Clusters of Abilities or Individual Cognitive Processes?

LO 16.14 Discuss how we’ve come to understand that the lateralization of function is better understood in terms of individual cognitive processes rather than clusters of abilities.

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Early theories of cerebral lateralization ascribed complex clusters of mental abilities to one hemisphere or the other. This conclusion is too simplistic.

The problem is that categories such as language, emotion, musical ability, and spatial ability are each composed of dozens of different individual cognitive activities, and you cannot assume that all those activities will be lateralized in the same hemisphere.

Exceptions to all broad categories of cerebral lateralization have emerged.

Researchers are now basing their studies on the work of cognitive psychologists, who have broken down complex cognitive tasks into their constituent cognitive processes.

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Chapter 16: Lateralization, Language, and the Split Brain •

Once the laterality of the individual cognitive element has been determined, it is possible to predict the laterality.

c. Anatomical Asymmetries of the Brain LO 16.15 Describe three anatomical asymmetries in the human brain.

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Documenting anatomical differences is complex since there are large individual differences, no clear boundaries around cortical areas, and no consensus on how to define them.

Anatomical asymmetries have been found in the planum temporale, Heschl’s gyrus, and the frontal operculum.

All of these are language-related areas and might be expected to be larger in the left hemisphere, but in fact this is not so. Only the planum temporale is larger on the left.

Heschl’s gyrus is usually larger on the right.

The laterality of the frontal operculum is less clear.

The pattern of anatomical asymmetries is weakly correlated with language lateralization but should not be interpreted as indicating a cause-effect relationship.

There is also evidence that the cortical microcircuitry differs between comparable areas of the left and right hemispheres, suggesting that cerebral asymmetry is expressed down to the level of how neurons communicate with one another.

In musicians with perfect pitch the planum temporale is much larger in the left hemisphere than the right hemisphere.

4. Evolutionary Perspective of Cerebral Lateralization and Language a. Theories of the Evolution of Cerebral Lateralization LO 16.16 Describe and evaluate three theoretical explanations for why cerebral lateralization of function evolved.

Why has cerebral asymmetry evolved? Three main theories have tried to account for cerebral asymmetry: Analytic-Synthetic Theory • This theory suggests that there are two fundamentally different modes of thinking: an analytic mode and a synthetic mode, and that the neural circuitry for each is fundamentally different.

• As a result, the two kinds of circuits are presumed to have become segregated during evolution, the analytic mode in the left hemisphere and the synthetic mode in the right.

• The left hemisphere, according to this theory, operates in a logical, sequential, analytic fashion; the right hemisphere makes immediate, overall synthetic judgments.

• This theory has become very popular in psychology, however, its vagueness is difficult to empirically test.

Motor Theory • Motor theory posits that the left hemisphere is specialized for fine motor movement, of which speech is but one example.

• Two lines of evidence support this theory: (1) lesions of the left hemisphere disrupt facial movements more than do right hemisphere lesions, even when they are not related to speech; (2) the degree of disruption of nonverbal facial movements is positively correlated with the degree of aphasia.

• A problem with this theory is that it does not suggest why motor function became lateralized in the first place.

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Linguistic Theory This is based on the idea that the primary function of the left hemisphere is language, and on studies of deaf people who communicate using American Sign Language; this ability is lost if these people suffer damage to the left hemisphere, even when they are able to make the movements required. b. When Did Cerebral Lateralization Evolve?

LO 16.17 Outline how cerebral lateralization evolved.

It has been suggested that lateralization of function may have been present when vertebrates emerged about 425 million years ago. And, lateralization of function may occur in invertebrates. c. What Are the Survival Advantages of Cerebral Lateralization?

LO 16.18 List two survival advantages of cerebral lateralization.

• •

It may be more efficient for the neurons performing a particular function to be concentrated in one hemisphere.

Two different kinds of cognitive processes may be more readily performed simultaneously if they are lateralized to different hemispheres.

d. Evolution of Human Language LO 16.19 Describe what the study of nonhuman primates has suggested about the evolution of human language.

• •

At 10 months of age, infants say little, but 30-month-old infants speak a great deal.

At 10 months, human infants can distinguish the sounds of all human languages, but by 30 months, they can readily discriminate only those sounds that compose their own language.

Vocal Communication in Nonhuman Primates • The left hemisphere plays a dominant role in birdsong, and the left hemispheres of dogs and monkeys have been found to be dominant in the perception of conspecific calls.

• There is typically a substantial difference between vocal production and auditory comprehension.

• Even the most vocal nonhumans can produce a few calls, yet they are capable of interpreting a wide range of sounds.

• This suggests that vocal language may be limited because of the inability to exert fine motor control over their voices.

Motor Theory of Speech Perception • The motor theory of speech perception proposes that the perception of speech depends on the words activating the same neural circuits in the motor system that would be activated if the listener said those words.

• Many brain-imaging studies have revealed activity in the primary and secondary motor cortex during language comprehension tests that do not involve language expression.

• Transcranial magnetic stimulation of the motor cortex administered while volunteers listened to syllables and words resulted in disruption of the perception of the syllables and words.

Gestural Language The gestures of chimps were much more like a human language than were their vocalizations.

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Chapter 16: Lateralization, Language, and the Split Brain 5. Cortical Localization of Language: Wernicke-Geschwind Model (see Figures 16.10 and 16.11 in Biopsychology) a. Historical Antecedents of the Wernicke-Geschwind Model LO 16.20 Describe the historical antecedents of the Wernicke-Geschwind model. Include descriptions of the following disorders: Broca’s and Wernicke’s aphasia, conduction aphasia, agraphia, and alexia.

• • •

• • •

In 1864, Broca hypothesized that the inferior portion of the left prefrontal lobe (Broca’s area) is the center of speech production; he suggested that Broca’s area controls the area of primary motor cortex that controls the muscles of the face and oral cavity.

In 1874, Wernicke concluded on the basis of ten clinical cases that the area in the left temporal lobe just posterior to the primary auditory cortex is another important language area; it became known as Wernicke’s area.

Wernicke’s area was hypothesized by Wernicke to play a role in language comprehension; Wernicke claimed that damage to Broca’s area produces aphasia that is primarily expressive (no deficits in language comprehension and speech that is meaningful, but slow, labored, disjointed, and poorly articulated).

By contrast, damage to Wernicke’s area was hypothesized to produce aphasia that is primarily receptive (deficits in language comprehension and speech that has the structure, rhythm, and intonation of real speech, but is incomprehensible—a word salad).

Wernicke also argued that damage to the left arcuate fasciculus, which connects Broca’s and Wernicke’s areas, should produce aphasia characterized by a difficulty in repeating words that were heard; he called this third hypothetical form of aphasia conduction aphasia.

Dejerine later proposed that damage to the left angular gyrus would also produce language deficits—alexia (inability to read) and agraphia (inability to write)—because such damage disconnected visual cortex from the rest of the left hemisphere.

b. The Wernicke-Geschwind Model LO 16.21 Describe the Wernicke-Geschwind model.

• •

•

The seven components of the Wernicke-Geschwind model are: primary visual cortex, angular gyrus, primary auditory cortex, Wernicke’s area, arcuate fasciculus, Broca’s area, and primary motor cortex.

When you are having a conversation, the auditory signals triggered by the speech of the other person are received by your primary auditory cortex and conducted to Wernicke’s area, where they are comprehended. If a response is in order, Wernicke’s area generates the neural representation of the thought underlying the reply, and it is transmitted to Broca’s area via the arcuate fasciculus. This signal activates the appropriate program of articulation that drives your primary motor cortex and the muscles of articulation.

When you are reading aloud, the signal received by your primary visual cortex is transmitted to your left angular gyrus, which translates the visual form of the word into its auditory code and transmits it to Wernicke’s area for comprehension. Wernicke’s area then triggers the appropriate responses in your arcuate fasciculus, Broca’s area, and motor cortex, respectively, to elicit the appropriate speech sounds.

6. Wernicke-Geschwind Model: The Evidence (see Figures 16.12–16.15 in Biopsychology) a. Effects of Cortical Damage on Language Abilities

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Biopsychology, Tenth Edition LO 16.22 Identify the effects of cortical damage and brain stimulation on language abilities, and evaluate the Wernicke-Geschwind model in light of these findings.

Evidence from Studies of the Effects of Cortical Damage • Patients with surgical lesions are particularly useful for such studies because the site of their lesion is well-known.

• In addition, patients rendered aphasic by accidental brain damage almost always have extensive subcortical damage, which leads to widespread degeneration and makes firm localizationist interpretations difficult, but this is less of a problem with surgical lesions of the cortex.

• Several large-scale studies of the language-related deficits experienced by patients with surgical lesions to different areas of the cortex have been conducted; the following are their conclusions: – Lesions that destroy Broca’s area, but little surrounding tissue, have no permanent effect on language-related abilities (there are temporary problems that develop a few hours after the operation and disappear in several days, which are presumably the result of edema); – Discrete lesions that cut through the left arcuate fasciculus or angular gyrus produce no permanent aphasia; – Because of the dire predictions of the Wernicke-Geschwind model, Wernicke’s area has rarely been totally removed, but there are some cases in which large portions of it have been removed with little permanent effect.

• Supporters of the Wernicke-Geschwind model discount the data from surgical-lesion studies; they argue that the cortical organization of patients requiring neurosurgery is abnormal.

• Several independent studies have assessed the degree to which the Wernicke-Geschwind model can account for the effects of nonsurgical brain damage; this is exactly the type of evidence on which the model was based.

• The best of these studies have included only cases in which the location of the damage was confirmed by subsequent postmortem examination or visual inspection during surgery.

• For example, a study by Hécaen and Angelergues (1964) assessed the performance on several objective tests of speech production, speech comprehension, and reading performed by 214 right-handed patients whose brain damage was located during a subsequent operation or a postmortem examination.

• They found that: (1) lesions restricted to Broca’s area seldom produced lasting deficits, whereas those restricted to Wernicke’s area sometimes did not; (2) no case was observed that was purely expressive (Broca’s aphasia) or purely receptive (Wernicke’s aphasia); and (3) extremely large (involving three lobes) anterior lesions of the left hemisphere tended to produce more expressive symptoms than receptive symptoms, and the opposite was true of very large posterior lesions.

Evidence from Functional Neuroimaging Studies • No aphasic patients have damage restricted to Broca’s area or Wernicke’s area • Aphasic patients almost always have significant damage to subcortical white matter.

• Large anterior lesions are more likely to produce expressive symptoms, whereas large posterior lesions are more likely to produce receptive symptoms.

• Global aphasia is usually related to massive lesions of anterior cortex, posterior cortex, and underlying white matter.

• Aphasic patients sometimes have brain damage that does not encroach on the WernickeGeschwind areas-aphasia has been observed in patients with visible damage to only the medial frontal lobe, subcortical white matter, basal ganglia, or thalamus.

Evidence from Electrical Stimulation to the Cortex 15 ..

Chapter 16: Lateralization, Language, and the Split Brain •

•

• •

•

In the 1940s, Penfield and his colleagues were the first to stimulate the brains of conscious human patients during brain surgery; at some sites the stimulation disrupted various speechrelated activities. This suggested that brain stimulation might be a valuable method for mapping the language areas of the cortex; stimulation produces a much more local disruption than a brain lesion.

In 1959, Penfield and Roberts reported the results obtained from over ten years of research; they found that: 1) aphasia-like responses to right-hemisphere stimulation were rare; 2) each deficit was produced by stimulation of sites scattered throughout much of the left hemisphere; and 3) there was no apparent tendency for the stimulation of Broca’s area to produce deficits different from those produced by stimulation of Wernicke’s area.

More recently, Ojemann (1983) assessed naming, reading of simple sentences, short-term verbal memory, ability to mimic orofacial movements, and the ability to recognize phonemes (units of sound) during cortical stimulation.

He found that: 1) sites at which stimulation could disrupt language extended beyond the Wernicke-Geschwind language areas; 2) all of the specific language abilities were represented in anterior and posterior sites; and 3) there were major differences across subjects in the organization of language abilities.

Based on his work, Ojemann has suggested that the language cortex is organized like a mosaic, with the discrete columns of tissue performing a particular function distributed widely throughout the language areas of the cortex.

b. Current Status of the Wernicke-Geschwind Model LO 16.23 Summarize the current status of the Wernicke-Geschwind model.

• •

Research has supported the model’s tenets that Broca’s area and Wernicke’s area are important to language, and that expressive aphasias are generally associated with anterior damage, whereas receptive aphasias are more often associated with posterior damage.

Little else of the Wernicke-Geschwind model has been supported; however, the model did guide research and clinical diagnosis in the area for almost forty years. This research led to a new approach to the study of language.

7. Cognitive Neuroscience of Language (see Figure 16.16 in Biopsychology) a.

Three Premises That Define the Cognitive Neuroscience Approach to Language LO 16.24 Describe the three premises that define the cognitive neuroscience approach to language, and compare them with the premises on which the Wernicke-Geschwind model is based.

The cognitive neuroscience approach to language is guided by three premises: • Premise 1: Language can be broken down into constituent cognitive processes that are much simpler than the cognitive activities that Geschwind (and others) tried to localize to a single part of the brain; these constituent processes include phonological analysis (analysis of sounds of language), grammatical analysis (analysis of language’s structure), and semantic analysis (analysis of the meaning of language).

• Premise 2: Areas of the brain involved in language are not exclusively involved with that function; for example, areas involved with reading might also be involved with functions like short-term memory or pattern recognition.

• Premise 3: The brain areas involved with language are small and widely distributed. b. Functional Brain Imaging and the Localization of Language 16 ..

Biopsychology, Tenth Edition LO 16.25 Describe two influential functional imaging studies of the localization of language, and explain what their findings indicate.

• •

Brain-imaging studies have revolutionized the study of the neural bases of language.

Numerous fMRI and PET studies have been particularly influential.

Bavelier’s fMRI Study of Reading For example, Bavelier and colleagues used a very sensitive fMRI to study the activity of the brain during periods of silent reading; they found: 1) that only small areas are activated at a given time in a single subject; 2) that these areas vary from subject to subject and also within a single subject from trial to trial; 3) that the activity was spread over very large areas of the brain; 4) that the active areas were more often in the left hemisphere than the right; and 5) that the activity spread far beyond those areas predicted by the Wernicke-Geschwind model.

Damasio’s PET Study of Naming • By contrast, Damasio and colleagues used PET to study brain activity in the left temporal lobes while a person named objects within particular categories; they found that the activated area varied as the category changed, although it was typically somewhere along the anteriorposterior extent of the middle of the left temporal lobe.

• It is important to remember lesion data showing that right hemisphere damage rarely disrupts language activity; thus, while imaging studies show that this hemisphere is active during language tasks, its role in language cannot be critical.

8. Cognitive Neuroscience of Dyslexia Dyslexia is an inability to read or write despite normal or superior intelligence; it may be developmental or acquired. It is a common disorder, affecting about 5-12% of children. It affects males 2-3 times more often than females. a. Developmental Dyslexia: Causes and Neural Mechanisms LO 16.26 Describe the causes and neural mechanisms of developmental dyslexia.

• • • •

There appears to be a genetic component, as it has a heritability estimate of about 0.5; in addition, some neural abnormalities are often present in dyslexics, although none have been convincingly linked to the disorder itself.

Dyslexics often display subtle sensory and motor deficits; the role of these deficits in dyslexia remains unclear.

Dyslexic children exhibit reduced fMRI activity in their left parietal and left occipito-temporal cortices.

There is widespread agreement that dyslexia results from a disturbance in phonological processing, not a disturbance of sensorimotor functioning.

b. Developmental Dyslexia and Culture LO 16.27 Describe research that helped discredit the notion that dyslexia could not be a brain disorder because it is influenced by culture.

Dyslexia has a cultural component; for example, English speakers are twice as likely to be dyslexic as Italian speakers. Researchers believe that this is due to the complexity of English relative to Italian; PET studies have shown that Italian readers displayed more activity in the left superior temporal lobe, whereas English readers displayed more activity in the left inferior temporal and frontal lobes.

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Chapter 16: Lateralization, Language, and the Split Brain

c. Cognitive Neuroscience of Deep and Surface Dyslexia LO 16.28 Describe the difference between the lexical procedure and the phonetic procedure for reading aloud. Then describe the difference between surface dyslexia and deep dyslexia.

• Cognitive researchers have found two strategies for reading: a lexical procedure, used when material is familiar; and a phonetic procedure, used when the words are novel.

• These two strategies led to a better understanding of the two main types of dyslexia produced by brain damage: surface dyslexia occurs when patients lose their lexical skills, whereas deep dyslexia occurs when patients lose their phonetic reading skills.

• Interestingly, deep dyslexics most often have damage to the left hemisphere language areas, suggesting that the phonetic skills are distributed widely over the frontal and temporal lobes of the left hemisphere. < Return to Table of Contents

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LECTURE LAUNCHERS Lecture Launcher 16.1: The Dichotic Listening Test You can demonstrate this classical test for cerebral asymmetry using the simulation available at https://www.millisecond.com/. Place “dichotic listening” in the search bar. Select the link to “Dichotic Listening Task.” To do this, you will need a computer and sound system in your classroom; you can run the simulation from your computer by downloading the software. The demonstration should be done using headphones for your subject; allow the rest of the classroom to hear the monosyllables and watch the student demonstrator respond. The results are graphed at the end of the simulation.

Lecture Launcher 16.2: What’s It Like to Have a Split Brain?

You can demonstrate some of the “disconnection” experienced by patients who have undergone the splitbrain surgery using a video located on http://www.scienceblogs.com. Place “What’s it like to have your brain split in half” in the search bar. Select the matching link that will lead you to a video featuring Michael Gazzaniga. Have students reflect on what things would change in their lives if they had the split-brain procedure.

Lecture Launcher 16.3: Living with Dyslexia It is often the case that students cannot identify with some of the problems that dyslexics experience when trying to read even the simplest passage. After introducing the topic of dyslexia, you can give your students a better idea of how people with dyslexia struggle with reading problems by asking them to participate in at least one of the simulations available from the Jarmin Demos page. Place “Jarmin Demos” in your favorite browser and select the link titled “Project – Module: Dyslexia.”

Lecture Launcher 16.4: Language “Center” of Brain Shifts with Age Maybe handedness and lateralization of language are not as definite as was thought? From childhood until about age 25, language capacity in right-handers grows stronger in the left hemisphere of the brain. This is usually related to a person’s “handedness,” where a right-handed person holds language in the left hemisphere, and vice versa. Using functional magnetic resonance imaging (fMRI), researchers have now shown that after about age 25, language capacity “evens out” somewhat, with older adults using more of both hemispheres relative to language skills.

Web Link 16.3 Language “Center” of Brain Shifts with Age Lecture Launcher 16.5: Case Studies Case studies are always a great way to begin a lecture. Stories are both interesting and memorable. This case study book can provide examples to be used to emphasize many of the phenomena referred to in the text.

References Classic Cases in Neuropsychology II (Brain Damage, Behaviour, and Cognition), Code, C., Wallesch, C.W. Joanette, Y. & Roch Lecours, A. (2001). Classic Cases in Neuropsychology II (Brain Damage, Behaviour, and Cognition. Psychology Press.

Chapter 2 − Wernicke’s 1903 case of pure agraphia—an enigma for classical models of written language processing, R. de Bleser.

Chapter 3 − Charcot’s case of impaired imagery, A.W. Young, C. van de Wal. Chapter 4 − A case reported by Serieux—the first description of a “primary progressive word deafness”? M. Ceccaldi et al.

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Chapter 16: Lateralization, Language, and the Split Brain Chapter 5 − 19th-century accounts of the nature of the lexicon and semantics—riddles posed by the case of Johann Voit, C. Bartels, C.-W. Wallesch.

Chapter 6 − Bodomer’s cases of prosopagnosia, H.D. Ellis.

Chapter 7 − Poppelreuter’s case of merk—neglect and visual disturbance following a gunshot wound, G.W. Humphreys et al.

Chapter 8 − Wilbrand’s case of “mind-blindness,” M. Solms et al.

Chapter 9 − Liepmann. (1900 & 1905)—a definition of apraxia and a model of praxis, L.J. Gonzales Rothi, K.M. Heilman Chapter 10 − Balint-Holmes’ syndrome, E. de Renzi.

Chapter 11 − Lewandowsky’s case of object-colour agnosia, J. Davidoff.

Chapter 12 − Monrad-Krohn’s “foreign accent” syndrome case, I. Moen.

Chapter 13 − Paterson and Zangwill’s case of unilateral neglect—insights from fifty years of experimental inquiry, J.B. Mattingly.

Chapter 14 − G.R.—the prime “deep dyslexic,” C. Barry.

Chapter 15 − W.L.P.—a case for the modularity of language function and dementia, E. Funnell.

Chapter 16 − Warrington & Shallice’s 1984 category-specific aphasic J.B.R., R. Carlo Semenza, P. Bisiacchi.

Chapter 17 − Broca’s first two cases—from bumps on the head to cortical convolutions, J. Ryalls, A.R. Lecours.

Chapter 18 − Phineas Gage—a case for all reasons, M. Macmillan Chapter 19 − Anomaly in relations of hand, language and brain—crossed aphasia in history crossexamined., A. Schweiger.

Chapter 20 − A psychosurgical chapter in the history of cerebral localization—the six cases of Gottlieb.Burckhardt 1891, H.A. Whitaker et al.

Chapter 21 − Akelaitis’ investigations of the first split-brain patients, H.C. Sauerwien, M. Lassonde.

Chapter 22 − Speech from the isolated right hemisphere?—Left hemispherectomy cases E.C. & N.F., C. Code.

Chapter 23 − H.M.—the medical temporal lobes and memory, A.J. Parkin.

Chapter 24 − Gail D.—Poizner, Kilma & Bellugi’s 1987 deaf agrammatic signer—form and function in the specialization of the left cerebral hemisphere for speech and language, J. Bradshaw.

Web Links 16.7 Remarks on the Seat of the Faculty of Articulated Language, Following an Observation of Aphemia (Loss of Speech) 16.8 Loss of Speech, Chronic Softening and Partial Destruction of the Anterior Left Lobe of the Brain < Return to Table of Contents

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ACTIVITIES Activity 16.1: Experiencing Dyslexia It is difficult for most college students to remember how difficult it was to learn to read.

There are several exercises available that break conventional rules of reading. These are an effective introduction to the problems someone might experience.

A classic is “Ladle Rat Rotten Hut.” This story is made up of common English words which, when read aloud, sound like the story of Little Red Riding Hood. The competition between what you see and its meaning are related to the Stroop test, in which you must name the color of the word and not read the color name (for example, the word red printed in blue).

Students then can discuss answers to the following questions: • Who would find this the most difficult to read aloud?

• Who would find this the easiest to read aloud?

• Who would find this the most difficult to understand?

• Who would find this the easiest to understand?

Handout 16.1 Ladle Rat Rotten Hut < Return to Table of Contents

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Chapter 16: Lateralization, Language, and the Split Brain

ASSIGNMENTS Assignment 16.1: Classical Articles A sense of the history of neuroscience and the source of the names of specific diseases and syndromes can be addressed by giving the students readings that discuss the research that first introduced these concepts.

You might find it useful to assign several students to an article and then have them report on it to the class or write reports to be made available to other class members.

References Classic Cases in Neuropsychology II (Brain Damage, Behaviour, and Cognition). Code, C., Wallesch, C.W. Joanette, Y. & Roch Lecours, A. (2001). Classic Cases in Neuropsychology II (Brain Damage, Behaviour, and Cognition. Psychology Press.

Web Links 16.7 Remarks on the Seat of the Faculty of Articulated Language, Following an Observation of Aphemia (Loss of Speech) 16.8 Loss of Speech, Chronic Softening and Partial Destruction of the Anterior Left Lobe of the Brain < Return to Table of Contents

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WEB LINKS Web Link 16.1: The Role of Handedness in Brain Lateralization Go to http://www.indiana.edu/ and place “Handedness in Brain Lateralization” in the search bar. Select the matching link.

What does handedness have to do with brain lateralization—and who cares?

Web Link 16.2: Brodmann Areas in the Human Brain with an Emphasis on Vision and Language Using your favorite browser, place “Brodmann Areas in the Human Brain with an Emphasis on Vision and Language” in your search bar. Select the link that comes up from the University of Colorado Boulder.

Brodmann areas in the human brain with an emphasis on vision and language.

Web Link 16.3: Language “Center” of Brain Shifts with Age Go to https://www.sciencedaily.com/ and place “Language Center of Brain Shifts with Age” in the search bar. Select the matching link from your search.

Web Link 16.4: The Whole Brain Atlas Place “Whole Brain Atlas” in your favorite browser’s search bar and select the link that leads you to the atlas on the Harvard University Web site. Once there, locate the following links to view pictures of the brain where damage has resulted in problems with speech.

Segments of this Web site include a series of MR scans of patients experiencing language problems.

• Acute stroke: speech arrest • Acute stroke: speaks nonsense words, “fluent aphasia” (time-lapse movies) • Acute stroke: writes, but can’t read, “alexia without agraphia” • Subacute stroke: hesitating speech, “transcortical aphasia” Web Link 16.5: National Institute of Deafness and Other Communication Disorders http://www.nidcd.nih.gov Web Link 16.6: Broca Go to http://www.whonamedit.com/ and place “Broca’s aphasia” in the search box. Select the matching link.

Some biographical facts.

Web Link 16.7: Remarks on the Seat of the Faculty of Articulated Language, Following an Observation of Aphemia (Loss of Speech) Go to http://psychclassics.yorku.ca/ and use the “Sorted by Author” link to move to the articles listed by authors. Page down the page to Broca and select the English translation of the article titled “Remarks on the Seat of the Faculty of Articulate Language.”

A classic article. Paul Broca (1861). First published in Bulletin de la Société Anatomique, 6, 330–357.

Translation by Christopher D. Green.

Web Link 16.8: Loss of Speech, Chronic Softening and Partial Destruction of the Anterior Left Lobe of the Brain Go to http://psychclassics.yorku.ca/ and use the “Sorted by Author” link to move to the articles listed by authors. Page down the page to Broca and select the English translation of the article titled “Loss of Speech, Chronic Softening and Partial Destruction of the Anterior Left Lobe of the Brain.”

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Chapter 16: Lateralization, Language, and the Split Brain Pierre Paul Broca (1861). First published in Bulletin de la Société Anthropologique, 2, 235–238. Translation

by Christopher D. Green.

Web Link 16.9: Wernicke Go to http://www.whonamedit.com/ and place “Wernicke” in the search bar. Select the matching link.

Some biographical facts.

Web Link 16.10: National Aphasia Association http://www.aphasia.org Web Link 16.11: Characteristics of Aphasia Go to http://www.asha.org/ and place “aphasia” in the search bar. Select the matching link.

Web Link 16.12: Conversations with Neil’s Brain: The Neural Nature of Thought & Language Go to http://williamcalvin.com/ and click on the link labeled “books.” Once there, page down the Web site until you reach the book called “Conversations with Neil’s Brain” and click on that link to reach the full text online.

An online book about a man who had an area of his brain removed to treat his epilepsy. Several chapters examine the resulting language disruption he experienced.

Web Link 16.13: Langbrain: Language and the Brain—Cognitive Neurolinguistics Go to http://www.rice.edu and place “Language and Brain: Neurocognitive Linguistics” in the search bar.

Select the matching link.

Major points from the book: Lamb, S. (1999). Pathways of the Brain: The Neurocognitive Basis of Language. Amsterdam and Philadelphia: John Benjamins Publishing Co. Web Link 16.14: Dyslexia and Language Brain Areas Go to http://www.wisc.edu and place “Dyslexia and language brain areas” in the search bar. Click on the matching link.

The learning disability dyslexia centers on difficulties in reading. Since dyslexics often have good intelligence and even may be gifted in some areas, it was thought that a little motivation could get them on the right track. Now researchers are getting closer to confirming the key brain areas that are affected. Nice brain image. A quick summary (April 1999).

Web Link 16.15: “Oh Say Can You Say”: The Brain and Language Go to http://www.faculty.washington.edu and place “Chudler Language” in the search bar. Select the page from “Neuroscience for Kids” that covers language.

This “Neuroscience for Kids” page has some useful links and diagrams and puts things in very simple language—sometimes a good beginning point for students having difficulty. < Return to Table of Contents

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HANDOUTS Handout 16.1: Laden Rat Rotten Hut Name: ________________________________________ Section: ___________ Date: ___________ Wants pawn term, dare worsted ladle gull hoe lift wetter murder inner ladle cordage, honor itch offer lodge, dock, florist. Disk ladle gull orphan worry putty ladle rat cluck wetter ladle rat hut, an fur disk raisin pimple colder Ladle Rat Rotten Hut. Wan moaning, Ladle Rat Rotten Hut’s murder colder inset. “Ladle Rat Rotten Hut, heresy ladle basking winsome burden barter an shirker cockles. Tick disk ladle basking tutor cordage offer groinmurder hoe lifts honor udder site offer florist. Shaker lake! Dun stopper laundry wrote! Dun stopper peck floors! Dun dailydoily inner florist, an yonder nor sorghum-stenches, dun stopper torque wet strainers!”

“Hoe-cake, murder,” resplendent Ladle Rat Rotten Hut, an tickle ladle basking an stuttered oft. Honor wrote tutor cordage offer groin-murder, Ladle Rat Rotten Hut mitten anomalous woof. “Wail, wail, wail!” set disk wicket woof, “Evanescent Ladle Rat Rotten Hut! Wares are putty ladle gull goring wizard ladle basking?”

“Armor goring tumor groin-murder’s,” reprisal ladle gull. “Grammar’s seeking bet. Armor ticking arson burden barter an shirker cockles.”

“O hoe! Heifer gnats woke,” setter wicket woof, butter taught tomb shelf, “Oil tickle shirt court tutor cordage offer groin-murder. Oil ketchup wetter letter, an den—O bore!”

Soda wicket woof tucker shirt court, an whinny retched a cordage offer groin-murder, picked inner windrow, an sore debtor pore oil worming worse lion inner bet. En inner flesh, disk abdominal woof lipped honor bet, paunched honor pore oil worming, an garbled erupt. Den disk ratchet ammonol pot honor groinmurder’s nut cup an gnat-gun, any curdled ope inner bet.

Inner ladle wile, Ladle Rat Rotten Hut a raft attar cordage, an ranker dough ball. “Comb ink, sweat hard,” setter wicket woof, disgracing is verse. Ladle Rat Rotten Hut entity betrum an stud buyer groinmurder’s bet.

“O Grammar!” crater ladle gull historically, “Water bag icer gut! A nervous sausage bag ice!”

“Battered lucky chew whiff, sweat hard,” setter bloat-Thursday woof, wetter wicket small honors phase.

“O Grammar, water bag noise! A nervous sore suture anomolous prognosis!”

“Battered small your whiff, doling,” whiskered dole woof, ants mouse worse waddling.

“O Grammar, water bag mouser gut! A nervous sore suture bag mouse!”

Daze worry on-forger-nut ladle gull’s lest warts. Oil offer sodden, caking offer carvers an sprinkling otter bet, disk hoard hoarded woof lipped own pore Ladle Rat Rotten Hut an garbled erupt.

Mural: Yonder nor sorghum stenches shut ladle gulls stopper torque wet straine. < Return to Table of Contents 25 ..

17 Biopsychology of Emotion, Stress, and Health: Fear, the Dark Side of Emotion TABLE OF CONTENTS Chapter-at-a-Glance

2

Learning Objectives

3

Brief Chapter Outline

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Teaching Outline

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Lecture Launchers

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Activities

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Demonstrations

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Web Links

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Handouts

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Chapter 17: Biopsychology of Emotion, Stress, and Health

CHAPTER-AT-A-GLANCE

Brief Outline Chapter Introduction (p. 450) 17.1 Biopsychology of Emotion: Introduction (pp. 450–457)

17.2 Fear, Defense, and Aggression (pp. 457–460) 17.3 Neural Mechanisms of Fear Conditioning (pp. 460–462) 17.4 Brain Mechanisms of Human Emotion (pp. 462–465) 17.5 Stress and Health (pp. 465–471)

Instructor’s Manual Resources Lecture Launcher 17.1, Activities 17.1, 17.2, 17.3, Demonstration 17.1 Lecture Launcher 17.2 Lecture Launchers 17.3, 17.4 Lecture Launchers 17.5, 17.6, 17.7

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Biopsychology, Tenth Edition

LEARNING OBJECTIVES After completion of this chapter, the student should be able to: LO 17.1 LO 17.2 LO 17.3 LO 17.4 LO 17.5 LO 17.6 LO 17.7 LO 17.8 LO 17.9 LO 17.10 LO 17.11 LO 17.12 LO 17.13 LO 17.14 LO 17.15 LO 17.16 LO 17.17 LO 17.18 LO 17.19

Summarize the major events in the history of research on the biopsychology of emotion.

Summarize the research on the relationship between the autonomic nervous system and emotions.

Describe research on the facial expression of emotions.

Describe the work that led to the distinction between aggressive and defensive behaviors in mammals.

Describe the relation between testosterone levels and aggression in males.

Describe the role of the amygdala in fear conditioning.

Describe the role of the hippocampus in contextual fear conditioning.

Describe the role of two amygdalar nuclei in fear conditioning.

Describe the current status of cognitive neuroscience research on emotion.

Describe the role of the amygdala in human emotion.

Describe the role of the medial prefrontal lobes in human emotion.

Describe the research on the lateralization of emotion.

Describe the current perspective on the neural mechanisms of human emotion that has emerged from brain-imaging studies.

Describe the components of the stress response.

Describe research on animal models of stress, including that on subordination stress.

Describe how our view of psychosomatic disorders has been refined by the results of research on gastric ulcers.

Define psychoneuroimmunology, and describe the four components that make up our bodies’ defenses against foreign pathogens.

Describe the effects of early exposure to severe stress.

Describe the effects of stress on the hippocampus.

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Chapter 17: Biopsychology of Emotion, Stress, and Health

BRIEF CHAPTER OUTLINE Lecture Launcher 17.1: The Case of Phineas Gage 1. Biopsychology of Emotion: Introduction a. Early Landmarks in the Biopsychological Investigation of Emotion b. Emotions and the Autonomic Nervous System c. Emotions and Facial Expression Lecture Launcher 17.2: Show Some Emotion 2. Fear, Defense, and Aggression a. Types of Aggressive and Defensive Behaviors b. Aggression and Testosterone Lecture Launcher 17.3: Time for Some Laughter 3. Neural Mechanisms of Fear Conditioning a. Amygdala and Fear Conditioning b. Contextual Fear Conditioning and the Hippocampus c. Amygdala Complex and Fear Conditioning 4. Brain Mechanisms of Human Emotion a. Cognitive Neuroscience of Emotion b. Amygdala and Human Emotion c. Medial Prefrontal Lobes and Human Emotion d. Lateralization of Emotion e. Neural Mechanisms of Human Emotion: Current Perspectives 5. Stress and Health a. The Stress Response b. Animal Models of Stress c. Psychosomatic Disorders: The Case of Gastric Ulcers d. Psychoneuroimmunology: Stress, the Immune System, and the Brain e. Early Experience of Stress f. Stress and the Hippocampus < Return to Table of Contents

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TEACHING OUTLINE 1. Biopsychology of Emotion (see Table 17.1 and Figures 17.1–17.8 in Biopsychology) a. Early Landmarks in the Biopsychological Investigation of Emotion LO 17.1 Summarize the major events in the history of research on the biopsychology of emotion.

• • • •

This chapter describes six early landmarks in the biopsychological investigation of emotion.

In 1848, Phineas Gage was the victim of a tragic accident that sent a tamping iron through his medial prefrontal lobes.

His personality was altered forever.

By observing Gage, researchers were able to infer the function of this brain area.

Darwin’s Theory of the Evolution of Emotion • Darwin’s The Expression of Emotions in Man and Animals was the first major event in the study of the biopsychological bases of emotion.

• Darwin believed that emotions evolved from behaviors that indicated what an animal would do next in a given situation. When these behaviors were advantageous to the animal (e.g., allowed it to avoid a fight), they evolved in a way that would enhance their communicative value, to the extent that the original behavior was lost, and that opposite messages are signaled by opposite types of behaviors (the principle of antithesis).

James-Lange and Cannon-Bard Theories of Emotion • The James-Lange theory was the first attempt to explain the physiological bases of emotion; in their theory, James and Lange suggested that emotion-inducing stimuli are received and interpreted by the brain, which triggers visceral changes that subsequently trigger the experience of emotion.

• Cannon, and subsequently Bard, proposed an alternative theory based on the idea that emotional stimuli evoke visceral and emotional responses that are independent of one another.

• It appears that neither theory was entirely correct; emotions can be induced by stimuli that cannot elicit a peripheral, visceral response (e.g., in patients suffering from a spinal cord transection), but visceral responses can often induce an emotional state in the absence of any obvious eliciting stimuli (e.g., a racing heartbeat and increased respiration can produce a feeling of fear in the absence of an eliciting stimuli).

• More recently, a third theory has been reached that suggests that each of the three factors in an emotional response—the perception of the emotion-inducing stimulus, the autonomic and somatic responses to the stimulus, and the experience of emotion—influence the other two factors.

Sham Rage In 1929, Bard reported that decorticate cats responded with unusual aggression to the slightest provocation; often, this behavior was not directed at any specific topic. Bard concluded that the hypothalamus is critical in the performance of these aggressive behaviors, which he called sham rage; he also believed that the cortex normally inhibited and directed these aggressive displays.

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Chapter 17: Biopsychology of Emotion, Stress, and Health Limbic System and Emotion This theory of hypothalamic function was followed by Papez’s proposal of a limbic system that controlled the expression of emotions by connections with the hypothalamus and mediated the perception of emotions by connections with the cortex.

The Klüver-Bucy Syndrome • In 1939, Klüver and Bucy observed that damage to the amygdala would produce a syndrome in which a subject was fearless, hypersexual, and inclined to explore objects with their mouths.

• The Klüver-Bucy syndrome has been observed in several species. b. Emotions and the Autonomic Nervous System LO 17.2 Summarize the research on the relationship between the autonomic nervous system and emotions.

A large body of research in the area has focused on the degree to which specific patterns of ANS activity are associated with specific emotions; the results suggest that both the James-Lange theory (which predicts a multitude of activity patterns, each generating a unique emotion) and the CannonBard theory (which predicts a single general pattern of activation) are partially correct.

Another focus of research is how effective is it to use ANS measures for lie detection.

Emotional Specificity of the Autonomic Nervous System • As noted above, both the James-Lange and Cannon-Bard theories differ in their views of the emotional specificity of the ANS. • The evidence suggests the answer lies somewhere between both theories—total emotional specificity and total emotional generality.

Polygraphy • In addition, the effectiveness of ANS measures in polygraphy has been extensively studied; these tests examine changes in emotions, as indexed by ANS activity, to assess the truthfulness of a person’s claims.

• Many of these studies employ a control-question technique in which a person’s answers to innocuous questions to which the answers are known (“Is your mother’s name Karen?”) are compared to answers to the target question of interest (“Did you steal the purse?”).

• In many cases, any normal person will react strongly to the target question and make it difficult for an investigator to determine whether or not they are lying; to circumvent this possibility, Lykken (1959) developed the guilty-knowledge technique in which the polygrapher asks a series of questions that contain possible details about the crime.

• Only some of these details are actually true, however; the polygrapher compares a subject’s responses to “true” details (that only a guilty suspect could know) to their responses to “false” details (that would make innocent parties equally uneasy) to determine if someone is not telling the truth. c. Emotions and Facial Expression LO 17.3 Describe research on the facial expression of emotions.

•

Ekman and Friesen have conducted much of the classic research on human facial expressions.

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Biopsychology, Tenth Edition Universality of Facial Expression Several studies have found that people of different cultures make similar facial expressions in similar situations. Ekman and Friesen found that isolated New Guinea tribe members could correctly identify Western facial expressions and that Westerners could correctly identify New Guinean expressions, further supporting the idea of the universality of emotions.

Primary Facial Expressions In the 1970s, Ekman and Friesen began analyzing hundreds of films and photographs of people experiencing various emotions. They concluded that there are six primary facial expressions of emotion and that all other expressions were mixtures of these; the six primary expressions were: (1) anger, (2) fear, (3) happiness, (4) surprise, (5) sadness, and (6) disgust.

Facial Feedback Hypothesis • One version of this hypothesis focuses on the idea that facial expression can influence emotional experience. This is called the facial feedback hypothesis: Can putting on a happy face make you feel better?

• The answer seems to be yes: Rutledge and Hupka (1985) asked subjects to hold various facial poses while they viewed slides; the subjects reported being slightly more happy when making happy faces, and slightly more angry when making angry faces.

Voluntary Control of Facial Expression • Because we can exert voluntary control over the facial muscles, we can inhibit true facial expressions and substitute false ones.

• It is difficult to fool an expert because microexpressions of the genuine emotion often break through the false one; although they are usually very short (about .05 seconds), they can often be spotted by an expert even without slow-motion analysis.

• Also, there tend to be subtle differences between genuine and false expressions that can be recognized by an expert. For example, Duchenne, a French neuroanatomist, pointed out in 1862 that genuine smiles (which have been known as Duchenne smiles) involve contraction of both the zygomaticus major (which pulls the lip corners up) and orbicularis oculi (which encircles the eyes), whereas false smiles involve only the zygomaticus major.

• According to Duchenne, the zygomaticus major can be controlled voluntarily, whereas the orbicularis oculi cannot.

Facial Expressions: Current Perspectives • Ekman’s work began before we had ready access to video recording. Now, video recording allows unlimited access to human facial expressions in real time and in response to real stimuli.

As a result of modern analyses of Ekman’s primaries, it is now clear that they never occur in their pure form.

• Also, the existence of other primary emotions has been recognized.

• Body cues, not just facial expressions, play a major role in expressions of emotion.

• There is evidence that Ekman’s six primary facial expressions may not be as universal as originally believed.

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Chapter 17: Biopsychology of Emotion, Stress, and Health 2. Fear, Defense, and Aggression (see Table 17.2 in Biopsychology) Fear is the emotional reaction to threat; defensive behaviors are intended to protect an animal from threat, while aggressive behaviors are intended to threaten or harm. a. Types of Aggressive and Defensive Behaviors LO 17.4 Describe the work that led to the distinction between aggressive and defensive behaviors in mammals.

• Considerable progress in understanding aggression and defensive behavior has come from the research of Blanchard and Blanchard on the colony intruder model of aggression and defense in rats.

• Two important concepts have emerged from this study: − Neither aggression or defense are unitary concepts; there are different kinds of aggression and defense, which occur in different situations, have a different topography, and have a different function. − Many of the complexities of aggressive and defensive behavior can be understood in terms of the concept of target sites, the idea that different kinds of aggression tend to be directed at particular sites on the defender’s body, and that various defensive maneuvers appear to be specifically designed to protect these sites.

• Recognition of different types of aggression and defense, and the stereotypical nature of many of the behaviors associated with them, has helped researchers studying the neural bases of these behaviors.

• For example, lesioning the septal nuclei in a rat produces a state commonly referred to as septal rage, in which the rat is very hard to handle. This lesion was believed to increase the aggressiveness of the rat, but closer analyses revealed that the septal lesions actually made the rat more defensive. b. Aggression and Testosterone LO 17.5 Describe the relation between testosterone levels and aggression in males.

• • • • •

Testosterone increases social aggression in the males of many species, and castration can abolish this aggression.

In some species, castration has no effect on social aggression; in still others, castration reduces social aggression during the breeding season but not at other times.

The relation between aggression and testosterone levels is difficult to interpret because engaging in aggressive activities can increase testosterone.

Blood levels of testosterone may give aberrant data.

It is likely that humans’ aggression is under different hormonal and neural regulation than that of other species.

3. Neural Mechanisms of Fear Conditioning (see Figure 17.9 in Biopsychology) • Fear conditioning is the establishment of fear in response to a previously neutral stimulus like a tone (the CS+) by pairing it with the presentation of an aversive stimulus like a footshock (the US).

• LeDoux and his colleagues have mapped the neural substrates for this form of auditory fear conditioning. a. Amygdala and Fear Conditioning LO 17.6 Describe the role of the amygdala in fear conditioning.

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• • • •

LeDoux found that lesions to the medial geniculate nucleus of the thalamus blocked fear conditioning, but lesions to primary auditory cortex did not.

This suggested that the medial geniculate nucleus projected to an alternate neural structure that was involved in the fear conditioning; this turned out to be the amygdala, as lesions there also blocked the auditory fear conditioning.

Pathways from the amygdala to the periaqueductal gray mediate many defensive behaviors; pathways to the lateral hypothalamus elicit the appropriate sympathetic responses.

Interestingly, there is a second pathway from the medial geniculate nucleus of the thalamus to the amygdala that passes through primary auditory cortex; if either the direct or the indirect route is intact, fear conditioning can occur.

b. Contextual Fear Conditioning and the Hippocampus LO 17.7 Describe the role of the hippocampus contextual fear conditioning.

• •

The context or environment in which fear-inducing stimuli are encountered can also come to elicit fear; this is called contextual fear conditioning.

Given the role of the hippocampus in spatial memory, it is not surprising that this brain structure is also involved in contextual fear conditioning; lesioning the hippocampus blocks the development of contextual fear conditioning without blocking conditioning to a CS+, and lesioning the hippocampus just after conditioning has taken place blocks the retention of the contextual fear conditioning without blocking retention of the fear response to an explicit CS+.

c. Amygdala Complex and Fear Conditioning LO 17.8 Describe the role of two amygdalar nuclei in fear conditioning.

• • • • • •

The amygdala is not a single structure—it is a cluster of many nuclei referred to as the amygdala complex.

Each nucleus is structurally distinct, has different connections, and is thus likely to have different functions.

The lateral nucleus of the amygdala, not the whole nucleus, is involved in the acquisition, storage, and expression of conditioned fear.

The prefrontal cortex is thought to act on the lateral nucleus of the amygdala to suppress conditioned fear.

The hippocampus is thought to interact with a part of the amygdala to mediate learning about the context of fear.

The amygdala is thought to control defensive behavior via outputs from the central nucleus of the amygdala.

4. Brain Mechanisms of Human Emotion (see Figures 17.10–17.12 in Biopsychology) a. Cognitive Neuroscience of Emotion LO 17.9 Describe the current status of cognitive neuroscience research on emotion.

This research has focused on neuropsychological studies of brain-damaged patients, and functional imaging studies in health subjects. Three findings have emerged: • Brain activity associated with each emotion is diffuse.

• When a person is experiencing or empathizing with another person, there is always activity in the sensory and motor cortices (embodiment of emotions).

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Chapter 17: Biopsychology of Emotion, Stress, and Health •

Similar activity in the brain is recorded when a person experiences, imagines, or sees someone else experiencing an emotion.

b. Amygdala and Human Emotion LO 17.10 Describe the role of the amygdala in human emotion.

• • •

Researchers have found that while the amygdala responds the most robustly to fear, it is activated by many others.

Lesioning the amygdala leaves a person or animal unable to perceive fearful emotions in others.

A similar deficit is seen in patients with Urback-Wiethe disease, in which the tissue forming the amygdala and medial temporal lobes is calcified and destroyed.

c. Medial Prefrontal Lobes and Human Emotion LO 17.11 Describe the role of the medial prefrontal lobes in human emotion.

• • • • •

The medial portion of the prefrontal lobes is the site for emotion-cognition interaction that has received the most attention.

Functional brain-imaging studies show that when emotional reactions are being cognitively suppressed or re-evaluated, the medial prefrontal areas are activated.

In studies that use the suppression paradigm, participants are directed to inhibit their emotional reaction to unpleasant films of pictures. In studies using the reappraisal paradigm, participants are instructed to reinterpret a picture to change their emotional reaction to it.

The medial prefrontal lobes have been hypothesized to monitor the difference between outcome and expectancy, to respond to personal choices that result in losses, to predict the likelihood of error, to guide behavior based on previous actions, and to respond to social rejection.

Single cell recordings have revealed that the medial aspects of the frontal lobes are most associated with negative emotions.

d. Lateralization of Emotion LO 17.12 Describe the research on the lateralization of emotion.

• •

• •

There is considerable evidence that emotional functions are lateralized.

The two dominant hypotheses are: − The Right Hemisphere Model: The right hemisphere is specialized for all aspects of emotional processing: perception, expression, and experience of emotion. − The Valence Model: Proposes that the right hemisphere is specialized for processing negative emotions and the left hemisphere is specialized for positive emotions.

Most studies have employed functional brain-imaging methods, and the results have been complex and variable.

Evidence suggests that the models are too general.

e. Neural Mechanisms of Human Emotion: Current Perspectives LO 17.13 Describe the current perspective on the neural mechanisms of human emotion that has emerged from brain-imaging studies.

• • • •

In general, emotional experiences produce widespread brain activation.

All brain areas activated by emotional stimuli are also activated during other psychological processes.

No one brain structure is linked to a particular emotion.

There is considerable individual variability in the neural substrates of emotion.

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5. Stress and Health (see Figures 17.13–17.14 in Biopsychology) When the body is exposed to harm, the result is a cluster of physiological changes called the stress response, or stress. a. The Stress Response LO 17.14 Describe the components of the stress response.

• • • • •

Selye first described the stress response in the 1950s; he identified several physiological responses to stress, emphasizing the role of the anterior pituitary-adrenal cortex system and the effects of stress on the release of ACTH, and glucocorticoids from the adrenal cortex.

Recent research has also implicated the importance of the sympathetic nervous system’s release (via the adrenal medulla) of epinephrine and norepinephrine in the response to stress.

Brief stressors produce an increase in blood levels of cytokines, hormones that are released by many cells and participate in physiological and immunological responses, causing inflammation and fever. The cytokines are now classified as major stress hormones.

McEwen (1994) hypothesized that the magnitude of the stress response was dependent upon three factors: the stressor, the individual, and strategies to cope with stress.

Selye’s work remains important to the psychological sciences because it provided a link through which psychological factors might impact upon physical illness.

b. Animal Models of Stress LO 17.15 Describe research on animal models of stress, including that on subordination stress.

• Early stress research on nonhumans tended to involve extreme forms of stress, such as repeated exposure to electric shocks or long periods of physical restraint.

• There are two problems with this research. The first is that it is unethical. The second is that studies that use extreme forms of stress are of questionable scientific value.

• Better animal models of stress involve the study of social threat from conspecifics that result in subordination stress.

• Subordination stress is most readily studied in social species that form dominance hierarchies.

Subordinate males are more likely to attack juveniles, have smaller testes, shorter life spans, lower blood levels of testosterone, and higher blood levels of glucocorticoids. This model mimics bullying in humans. c. Psychosomatic Disorders: The Case of Gastric Ulcers LO 17.16 Describe how our view of psychosomatic disorders has been refined by the results of research on gastric ulcers.

• • • •

Psychosomatic illnesses are those that have a physical basis that is greatly influenced by psychological factors. One example of a psychosomatic illness is ulcers.

Gastric ulcers are painful lesions to the lining of the stomach and small intestine. Stress has been implicated in their development, with the key factor being a stress-induced increase in acidic gastric secretions accompanied by decreased blood flow through the wall of the stomach.

Research had suggested that the bacteria Helicobacter pylori are responsible for all ulcers, except by those caused by nonsteroidal anti-inflammatory drugs.

However, it seems as though H. pylori by itself is not sufficient to induce the formation of ulcers, as it is found in about 75% of all control subjects, too. Currently, researchers believe that stress-induced increases in gastric secretions and decreases in blood flow interact with H. pylori to produce ulcers.

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Chapter 17: Biopsychology of Emotion, Stress, and Health

d. Psychoneuroimmunology: Stress, the Immune System, and the Brain LO 17.17 Define psychoneuroimmunology, and describe the four components that make up our bodies’ defenses against foreign pathogens.

• •

Stress can also increase susceptibility to infectious diseases.

This led to the emergence of a new field of research in the 1980s: psychoneuroimmunology— the interactions among psychological factors, the nervous system, and the immune system.

Innate Immune System • The immune system puts up barriers to keep the body from being taken over by invading microorganisms.

• It is triggered when receptors called toll-like receptors bind to molecules on the surface of the pathogens or when injured cells send out alarm signals.

• One of the first reactions is inflammation that attracts leukocytes and phagocytes.

• Phagocytosis is a nonspecific mechanism by which foreign microorganisms are destroyed.

Adaptive Immune System • There is also a second, more specific mechanism for dealing with foreign microorganisms and debris.

• Antigens are protein molecules on a cell’s surface that identify it as foreign or native.

• Lymphocytes are specialized white blood cells, produced in the bone marrow, and stored in the lymphatic system; there are two types of lymphocytes, and each mediates a form of immunological defense: − T-cells are lymphocytes that destroy invading microorganisms in a process called cellmediated immunity; where a foreign microorganism is detected by a phagocyte, which displays the foreign organisms’ antigens. T-cells with the appropriate receptors are attracted to the antigens, multiply to create more T-cells, and destroy the microorganisms. − B-cells are lymphocytes that manufacture antibodies (lethal receptor molecules) against antigens encountered on foreign cells and debris, in a process called antibody-mediated immunity. B-cells bind to foreign cells and release antibodies into the extracellular fluid to destroy the foreign microorganism. − The production of memory B cells accelerates the antibody-mediated immune response during subsequent infections. This memory is what gives vaccination its prophylactic effect.

What Effect Does Stress Have on Immune Function: Disruptive or Beneficial?

• Based on the meta-analysis of Segerstrom and Miller, acute stress actually improves immune function in humans.

• However, chronic stress impairs immune function.

• Stress that disrupts health is called distress, and stress that improves health is eustress.

How Does Stress Influence Immune Function?

• Stress produces widespread changes in the body that have been difficult to causally link to specific immune functions.

• People experiencing stress can also change their health behaviors (diet, sleep, etc.), which can increase their susceptibility to many infectious diseases.

Does Stress Affect Susceptibility to Infectious Disease?

• Stress is correlated with ill health in humans.

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Biopsychology, Tenth Edition • •

The duration of the stressor can be important, as well as the presence of a compensatory immune response or redundant immune system component.

Three types of evidence suggest stress leads to more infection: − Correlational studies have found correlations between stress levels and numerous measures of health. − Controlled experiments conducted with lab animals show that stress increases susceptibility to infectious disease. − A few partially controlled studies of humans have found similar results.

e. Early Experience of Stress LO 17.18 Describe the effects of early exposure to severe stress.

• • •

f.

Early experience of stress can adversely affect subsequent development; in addition, it often increases the intensity of subsequent stress responses.

Sensitivity to stress begins in utero and may play a key role in determining how animals will deal with stress as adults; for example, rat pups that are handled or groomed the most by their mothers are less responsive to stress as adults.

These salutary effects appear to be mediated by increased glucocorticoid receptors in the hippocampus, resulting in increased negative feedback to the hypothalamus.

Stress and the Hippocampus LO 17.19 Describe the effects of stress on the hippocampus.

• • •

The hippocampus is particularly rich in glucocorticoid receptors, a fact that makes the hippocampus particularly sensitive to the effects of stress.

These changes include shrinking of dendrites of hippocampal neurons and reduced neurogenesis in the hippocampus after a stressful experience.

The effects are mediated by stress-related increases in corticosteroids.

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Chapter 17: Biopsychology of Emotion, Stress, and Health

LECTURE LAUNCHERS Lecture Launcher 17.1: The Case of Phineas Gage Pinel opens Chapter 17 of Biopsychology with a description of the celebrated case of Phineas Gage. You can build on this opener with the images provided at http://content.nejm.org/ (place “The Tale of Phineas Gage” in the search bar and select the matching link) courtesy of Peter Ratiu, M.D. and Ion-Florin Talos, M.D. at the New England Journal of Medicine. It includes a text description of the accident and injury and a two-perspective view of the accident itself—one showing the tamping bar passing through Gage’s skull from the outside, and another from the inside!

Lecture Launcher 17.2: Are There Universal Facial Expressions?

Researcher Paul Ekman revolutionized the study of emotion through facial expression. You can begin your discussion of Ekman’s work by visiting his Web site, where he shows the facial expressions of a man from New Guinea (an isolated preliterate culture) to see if facial expressions are universal. Place “Ekman Universal Facial Expression” in your browser’s search bar and select the Web site available from the Paul Ekman Group.

Lecture Launcher 17.3: Time for Some Laughter Laughter is discussed much less than it deserves. To lighten things up a bit after all your talking about fear and aggression, you can show the video from the Ted Talk presented by Anthony McCarten on laughter and its roll in our lives. Find it by placing “Anthony McCarten Laughter” in the search bar of your favorite browser. Select the link to his You Tube video.

Lecture Launcher 17.4: Projections from the Central Nucleus of the Amygdala Map projections from the central nucleus of the amygdala to other brain areas using the information from Figure 11.2. This will encourage review of brain structures.

What behaviors might you expect would be impaired or increased with lesions or stimulation to various parts of the brain? Is there any research mentioned in the text that supports these conclusions?

Lecture Launcher 17.5: The Role of the Amygdala in Emotions This study looks at another aspect of the role of the amygdala in emotion. The connection to real emotional events of traumatic memories and eyewitness testimony makes this an interesting topic for discussion.

Abstract: “Neurobiological studies demonstrate the amygdala’s role in emotional memory, and psychological studies suggest a particular pattern: enhanced memory for the gist but not the details of complex stimuli. We hypothesized that these two findings are related. Whereas normal (n = 52) and braindamaged (n = 22) controls showed the expected enhancement of gist memory when the encoding context was emotional, persons with unilateral damage to the medial temporal lobe including the amygdala (n = 16) did not show this pattern.... A further study in four subjects with selective medial temporal damage sparing the amygdala, and one with selective damage confined to the amygdala, confirmed the specificity of this effect to the amygdala. The data support a model whereby the amygdala focuses processing resources on gist, possibly accounting for features of traumatic memories and eyewitness testimony in real life.”

Adolphs, R., Tranel, D., Buchanan, T.W. (2005) Amygdala damage impairs emotional memory for gist but not details of complex stimuli. Nature Neuroscience, 8 (4):512–8.

Lecture Launcher 17.6: Natural Experiments: Urbach–Wiethe Disease Urbach–Wiethe disease provides a unique nature experiment, as more than half of the individuals with this disorder have bilaterally symmetrical damage in the amygdaloid region. Neuropsychological evaluation,

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Biopsychology, Tenth Edition static (CT) and functional imaging techniques (single-photon emission computed tomography [SPECT] and PET) were used to examine a group of these individuals.

Neuropsychologically, the patients showed cognitively little deviation from normal subjects, while they differed emotionally. This was evident in their judgment of all emotions in facial expressions, in an odor– figure association test, as well as in remembering negative and positive pictures. This suggests that the human amygdala influences both negative and positive emotional processing.

Siebert, M., Markowitsch, H.J., & Bartel, P. (2003). Amygdala, affect and cognition: evidence from 10 patients with Urbach–Wiethe disease. Brain, 126 (12) 2627–2637.

Lecture Launcher 17.7: Women’s Better Emotional Recall Explained Differences between the sexes often catch students’ imaginations. This should begin a good discussion.

Men and women’s brains may use different strategies to remember highly emotional images. In the study, twelve women and twelve men were asked to view a selection of images while their brains were being scanned by functional MRI. Some were neutral pictures (fire hydrants and bookshelves). Others were disturbing (mutilated bodies and autopsies). Volunteers had to rate each image on a four-point scale for emotional intensity. Three weeks later, the volunteers were shown all the images again, plus forty-eight previously unseen images. They were asked to say whether they remembered the images clearly, only vaguely, or not at all.

Women remembered the emotional events better than the men. One hypothesis is that women experience images and events with the same brain activation as men, but it is stronger. Another theory is that men and women experience and encode emotional memories in completely different ways. The researchers found that even when both sexes rated an image as “highly emotionally intense,” women were better at remembering it three weeks later. Women had more activation in their left brains during emotional experiences, and men in their right.

Web Link 17.10 Women’s Better Emotional Recall Explained < Return to Table of Contents

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Chapter 17: Biopsychology of Emotion, Stress, and Health

ACTIVITIES Activity 17.1: Can Thought Influence Emotional Arousal?

Ask your students to take a one-minute pulse rate. (They should be able to find their pulse at the wrist or on the neck over the carotid artery.)

Ask half the class to imagine a time when they were frightened.

Have the class do a pulse rate estimate again.

The people who imagine an arousing situation should have a higher average pulse rate.

You can do the same thing by suggesting a place where the student feels safe and relaxed. This should lower pulse rate.

While sympathetic nervous system arousal, and corresponding increases in heart rate, are often related to emotional arousal, they are only part of emotional responses.

Activity 17.2: The Original William James and George Lange!

Read at least part of the original papers by William James and/or George Lange in class.

Contemporary students often have trouble reading classical literature because of its language and style.

Going over some of the text with them will increase their understanding and interest in the writing and history of the discipline. This can also be an excellent assignment for an honors course.

Web Links 17.6 What Is an Emotion?

17.7 The Mechanism of the Emotions Activity 17.3: Ekman’s Facial Feedback Hypothesis A simple demonstration of the facial feedback hypothesis comes in a brief experiment.

Ask half the class to hold a pencil horizontally between their teeth, forcing a wide grin. Have the other half of the class hold the pencil in their lips in a “fish face.” Present a series of cartoons to the class using an overhead or digital projector. Ask the students to rate the cartoon’s “funniness” on a scale of 1 to 5, with 5 being the funniest you have ever seen and 1 being not funny at all.

Average the estimates from the two halves of the room. If the “grinning” students have a higher average mood than the “fish face” half, you have support for facial expressions predisposing us to emotions, as we would expect the two halves of the class to have an average mood that is very similar. < Return to Table of Contents

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Biopsychology, Tenth Edition

DEMONSTRATIONS Demonstration 17.1 Galvanic Skin Response You will need: • A Galvanic Skin Response (GSR) meter • A boat foghorn, two blocks of wood, or some other device that will generate a loud sudden sound • The list of words in Handout 17.1 • Copies of the list for each student in the class • Two volunteers Many laboratories will have an apparatus for measuring galvanic skin response tucked away in a corner, or they are available from Lafayette Equipment Company.

Place the meter so that students can see the fluctuations of the needle. (I have found that a camera hooked to a projection device works well for this.) Have one volunteer sit so that she cannot see the meter. The other is positioned behind the seated student holding the foghorn or the two blocks of wood. Ask the class to record the meter reading for each word.

Begin reading the words at a rate of about one per second. When you read the word “boat,” have your assistant honk the horn briefly, or slap the two wood blocks together. (Be careful not to direct the sound directly toward the ear of the seated student.) You will probably need to stop briefly after the first time, as all of the students will be startled. The GSR reading should increase dramatically, indicating emotional arousal. Then continue with the list, evoking the startle reflex after each repetition of the word “boat.” After about three or four startle stimuli, read the word without the startle stimulus. You should see a conditioned emotional response. Continue reading. You will notice several words related to boat (water, sail, fishing, etc.). You may see the conditioned response generalize to these words as well.

Debrief by asking the startled student about her experience. Then ask the class what they thought. You may wish to average the values recorded by several students and plot them for students to see the pattern of arousal and the appearance of a conditioned emotional response.

What does this say about emotional arousal? < Return to Table of Contents

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Chapter 17: Biopsychology of Emotion, Stress, and Health

WEB LINKS Web Link 17.1: Health and Emotions Research Institute http://www.healthemotions.org/ The Health Emotions laboratory conducts basic research on the link between positive emotion, stress, and health.

Web Link 17.2: Ask the Geneva Emotion Analyst!

Go to http://www.unige.ch/ and place “emotion analyst” in the search bar. Click on the first link titled “Demos.” Once on that page, click on the link to “Geneva Emotion Analyst.”

Web Link 17.3: Paul Ekman’s Homepage http://www.paulekman.com/ Web Link 17.4: Joseph LeDoux Laboratory Go to http://www.cns.nyu.edu/ and place “Joseph LeDoux Laboratory” in the search bar. Visit the webpage that covers what research is being done in this lab.

How well do you know your emotions?

Web Link 17.5: Body Language vs. Micro-Expressions Go to https://www.psychologytoday.com and place “Body Language vs. Micro-Expressions” in the search bar. Click on the matching link. Debunking the myths of “micro-expressions” Web Link 17.6: What Is an Emotion?

Go to http://psychclassics.yorku.ca/ and click on the “sorted by author” link. Click on the “J” in the alphabetic bar at the top of the page. When you arrive at the articles written by William James, scroll down until you find the article titled “What is an Emotion?” William James (1884). First published in Mind, 9, 188–205.

Web Link 17.7: The Mechanism of the Emotions Go to http://psychclassics.yorku.ca/ and click on the “sorted by author” link. Click on the “L” in the alphabetic bar at the top of the page. Scroll down the page to find the article written by Carl Lange on “The Mechanism of the Emotions.”

Carl Georg Lange (1885–1912). Translated by Benjamin Rand.

Web Link 17.8: The Autonomic Nervous System Go to http://faculty.washington.edu/ and place “Chudler Autonomic” in the search bar. Click on the link to the “Neuroscience for Kids” page.

Web Link 17.9: Overview of the Autonomic Nervous System Go to http://www.merckmanuals.com/ and click on the “professional” button at the bottom of the homepage. Click the search bar and type in “Overview of the Autonomic Nervous System” and click enter.

You will arrive at the page you need.

Web Link 17.10: Women’s Better Emotional Recall Explained Go to http://www.newscientist.com/ and place “Women’s Better Emotional Recall Explained” in the search bar. Click on the link that matches that string of words. < Return to Table of Contents

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Biopsychology, Tenth Edition

HANDOUTS Handout 17.1: Record the Galvanic Skin Response Values for Each Word Name: ________________________________________ Section: ___________ Date: ___________

_______ Hat

_______ Red

_______ Hand

_______ Boat

_______ Car

_______ Bowl

_______ Harp

_______ Knob

_______ Boat

_______ Boat

_______ Step

_______ Boat

_______ Board

_______ Water

_______ Catch

_______ Phone

_______ Door

_______ Cow

_______ Ten

_______ Dog

_______ House

_______ Ride

_______ Foot

_______ Boy

_______ Go

_______ Fork

_______ Stair

_______ Lamp

_______ Girl

_______ Pop

_______ Blue

_______ Race

_______ Sail

_______ Drape

_______ Light

_______ Boat

_______ Friend

_______ Lamp

_______ Book

_______ Boat

_______ Stool

_______ Truck

_______ Rose

_______ Bird

_______ Star

_______ Game

_______ Vase

_______ Mark

_______ Story

_______ View

_______ Fish

< Return to Table of Contents

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18 Biopsychology of Psychiatric Disorders: The Brain Unhinged TABLE OF CONTENTS Chapter-at-a-Glance

2

Learning Objectives

3

Brief Chapter Outline

4

Teaching Outline

5

Lecture Launchers

15

Activities

17

Assignments

18

Web Links

19

Handouts

22

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Chapter 18: Biopsychology of Psychiatric Disorders

CHAPTER-AT-A-GLANCE

Brief Outline Chapter Introduction (p. 474) 18.1 Schizophrenia (pp. 475–481)

18.2 Depressive Disorders (pp. 481– 487) 18.3 Bipolar Disorders (pp. 487–489) 18.4 Anxiety Disorders (pp. 489–492 18.5 Tourette’s Disorder (pp. 492–495) 18.6 Clinical Trials: Development of New Psychotherapeutic Drugs (pp. 495–499)

Instructor’s Manual Resources Lecture Launchers 18.1, 18.4, 18.5, 18.6 Activity 18.1, Assignments 18.1, 18.2 Lecture Launcher 18.2

Lecture Launcher 18.7 Activity 18.2 Lecture Launcher 18.3

< Return to Table of Contents

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Biopsychology, Tenth Edition

LEARNING OBJECTIVES After completion of this chapter, the student should be able to: LO 18.1 LO 18.2 LO 18.3 LO 18.4 LO 18.5 LO 18.6 LO 18.7 LO 18.8

LO 18.9 LO 18.10 LO 18.11 LO 18.12 LO 18.13 LO 18.14 LO 18.15 LO 18.16 LO 18.17 LO 18.18 LO 18.19 LO 18.20 LO 18.21 LO 18.22 LO 18.23 LO 18.24 LO 18.25 LO 18.26 LO 18.27

Describe the positive and negative symptoms of schizophrenia, and provide specific examples of each.

Describe the causal factors that have been implicated in the development of schizophrenia.

Describe the discovery of the first two widely prescribed antipsychotic drugs.

Describe the evolution of the dopamine theory of schizophrenia.

Describe four current lines of research on schizophrenia.

Explain what a clinical depression is.

Describe the causal factors that have been implicated in the development of major depressive disorder.

Describe the early research that led to the discovery of anti-depressant medications. Also, list each of the five major classes of antidepressant drugs, and provide one specific example of each.

Describe the various brain differences associated with major depressive disorder.

Describe two theories of the etiology of major depressive disorder.

Describe two forms of treatment for depression that utilize brain stimulation.

Describe the symptoms associated with each of the two categories of bipolar disorders.

Describe the various causal factors that have been identified for bipolar disorders.

Describe the discovery of the first mood stabilizer.

Describe the brain differences associated with bipolar disorder.

Describe some of the theories of the etiology of bipolar disorders.

Describe four anxiety disorders.

Describe the etiological factors that have been implicated in anxiety disorders.

Describe drugs used in the treatment of anxiety disorders.

Describe three animal models of anxiety disorders.

Describe research findings related to the neural bases of anxiety disorders.

Describe the symptoms of Tourette’s disorder.

Describe research findings related to the neural bases of Tourette’s disorder.

Describe how Tourette’s disorder is treated.

Describe the three phases of clinical trials.

Identify five controversial aspects of clinical trials.

Discuss the relative effectiveness of clinical trials.

< Return to Table of Contents

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Chapter 18: Biopsychology of Psychiatric Disorders

BRIEF CHAPTER OUTLINE Lecture Launcher 18.1: The Epidemic of Mental Illness 1. Schizophrenia a. What Is Schizophrenia? b. Causal Factors in Schizophrenia c. Discovery of the First Antipsychotic Drugs d. Dopamine Theory of Schizophrenia e. Schizophrenia: Current Research and Treatment Lecture Launcher 18.2: Antidepressants Change the Activity of the Brain 2. Depressive Disorders a. Defining Depressive Disorders b. Causal Factors in Major Depressive Disorder c. Antidepressant Drugs d. Brain Differences in Depression e. Theories of Depression f. Treatment of Depression with Brain Stimulation 3. Bipolar Disorders a. Defining Bipolar Disorders b. Causal Factors in Bipolar Disorders c. Mood Stabilizers d. Brain Differences Associated with Bipolar Disorders e. Theories of Bipolar Disorders 4. Anxiety Disorders a. Four Anxiety Disorders b. Etiology of Anxiety Disorders c. Pharmacological Treatment of Anxiety Disorders d. Animal Models of Anxiety e. Neural Bases of Anxiety Disorders 5. Tourette’s Disorder a. What Is Tourette’s Disorder? b. Neural Basis of Tourette’s Disorder c. Treatment of Tourette’s Disorder Lecture Launcher 18.3: The Placebo Effect 6. Clinical Trials: Development of New Psychotherapeutic Drugs a. Clinical Trials: The Three Phases b. Controversial Aspects of Clinical Trials c. Effectiveness of Clinical Trials < Return to Table of Contents

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Biopsychology, Tenth Edition

TEACHING OUTLINE • • •

A psychiatric disorder is a psychological disorder that is severe enough that it requires treatment by a clinical psychologist or a psychiatrist.

The specific brain pathologies associated with each psychiatric disorder are not known.

Consequently, making an accurate diagnosis is difficult because it must be made based entirely on a patient’s symptoms. Currently diagnoses are guided by the DSM-5.

1. Schizophrenia (see Table 18.1, Figures 18.1–18.4 in Biopsychology) a. What Is Schizophrenia?

LO 18.1 Describe the positive and negative symptoms of schizophrenia and provide specific examples of each.

•

• • •

b.

Schizophrenia literally means a splitting of psychic function (“the shattered mind”); it is characterized by a complex and diverse set of symptoms that often overlap with other forms of mental illness and may change with time. The current DSM prefers to use the label schizophrenia spectrum disorders.

Positive symptoms (symptoms that seem to represent an excess of typical function) include delusions, hallucinations, inappropriate affect, disorganized speech or thought, and odd behavior.

Negative symptoms (symptoms that seem to represent a reduction or loss of typical function) include affective flattening, avolition, and catatonia.

The frequent recurrence of any two of these symptoms for one month is currently sufficient for the diagnosis of schizophrenia (provided that one of the symptoms is delusions, hallucinations, or disorganized speech.

Causal Factors in Schizophrenia LO 18.2 Describe the causal factors that have been implicated in the development of schizophrenia.

• • • •

A genetic basis for the disease emerged when it was recognized that the concordance rate of schizophrenia in identical twins is about 45%; in fraternal twins or siblings, it is about 10%.

Regions of several different chromosomes have been implicated in the vulnerability to schizophrenia.

In addition to a genetic predisposition, experiences such as birth complications, maternal stress, prenatal infections, socioeconomic factors, urban birth or residing in an urban setting, and childhood adversity may all be susceptibility factors.

Clearly schizophrenia is influenced by both genetics and experience; the current view is that people inherit a predisposition for schizophrenia, which may or may not be activated by experience.

c. Discovery of the First Antipsychotic Drugs LO 18.3 Describe the discovery of the first two widely prescribe antipsychotic drugs.

• Chlorpromazine was initially developed by a drug company as a new antihistamine; in the early 1950s, a French physician used the drug to prevent the swelling associated with surgery; by chance, he noticed that chlorpromazine also seemed to calm his patients down.

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Chapter 18: Biopsychology of Psychiatric Disorders • • • • • •

• •

The physician recommended that chlorpromazine be used as a sedative in difficult-to-manage psychiatric cases; in most cases it didn’t seem to work, however, one psychiatrist noticed a marked improvement in several schizophrenic patients after three weeks.

Amazingly, chlorpromazine seemed to calm agitated schizophrenic patients and to activate catatonic ones; therefore, the effect seemed specifically antipsychotic, not just sedative (sleep-inducing).

At the same time, an American psychiatrist became interested in reports that the snake root plant had been used for centuries in India as a cure for various psychiatric disturbances.

Reserpine, the active ingredient of the snakeroot plant, had been isolated, so he gave it to some of his schizophrenic patients.

It proved to be an effective antipsychotic. However, it is no longer used for treatment of schizophrenia due to its effect of dangerously lowering blood pressure.

Given the dissimilarity of the structures of chlorpromazine and reserpine, the similarity of their effects was remarkable; their therapeutic effects did not occur until two or three weeks after the beginning of therapy, and at that time, both drugs started to produce side effects— mild tremors at rest, muscular rigidity, and a decrease in voluntary movement.

You should recognize these as the symptoms of Parkinson’s disease; it seemed that the neurochemical changes that were the basis of these drugs’ antipsychotic action were related to the pathology that underlies Parkinson’s symptoms.

In 1960, it was discovered that there was a deficiency of dopamine in the brains of Parkinson’s patients. Thus, it seemed that both chlorpromazine and reserpine reduced brain dopamine levels and that this reduction was alleviating the symptoms of schizophrenia; on the basis of these two inferences, it was proposed that schizophrenia is associated with excessive activity in dopaminergic systems in the brain.

d. Dopamine Theory of Schizophrenia LO 18.4 Describe the evolution of the dopamine theory of schizophrenia.

•

•

• •

•

•

Two previous findings lent support to this dopamine theory of schizophrenia: – Reserpine was known to be a dopamine antagonist (it depleted the brain of dopamine and other monoamines by causing them to leak from their vesicles).

– Stimulants, which are agonists of dopamine and other monoamines, trigger schizophrenic episodes in healthy subjects at high doses (e.g., amphetamine psychosis).

In 1963, Carlsson and Lindqvist tested the dopamine theory; they expected to show that chlorpromazine, like reserpine, depletes the brain of dopamine—but they didn’t; instead, they found that chlorpromazine left dopamine levels unchanged, but that it produced a great increase in dopamine metabolites.

They concluded that, like reserpine, chlorpromazine is a dopamine receptor blocker, binding at dopamine receptors without activating them.

A feedback signal produced by the inactivity of the postsynaptic neurons causes the presynaptic neurons to release more dopamine; this excess of dopamine is immediately broken down by enzymes in the synapse because all of the binding sites are taken up by chlorpromazine; as a result, dopamine levels stay about the same but metabolite levels increase.

A technique developed in the mid-1970s allowed Snyder and his colleagues to measure the degree to which various antipsychotic drugs bind to dopamine receptors, and to relate this binding affinity to the potency with which each drug alleviated schizophrenic symptoms in human patients.

The correlation was positive, but there were some disturbing exceptions; for example, haloperidol, one of the most potent antipsychotic drugs, bound only weakly to dopamine receptors.

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Biopsychology, Tenth Edition • • • •

The answer to this puzzle was suggested by the discovery that there is more than one type of dopamine receptor; to date, a total of five dopamine receptors have been identified D1 and D2.

It turned out that chlorpromazine and all other antipsychotic drugs of the same chemical class (i.e., the phenothiazines) bind with equal affinity to both D1 and D2 receptors; in contrast, haloperidol and the other butyrophenones bind with highest affinity to D2 receptors.

This suggested a modification to the dopamine theory of schizophrenia, as schizophrenia could now be viewed as being caused by excess activity at D2 receptors and alleviated by drugs that block activity at D2 receptors.

However, there are several key findings that cannot be explained by the D2 receptor theory: – Timecourse: Therapeutic effects are not experienced for several weeks.

– Neuroleptics help only a small proportion of patients and usually with their positive symptoms only.

e. Schizophrenia: Current Research and Treatment LO 18.5 Describe four current lines of research on schizophrenia.

Atypical Neuroleptics • Schizophrenia also appears to involve alterations in glutamate, glycine, and other dopamine receptors.

• This is illustrated by the effectiveness of clozapine, an atypical neuroleptic that binds poorly to D2 receptors, but also binds to D1 and D4 receptors and some serotonin receptors.

• However, all atypical neuroleptics do bind somewhat to D2 receptors, and recent evidence suggests that newly diagnosed schizophrenics, who have not yet been medicated, have elevated numbers of D2 receptors in their brains.

• Drugs that affect glycine or block the effects of glutamate are proving to be effective treatments for schizophrenia in preliminary testing.

Renewed Interest in Hallucinogenic Drugs • There is renewed interest in understanding why classical hallucinogens mimic positive symptoms of schizophrenia through interaction at serotonin receptors.

• The anesthetic drug ketamine (a dissociative hallucinogen) is a glutamate antagonist and can produce negative symptoms.

Mechanisms of Schizophrenia-Related Genes • Numerous genes have been linked to schizophrenia. Some of these genes are linked to other disorders as well.

• Some of these genes have been linked to abnormal development or abnormal GABA or glutamate neurotransmission.

Schizophrenia and Brain Damage • Imaging studies have revealed many changes, including small cerebral cortices and large ventricles. Specifically, the hippocampus, amygdala, thalamus and nucleus accumbens are smaller in schizophrenics.

• There is some evidence that schizophrenia is a neurodevelopmental disorder; there is no obvious ongoing degeneration in the brains of schizophrenic patients, and the pathology observed is largely developed by the time diagnosis is first made.

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Chapter 18: Biopsychology of Psychiatric Disorders

2. Depressive Disorders (see Figures 18.5–18.8 in Biopsychology) a. Defining Depressive Disorders LO 18.6 Explain what a clinical depression is.

• • • •

Depression is characterized by intense feelings of despair, hypoactivity, sleep problems, withdrawal, lack of appetite, and an inability to care for oneself. When these symptoms last longer than two weeks, the person is said to suffer from clinical depression.

Depression can be reactive (triggered by negative experiences) or endogenous, (no apparent external triggers).

About 10% of people will suffer from unipolar affective disorder. It is found in women two times more than men. and 1% from bipolar affective disorder at some point in their lives; about 4-15% of people suffering from depressive disorder will commit suicide.

Depression is often comorbid (occurs together) with other disorders such as diabetes, heart problems, and anxiety disorders.

b. Causal Factors in Major Depressive Disorder LO 18.7 Describe the causal factors that have been implicated in the development of major depressive disorder.

• • •

•

The concordance rate major depressive disorder is 30-40%.

Two loci on chromosome 10 have been implicated.

Like schizophrenia, stress plays a major role in the etiology of depressive disorders; stress can trigger attacks of depression, and there is some indication that early exposure to stress increases the likelihood of developing depression in adulthood. Epigenetic mechanisms are currently being studied.

Seasonal affective disorder and postpartum depression are two examples with more obvious environmental factors.

c. Antidepressant Drugs LO 18.8 Describe the early research that led to the discovery of antidepressant medications.

Also, list each of the five major classes of antidepressant drugs, and provide one specific example of each.

Monoamine Oxidase Inhibitors • The first antidepressant drug, iproniazid, was developed as a treatment for tuberculosis; it had no effect on tuberculosis, but it did leave the patients less depressed about their condition and its clinical usefulness in this regard was soon exploited.

• Iproniazid is a monoamine oxidase (MAO) inhibitor; MAO inhibitors in combination with tyramine-rich foods (e.g., cheese, wine, or pickles) cause life-threatening surges in blood pressure; this is called the cheese effect.

Tricyclic Antidepressants • Imipramine, the first tricyclic antidepressant, was initially developed as an antipsychotic drug. When it was tried on a mixed group of psychiatric patients, it was found to be ineffective against schizophrenia, but effective against depression. Tricyclic antidepressants block the reuptake of both serotonin and norepinephrine and are safer than MAO inhibitors.

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Biopsychology, Tenth Edition • • •

Selective serotonin reuptake inhibitors (SSRIs), such as Prozac, are a variation of tricyclic antidepressants, which selectively block serotonin uptake.

SSRIs are not more effective than imipramine and other tricyclics against depression, but they have fewer side effects, and they are effective against many types of psychological disorders.

Recently, selective norepinephrine reuptake inhibitors (SNRIs) have proven equally effective in the treatment of depression.

Atypical Antidepressants • Drugs that do not fit neatly into existing classifications of antidepressants are called atypical antidepressants. An example is Buproprion, which blocks uptake of dopamine and norepinephrine and blocks nicotinic acetylcholine receptors.

• Another example is agomelatine, a melatonin receptor agonist.

NMDA-Receptor Antagonists • The dissociative hallucinogen Ketamine was shown to reduce depression by blocking NMDA receptors. Unfortunately, the side effects of Ketamine make it undesirable.

Effectiveness of Drugs in the Treatment of Depressive Disorders • Research shows about 25% of the population is helped with antidepressant medications. No classification of drug seems better than the others and they seem to be most effective in severely depressed individuals. d. Brain Differences in Depression LO 18.9 Describe the various brain differences associated with major depressive disorder.

• • •

Consistent reduction in gray matter volumes in the prefrontal cortex, hippocampus, amygdala, and cingulate cortex have been observed.

White matter reductions have been noted in several regions, but most reliably in the frontal cortex. fMRI studies show atypical activation in frontal, cingulate, insular cortices and the amygdala, striatum, and thalamus.

e. Theories of Depression LO 18.10 Describe the two theories of the etiology of major depressive disorders.

Monoamine Theory of Depression • The most widely accepted theory of depression is based on the fact that all clinically effective tricyclic antidepressants, serotonin-reuptake inhibitors, or norepinephrine reuptake inhibitors are serotonin and/or norepinephrine agonists. Thus, depression may be due to underactivity at serotonin and norepinephrine synapses.

• In support of this theory, there is evidence that certain norepinephrine and serotonin receptors are elevated in untreated depressed patients; this may be due to low levels of transmitters eliciting a compensatory increase in receptors called receptor up-regulation.

• Overall, this theory is rather weak. Many patients are not helped by 5-HT or NE agonists, and other neurotransmitters are known to be involved with depression.

Neuroplasticity Theory of Depression • Altered neuroplasticity may account for the fact that the beneficial effects of antidepressants are often not seen until weeks after treatment onset.

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Chapter 18: Biopsychology of Psychiatric Disorders • •

f.

Key neuroplastic processes that might be reversed by antidepressants include: neural loss, reduced synthesis of neurotrophins, and decreased adult neurogenesis. These processes have been observed in the prefrontal cortex, hippocampus and amygdala.

Most recently a role for brain-derived-neurotrophic-factor (BDNF) in plasticity has been proposed.

Treatment of Depression with Brain Stimulation LO 18.11 Describe two forms of treatment for depression that utilizes brain stimulation.

Repetitive Transcranial Magnetic Stimulation • High frequency and low frequency rTMS to the prefrontal cortex has been shown to relieve symptoms of depression.

Deep Brain Stimulation • Chronic stimulation of the anterior cingulate gyrus has been shown to alleviate symptoms in treatment-resistant patients.

3. Bipolar Disorders a. Defining Bipolar Disorders LO 18.12 Describe the symptoms associated with each of the two categories of bipolar disorder.

• Hypomania is characterized by a reduced need for sleep, high energy, and positive affect.

• Mania is hypomania but to an extreme. It includes delusions of grandeur, overconfidence, impulsivity, and distractibility. It usually involves psychosis.

• Bipolar I is described as those who experience mania episodes, while Bipolar II is described as those who experience bouts of hypomania and depression.

• Rapid cycling is when a person fluctuates between mania and depression more than 4 times per year. b. Causal Factors in Bipolar Disorders LO 18.13 Describe the various causal factors that have been identified for bipolar disorders.

• Heritability estimates of bipolar disorder range from 80-90%.

• Genes that code for particular calcium channels and particular proteins found at Nodes of Ranvier have been implicated. c. Mood Stabilizers LO 18.14 Describe the discovery of the first mood stabilizers.

• Lithium was the first drug found to be a mood stabilizer. It was found by accident by Cade during experiments with guinea pigs.

• Other drugs used for mood stabilization include anticonvulsants and antipsychotics. d. Brain Differences Associated with Bipolar Disorders LO 18.15 Describe the brain differences associated with bipolar disorders.

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Biopsychology, Tenth Edition • MRI studies reveal several specific brain structures being smaller in patients with bipolar disorders. These include the medial prefrontal cortex, the left anterior cingulate, the left superior temporal gyrus, certain prefrontal regions and the hippocampus.

• fMRI studies show atypical activation in the frontal cortex, medial temporal lobe structures, and basal ganglia. e. Theories of Bipolar Disorder LO 18.16 Describe some of the theories of the etiology of bipolar disorders.

• There is evidence of HPA axis dysregulation, marked disruptions in circadian rhythms, and alterations in GABA, glutamate, and monoamine neurotransmission.

• There is evidence that BDNF levels are lower in patients with bipolar disorders.

4. Anxiety Disorders • Anxiety is a fear that disrupts normal functioning and persists in the absence of a direct threat; symptoms include feelings of fear, worry, tachycardia, hypertension, nausea, sleep disturbances, and high glucocorticoid levels. a. Four Anxiety Disorders LO 18.17 Describe the four anxiety disorders.

These are the most prevalent of all psychiatric disorders; there are four major classes of anxiety disorders: • Generalized anxiety is a stress response in the absence of an obvious stimulus.

• Specific phobias are caused by exposure to a specific object or situation (snakes, heights, etc.).

• Panic disorders are rapid-onset attacks characterized by extreme fear and stress symptoms (tachycardia, choking, etc.).

• Agoraphobia is a fear of public places and open spaces. b. Etiology of Anxiety Disorders LO 18.18 Describe the etiological factors that have been implicated in anxiety disorders.

•

The role of environmental stressors is obvious in the etiology of anxiety disorders; however, there is also a genetic contribution, as the concordance rate for identical twins is 30-50%.

c. Pharmacological Treatment of Anxiety Disorders LO 18.19 Describe three categories of drugs used in the treatment of anxiety disorders.

• •

• •

Benzodiazepines Treatment often includes benzodiazepines (Librium, Valium) that increase the binding of GABA-A to its receptors.

Benzodiazepines are also clinically used as hypnotics, muscle relaxants, and anticonvulsants; problematic side effects include tremors, nausea, and addiction.

Serotonin Agonists The efficacy of the anxiolytic buspirone, which is an agonist at 5-HT1-A receptors, suggests that serotonergic systems may also be involved in anxiety; this idea is supported by the fact that antidepressants that alter serotonergic function are also effective anxiolytics.

Buspirone has fewer and less significant side effects than the benzodiazepines.

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Chapter 18: Biopsychology of Psychiatric Disorders Antidepressant Drugs • The comorbidity of anxiety disorders and depression, as well as the positive response of anxiety symptoms to antidepressant drugs, suggests the two disorders may be very related.

• Some anxiolytic drugs lessen depressive symptoms and drugs to treat bipolar disorders can be effective treatments for certain anxiety disorders. d. Animal Models of Anxiety Disorders LO 18.20 Describe three animal models of anxiety disorders.

• •

•

The elevated plus maze involves placing rats on a four-armed plus-sign-shaped maze that rests about 40 centimeters above the floor. Two arms have sides and two do not. The measure of anxiety is the proportion of time the rats spend in the enclosed arms rather than the open arms.

The defensive-burying test is when rats are shocked by a wire-wrapped wooden dowel mounted on the wall of a familiar test chamber. The measure of anxiety is the amount of time the rats spend spraying bedding material at the source of the shock with forward thrusting movements.

The risk-assessment test involves exposing a rat to a cat. After this exposure rats will engage in risk assessment behaviors. The measure of anxiety is how long the rat spends doing these behaviors.

e. Neural Bases of Anxiety Disorders LO 18.21 Describe research findings related to the neural bases of anxiety disorders.

• •

Many anxiolytic drugs are GABA-A receptor or serotonergic agonists. The hippocampus, amygdala, and medial prefrontal cortex are implicated in both affective and anxiety disorders.

While depressive disorders show shrinkage of these structures, in anxiety, activity in these areas is altered.

5. Tourette’s Disorder (see Figure 18.9 in Biopsychology) a. What Is Tourette’s Disorder?

LO 18.22 Describe the symptoms of Tourette’s disorder.

• • • • • • •

Tourette’s disorder is a disorder characterized by tics, or involuntary, repetitive movements or vocalizations.

It usually begins in childhood; symptoms become progressively more complex and severe with time.

Common motor tics include lewd gestures, hitting, touching, squatting, hopping, and twirling.

Common vocal tics include barking, grunting, copralalia (uttering obscenities), echolalia (repeating other’s words) and palilalia (repeating oneself).

Tourette’s disorder is four times more likely in males than females; it has a major genetic component, as there is a concordance rate of 50% for identical twins and 8% for fraternal twins.

It is often accompanied by attention-deficit-hyperactivity disorder or obsessive-compulsive disorder.

The tics of Tourette’s can be suppressed for brief periods of time; and there does not seem to be a rebound after this suppression.

b. Neural Bases of Tourette’s Disorder LO 18.23 Describe the research findings related to the neural bases of Tourette’s disorder.

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Biopsychology, Tenth Edition • • • •

Although Tourette’s has well-defined symptoms, it tends to get better with age. Therefore, few patients are in treatment at the time of their death and so anatomical studies are few.

Brain imaging studies have consistently found abnormalities in the caudate nucleus and prefrontal cortex, leading researchers to believe that the neuropathology of Tourette’s may be due to alterations in neural circuits between the basal ganglia and cortex.

There is also evidence of dysfunctional dopaminergic and GABAergic signaling in the corticalstriatal-thalamic-cortical brain circuit.

Neural bases of Tourette’s may be more widespread than previously thought.

c. Treatment of Tourette’s Disorder LO 18.24 Describe how Tourette’s disorder is treated.

•

•

Treatment of Tourette’s typically begins by educating the patient and family about the disorder and dealing with the anxiety and depression that often accompanies it.

The tics of Tourette’s are often treated with D–2 blocking antipsychotics; this fact supports the idea that Tourette’s is due to a disorder of the basal ganglia, possibly excessive dopaminergic innervation of the striatum and associated limbic cortices.

6. Clinical Trials: Development of New Psychotherapeutic Drugs (see Table 18.2 and Figures 18.10– 18.11 in Biopsychology) • • • •

Research designed to translate basic scientific discoveries into effective clinical treatments is called translational research.

The development of new psychotherapeutic drugs is an exceedingly slow, expensive and complex task that begins with the synthesis of a new drug and the collection of evidence from nonhuman subjects to support its putative therapeutic efficacy.

The importance of nonhuman subjects during this phase of drug development cannot be overestimated; without a solid foundation of comparative research, the development of drugs for human consumption is very difficult.

These initial steps take at least five years; if they are successful, the drug is eligible for clinical trials conducted on human subjects to assess the drug’s safety and therapeutic efficacy.

a. Clinical Trials: The Three Phases LO 18.25 Describe the three phases of clinical trials.

• Phase 1: Screening for Safety This stage determines whether a drug is actually safe for humans and the dose range that can be tolerated; subjects are usually healthy, paid volunteers. This stage usually takes 18 months and costs $10,000,000 to complete.

• Phase 2: Establishing the Test Protocol − This establishes the conditions under which the final tests will be conducted; therapeutic dose, interdose interval, duration of drug treatment, likely benefits, and patients most likely to be helped are all determined. − Subjects are usually patients suffering from the disorder of interest and placebo control groups; the studies are usually done double blind, so that neither the subjects nor the attending physicians know which treatment a particular subject is getting. − This phase normally takes about two years and costs about $20,000,000 to complete.

• Phase 3: Final Tests − This is typically a large, double-blind, placebo-controlled study involving thousands of patients suffering from the target disorder.

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Chapter 18: Biopsychology of Psychiatric Disorders −

Often, two independent tests must be conducted to determine a successful drug candidate—that is, one that has greater therapeutic effects than noxious side effects.

b. Controversial Aspects of Clinical Trials LO 18.26 Identify five controversial aspects of clinical trials.

• The need for double-blind, placebo-controlled studies means that some subjects, who might only recover from their illness if they receive the latest experimental treatment, will go untreated.

• However, the only way that researchers can be sure a drug is effective is to control for the very real possibility of placebo effects in patients; if an active placebo is employed, that is even better.

• The need for extensive testing of new drugs also means that it takes a long time for a drug to come to market, often frustrating patients and drug companies alike.

• The amount of money required to develop a new drug means that drug costs are high, and many question the impartiality of clinical trials conducted by the drug companies themselves.

• A major impediment to drug development is it is often aimed at curing disease entities as currently conceived (psychiatric disorders are more complicated than can benefit from this practice).

Conclusion The diagnosis of psychiatric disorders needs to improve. It does seem that each diagnosis contains several different disorders and that research and treatment could benefit from distinguishing among them. < Return to Table of Contents

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Biopsychology, Tenth Edition

LECTURE LAUNCHERS Lecture Launcher 18.1: The Epidemic of Mental Illness For many years, E. Fuller Torrey (“the most famous psychiatrist in America,” according to the Washington Post) has argued that there has been an alarming, though largely ignored, increase in the incidence of major mental illness in the United States. You can begin your lectures on the biology of psychiatric disorders by discussing this topic with your class, aided with information from a review of Torrey’s book on the subject.

It’s available at http://ajp.psychiatryonline.org. Place “Invisible Plague” into the search bar and follow the link with the same name.

Lecture Launcher 18.2: Brain Images Reveal Effects of Antidepressants Modern imaging techniques have clearly shown changes in brain activity following treatment with antidepressant medications. You can discuss these changes by building a foundation from the article provided by the University of Wisconsin. Go to http://www.wisc.edu and place “Brain Images Reveal Effects of Antidepressants” in the search bar. Select the link with the matching name.

Lecture Launcher 18.3: The Wonder Pill One of the most interesting clinical drug effects is not a drug effect at all, but the placebo effect—a clinically effective response to an inert substance. You can stimulate a great discussion of the placebo effect just by mentioning the term; for some interesting background information, show your class one or more of the online video clips from “The Wonder Pill,” a show from the “Scientific American Frontiers” series on PBS available at http://www.chedd-angier.com. Once there, click on “projects” at the top of the page and click on “Scientific American Frontiers” toward the bottom of the page. Once there, select season 13, episode 7 titled “The Wonder Pill.”

Lecture Launcher 18.4: What Causes Schizophrenia?

While researchers are convinced that schizophrenia has a biological cause or causes, exactly what these causes might be is still a subject of some interesting research. At present, the correlational research conducted with large populations in several countries has suggested many connections. An interesting discussion in class might begin with a statement of some of the observations and a critical assessment of these possibilities.

Web Links 18.2 The Schizophrenia Home Page 18.3 Schizophrenia Might Be Several Disorders 18.4 Schizophrenia 18.5 Schizophrenia Screening Quiz 18.6 Schizophrenia Possibly Linked to Early Brain Development 18.7 Fetal and Birth Complications Increase Mental Illness Risks 18.8 Schizophrenia “Linked to Lack of Sun” Handouts 18.2 Causes of Schizophrenia

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Chapter 18: Biopsychology of Psychiatric Disorders Lecture Launcher 18.5: What Causes Schizophrenia? Part 2 When first described, the category of schizophrenia was used very broadly. As understanding has increased, the definition has become more specific. Schizophrenia might not be a single disease as traditionally thought, but instead a collection of multiple disorders with similar symptoms that affect the brain differently. A study of more than 100 schizophrenics found they could be divided into at least two different groups based on memory impairment and structural and functional differences in their brains (Bruce Turetsky, associate director of neuropsychology at the University of Pennsylvania and principal investigator of the study).

Web Links 18.2 The Schizophrenia Home Page 18.3 Schizophrenia Might Be Several Disorders Lecture Launcher 18.6: Developmental Abnormalities and Schizophrenia Schizophrenia appears to be related to developmental abnormalities in the brain. Clues may be found in the rest of the body as well. Prenatal development includes critical periods when organs and structures are going through rapid growth and cell division. During these periods, the cells are more susceptible to damage. One might expect that if there is a period of damaging influence, several structures might be damaged, including those responsible for schizophrenia.

Scientific evidence points to a possible link between schizophrenia and altered brain development in the first three months of pregnancy. Babies born with minor physical abnormalities may be at increased risk of developing psychological problems such as schizophrenia—especially if one or both of the parents suffers from schizophrenia. A new study published in the American Journal of Psychiatry found that children who were born with several physical deviations such as wide-set eyes, a high palate, low-set ears, or a curved fifth finger, among other anomalies, were more likely to suffer from schizophrenia-related disorders than no mental illness at all. Those with a high number of slight physical irregularities were also more likely to suffer from schizophrenia than other mental problems. (Web Link 18.6) The perspective on schizophrenia developed over the last ten years is that there is an early insult in the first trimester of pregnancy that basically pushes brain development in a somewhat aberrant direction.

Web Links 18.6 Schizophrenia Possibly Linked to Early Brain Development 18.7 Fetal and Birth Complications Increase Mental Illness Risks Lecture Launcher 18.7: Activity in the Brain View SPECT images of normal brains and those of people diagnosed with ADHD, anxiety disorders, PTSD, obsessive-compulsive disorder, etc. Help the students to read the SPECT images and make the comparisons between the different disorders. See Images into Human Behavior: A Brain SPECT Atlas by Daniel G. Amen, M.D. “This color atlas contains 115 pages of brain SPECT images. It compares normal to abnormal brain images and looks at functional neuroanatomy, strokes, dementia, brain trauma, depression, bipolar disorder, schizophrenia, PMS, anxiety, attention deficit disorder, obsessive compulsive spectrum disorders, violence, alcohol and drug abuse, and before and after treatment studies.”

Images can also be found on the Internet. < Return to Table of Contents

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Biopsychology, Tenth Edition

ACTIVITIES Activity 18.1: Case Studies Have the students work in pairs or small groups to determine the positive and negative symptoms of schizophrenia from the case studies.

Handout 18.1 Case Studies Activity 18.2: Tourette’s Disorder Awareness These activities are suggested as a way to have more understanding of the difficulty that someone with Tourette’s disorder might have in making sense out of a normal world, on top of the social difficulties caused by the disorder. Does the brain seem to have biological areas of activity or inactivity that would suggest the processing difficulties described? Does the behavior cause the brain activity irregularities or do the brain abnormalities cause the behavior?

Web Links 18.15 Tourette's Disorder Awareness < Return to Table of Contents

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Chapter 18: Biopsychology of Psychiatric Disorders

ASSIGNMENTS Assignment 18.1: Causes of Schizophrenia Have students organize the information on schizophrenia in a table to assist them in keeping track of the relationship between the putative causes of schizophrenia and the evidence for each. You could ask them to choose one cause and search for more detailed information and evidence, or to write a brief paper supporting their choice for the cause.

Assignment 18.2: Causes of Schizophrenia Literature Search A web-based search should include indications of the validity of the information through some type of evaluation of the sources used.

Have students do research to add to the causes listed in the text and then answer the questions, such as: Are these causes related to any of the other factors already described? For example: There are several possible causes that have their effect during prenatal development, such as viral infections during the first trimester, or levels of nutrients such as vitamin D. Another possibility is the effect of maternal diuretics administered during pregnancy. Can students evaluate this information in line with the summaries of the studies already described?

Web Links 18.4 Schizophrenia 18.6 Schizophrenia Possibly Linked to Early Brain Development 18.7 Fetal and Birth Complications Increase Mental Illness Risks 18.8 Schizophrenia “Linked to Lack of Sun” Handouts 18.2 Causes of Schizophrenia < Return to Table of Contents

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Biopsychology, Tenth Edition

WEB LINKS Web Link 18.1: Dana Brain Web Go to http://www.dana.org/ and place “Brain Web” into the search bar. Select the matching link.

The focus of the Dana Brain Web is on sites relating to brain diseases and disorders. Lots of brief news articles.

Web Link 18.2: World Fellowship for Schizophrenia and Allied Disorders Go to http://www.world-schizophrenia.org and search around for any information on schizophrenia you may need.

Web Link 18.3: Schizophrenia Might Be Several Disorders Go to https://source.wustl.edu/ and place “Schizophrenia not a single disease” in the search bar. Select the first link that appears from your search. Schizophrenia might not be a single disease as traditionally thought, but instead a collection of multiple disorders with similar symptoms that affect the brain differently.

Web Link 18.4: Schizophrenia Go to https://www.nimh.nih.gov/index.shtml and click on the drop down menu labeled “Health and Education” and select “schizophrenia” from the listed options.

A comprehensive overview of what is currently known about schizophrenia.

Web Link 18.5: Schizophrenia Screening Quiz Go to http://psychcentral.com/ and click on “quizzes.” Scroll down the quiz page until you get to “Schizophrenia.” For helping to determine whether you have symptoms commonly associated with schizophrenia.

Web Link 18.6: Schizophrenia Possibly Linked to Early Brain Development Go to http://www.sciencedaily.com/ and place “Schizophrenia Linked to Early Brain Development” in the search bar. Select the link at the top of the search results.

“Scientific evidence points to a possible link between schizophrenia and altered brain development in the first three months of pregnancy, according to a new report from the University of North Carolina at Chapel Hill. Writing in the July issue of Biological Psychiatry, Dr. Anthony-Samuel LaMantia, associate professor of cell and molecular physiology at the UNC-CH School of Medicine, for the first time brings together compelling interdisciplinary findings, including new research from his laboratory, to support a neurodevelopmental theory of schizophrenia. ‘The idea of schizophrenia developed over the last 10 years is there’s an early insult in the first trimester of pregnancy that basically pushes brain development in a somewhat aberrant direction,’ he said.”

Source: University of North Carolina School of Medicine. Date: 1999–07–08.

Web Link 18.7: Hypoxic-Ischemia-Related Fetal/Neonatal Complications and Risk of Schizophrenia Go to http://www.ajp.psychiatryonline.org and place “Hypoxic-Ischemia-Related Fetal/Neonatal Complications and Risk of Schizophrenia and Other Nonaffective Psychoses: A 19-Year Longitudinal Study” in the search bar. Select the matching article.

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Chapter 18: Biopsychology of Psychiatric Disorders “New mental illness research offers bold insights into mental health risks associated with fetal and birth complications according to several papers published in the February 2000 issue of the American Journal of Psychiatry. In a study at Columbia University and the New York State Psychiatric Institute, researchers learned the risk of developing major mental illness after fetal and birth complications.

Web Link 18.8: Schizophrenia Linked to Lack of Sun Go to http://news.bbc.co.uk/ and place “Schizophrenia linked to lack of sun” in the search bar. Select the matching link.

“Sun deprivation could cause a seasonal peak in babies born with schizophrenia. Some cases of schizophrenia may be caused by mothers being deprived of sunshine during pregnancy, an expert has suggested. It has been known for more than 80 years that there was a seasonal peak of cases in North America and Europe in March. Babies born between February and April are 10% more likely to develop schizophrenia than those born at other times of the year.”

Web Link 18.9: All About Depression Go to http://www.mentalhelp.net/ and place “depression” in the search bar. Select the link for “major depression and other unipolar depressions.”

This site from the Mental Health Network contains links on depression diagnosis, therapy, and organizations.

Web Link 18.10: Depression Central Go to http://www.depressioncentral.net/. This is a reference Web site on depression that includes information on books, videos, associations, as well as sites related to the assessment and treatment of bipolar disorder, unipolar disorder, and SAD. Web Link 18.11: Medical Conditions and Depression http://www.allaboutdepression.com/ We all are vulnerable to depression, but people with some serious or chronic diseases may be at greater risk. It may also be true that those who are depressed could be at greater risk for developing certain medical conditions.

Web Link 18.12: Anxiety Disorder Resources Go to http://www.nimh.nih.gov/ and place “anxiety disorders” in the search bar. This NIMH site provides links to articles and fact sheets on anxiety disorders including panic disorder, phobias and generalized anxiety disorder.

Web Link 18.13: Phobia List http://www.phobialist.com/ Students will enjoy visiting this site on naming phobias.

Web Link 18.14: Social Phobia http://www.socialphobia.org The topic of this association site is social phobia; the site includes fact pages as well as links to other sites relating to phobia and anxiety.

Web Link 18.15: Tourette’s Disorder Awareness Go to http://www.ninds.nih.gov/ and place “Tourette Syndrome” in the search bar. Select the “Tourette Syndrome Information Page” from the results.

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Biopsychology, Tenth Edition Web Link 18.16: National Center for PTSD http://www.ptsd.va.gov/ “The National Center for Post-Traumatic Stress Disorder (PTSD) was created within the Department of Veterans Affairs in 1989, in response to a Congressional mandate to address the needs of veterans with military-related PTSD. Its mission was, and remains: To advance the clinical care and social welfare of America’s veterans through research, education, and training in the science, diagnosis, and treatment of PTSD and stress-related disorders. This website is provided as an educational resource concerning PTSD and other enduring consequences of traumatic stress.”

• • • • •

Information on the war in Iraq Latest fact sheets and literature on the war in Iraq Topics in PTSD Information related to traumatic stress PILOTS Database

Access information from the PILOTS Database, the largest interdisciplinary index to the worldwide literature on traumatic stress, which contains over 22,000 abstracts.”

Web Link 18.17: Understand the Facts about Post-Traumatic Stress Disorder Go to https://www.adaa.org/ and place “Post-traumatic Stress Disorder” in the search bar. Select the link with the matching name.

Web Link 18.18: Bipolar Disorder Go to https://www.nimh.nih.gov and select “Bipolar Disorder” on the menu on the right-hand side of the page.

Web Link 18.19: FDA Drug Development Go to http://www.fda.gov and click on the “Drugs” tab at the top of the page. Scroll down that page to the link for “Drug development and approval process.” < Return to Table of Contents

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Chapter 18: Biopsychology of Psychiatric Disorders

HANDOUTS Handout 18.1: Case Studies Hannah Hannah sits quietly in the corner of a room at the local homeless shelter. She stares at the floor and occasionally begins to cry softly as she repeats “Please don’t leave me, please don’t leave me…” Sometimes she will get up and join the line for meals or use the bathroom. If someone tries to disturb her, she screams loudly, and the staff has learned to leave her alone.

Tommy Tommy has just started his first semester at Old State U. This is the first time he has been away from home and he is lonely. Tommy has never made friends easily. His roommate is from a nearby town and seldom even enters the room. Many of the other young men on his floor seem to know each other from athletics or parties at local high schools. Tommy has always been rather quiet and studious.

Last night, Tommy was found in the shower by the resident assistant. He was soaking wet and fully dressed.

Tommy kept mumbling something about the speakers that had been secretly installed in his ears and how the water would short them out and stop the messages.

Asa Asa works in the mailroom at Zip-It-Up Bags. Everyone thinks of him as a nice enough guy and a reasonably reliable employee, though he is a little strange. He never seems to get excited about anything, and sometimes does not understand the jokes the others tell. He usually eats his lunch in the janitor’s closet and does not associate much with the other employees.

Occasionally, he will get part of the way through sorting the mail and just stop and go outside for anywhere from a few minutes to several hours. Luckily, Zip-It-Up doesn’t get too much mail, and what doesn’t get done today can be taken care of tomorrow.

Tammy Lou Tammy Lou is a clerk at Randy’s Shop and Drop laundry and grocery store. She has always been a bit quiet and unassuming, but very pleasant, and the staff is very fond of her. Wilma, the part owner of Randy’s, has been encouraging her to be less shy, to spruce herself up, and get out more.

Two weeks ago, Tammy Lou came to work in a new pink ruffled dress. She seemed very happy about something. (Wilma thought she might actually have a boyfriend!) As the week has progressed, she has had a new outfit every day.

This Monday, she came in wearing blue eye shadow and bright red lipstick, and she had her fingernails and toenails painted bright red to match. (They go with her red shorts, white sandals with three-inch heels, and red, white and blue flag printed shirt—just in time for the 4th of July.) She brought in a bag full of patriotic decorations and began running all over the store, draping crepe paper and hanging flags while singing “America the Beautiful” and dancing on the dryers.

On Tuesday and Wednesday, she dropped in only long enough to tell Wilma that she was planning to start her own grocery store and needed time off to go to the bank for a loan. Thursday and Friday she did not appear at all. < Return to Table of Contents 22 ..

Biopsychology, Tenth Edition Handout 18.2: Causes of Schizophrenia Literature Search Your text discusses several options that have been investigated in the search for the cause of schizophrenia, but gives only brief summaries of the research.

Choose one of the causes mentioned, or another possibility, and conduct your own search for evidence using the Web and your library.

Try to find primary sources, that is, work written by the original researchers, not summarized by someone else in a textbook or newspaper article.

Write a brief paper discussing the evidence available for this proposed cause.

Make the points you have gleaned from your research and consideration of the data and then provide evidence, both for and against, for each point, before you draw your conclusions.

< Return to Table of Contents

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