Vanders human physiology the mechanisms of body function 14th edition widmaier solutions manual

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6: NEURONAL SIGNALING AND THE STRUCTURE OF THE NERVOUS SYSTEM CHAPTER OVERVIEW The chapters preceeding Chapter 6 provided an important overview of physical and chemical properties that contribute to human physiological function. In Chapter 6, these principles are applied to the first organ system to be studied, the Nervous System. The Nervous System is an important means for communication across the body, and this communication occurs via changes in the electrical activity of neurons. This chapter will first describe the cells of the Nervous System. Next, the mechanisms that determine the difference in charge across a neuron cell membrane and how it is used as a means for communication from one neuron to another is described. This chapter also summarizes the different classes of neurotransmitters, one of the intercellular signaling molecules, that are used for neuron-to-neuron (or effector) communication. The last section of this chapter summarizes the structural and functional organization of the Nervous System CONTEXT FOR CHAPTER 6 One of the most fascinating stories in the history of physiology is the discovery of neurotransmitters by the German scientist Otto Loewi, who was awarded the 1936 Nobel Prize for Physiology or Medicine for his discovery. Part of the fascination lies in the report that the idea for the critical experiment proving the existence of chemical messengers from nerves came to Loewi in a dream. Loewi knew that stimulating the vagus nerve in frogs, as in humans, causes the heart rate to slow. The question was: how? Was the cause an electrical “spark” that inhibited the heart's pacemaker? Or was it a chemical messenger released by the nerve? Loewi also knew that the frog heart can keep beating long after its removal from the animal if placed in an isotonic salt solution approximating extracellular fluid. Loewi performed a simple, yet brilliant, experiment: He placed one frog heart, with its vagus nerve still attached, into a dish of isotonic saline (dish A) and another heart without the vagus into another dish with the same saline (dish B). He then electrically stimulated the vagus nerve of the heart in dish A and watched the heart rate slow. After some time, he removed the stimulated heart and transferred the other heart from dish B to dish A—and observed that the beating of the second heart slowed to match that of the first one! Something in the saline acted like a stimulated vagus nerve in affecting heart rate. The signal from nerve to muscle thus had to be a chemical.

The junction between a nerve and a muscle is a neuromuscular junction, not a synapse. But scientists soon realized that most nerve cells “talk” to each other as well as to the heart and other muscles. This communication takes place by means of chemical messengers called neurotransmitters.

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Chapter 6 is divided into four different sections to provide an overview of the structures and functions of the Nervous System.

Section A: Cells of the Nervous System. Generalized cell structure was presented in Chapter 3. This chapter describes the specific cellular structures and functional classes of neurons, the “nerve cells”. Glial cells, the second type of cells found in the Nervous System are also described.

Section B: Membrane Potentials. This section brings together electrical principles from physics and the movement of ions across the neurolemma to explain the how neurons changes in membrane potential for communication. The differences between graded potentials and action potentials are especially important to highlight and will be applied to many organ systems: the Muscular System, the Cardiovascular System, and so on.

Section C: Synapses. Once a “message” has reached an axon terminal in one neuron, how can it be relayed to a second neuron or other target tissue? The answer is via neurotransmitter release into the synapse, or the junction between the presynaptic neuron and a postsynaptic neuron/effector. If the neurotransmitter binds to receptors in the postsynaptic neuron, graded potentials are generated and if they reach threshold an action potential will be created for the continued propagation of the “message”. The different classes of neurotransmitters are also described.

Section D: Structure of the Nervous System. This section begins with an overview of the structural and functional organization of the Nervous System. It highlights information flow between different divisions. Importantly, the autonomomic division of the Nervous System is highlighted. The autonomic nervous system is a vital component of many homeostatic reflex mechanisms as it innervates many different organs throughout the body. Upcoming discussion of other organ systems throughout the body will hinge upon the understanding of autonomic function.

CONCEPTS COMMONLY FOUND TO BE CHALLENGING – TEACHING HINTS This is an expansive chapter covering many important aspects of Nervous System function.

Instructors may find areas to highlight or skim over depending upon the specific focus of the course and time availability.

1. To give context, instructors may want to provide a very general overview of the Nervous System as an introduction: explain that communication among the different divisions of the Nervous System is vital for homeostatic regulation and human function. How is this communication possible? To answer this question, students must understand neuron function.

2. The factors contributing to resting membrane potential and how it is maintained are important and tie together several concepts from chemistry, physics, and previous chapters: the difference between the intracellular and extracellular fluid compartments, ©2017 by McGraw-Hill Education. This is proprietary material solely for authorized instructor use. Not authorized for sale or distribution in any manner. This document may not be copied, scanned, duplicated, forwarded, distributed, or posted on a website, in whole or part.

membrane transport mechanisms and specifically voltage- gated ion channels, the Na+/K+ATPase pump, and as a positive feedback example during action potential generation.

There are numerous instructor resources available for this very important topic; pay specific attention to figures and tables in the text and consider the inclusion of animations during class sections or as recommendations for out-of-class activities.

3. It is common for students to have questions about the similarities/differences for graded potentials and action potentials. Temporal and spatial summation are sometimes also not immediately clear to students. One suggestion is to approach summation like it is a math problem, and actually find the sum of the changes in membrane potential in response to EPSPs and IPSPs to see if it reaches threshold.

4. Fig. 6.27 is a great one to carefully review. It summarizes the sequence of events at a chemical synapse, which can lead into a discussion of mechanisms for pre/post synaptic modulation of the “message” being sent, EPSP/ IPSP generation on the postsynaptic membrane, etc. These factors can be added in to the model depicted in Fig. 6.27.

5. Fig. 6.46 is also an excellent review to compare and contrast the somatic and autonomic divisions of the peripheral nervous system. It highlights: general structural organization, neurotransmitters released, classes of neurotransmitter receptors, epinephrine as a neurohormone, dual innervation and antagonistic control of autonomic effectors.

6. Suggested topic for discussion: 

Research efforts toward restoring function to damaged brain and spinal cord



Drugs and the blood-brain barrier. Suggested examples: Treatment of Parkinson’s disease includes administering L-dopa but not dopamine because dopamine cannot cross the blood-brain barrier. Allergy sufferers benefit from antihistamines but many of the classical drugs (e.g., Benadryl) cross the blood-brain barrier and make the person drowsy. Newer drugs (e.g., Claritin, Allegra) are effective antihistamines for sinus and nasal allergy symptoms, but they do not cross the blood-brain barrier and thus cannot affect one’s state of alertness.

LECTURE OUTLINE SECTION A: Cells of the Nervous System I. The central and peripheral nervous systems II. Neurons A. Structures: cell body, dendrites, axons, initial segment, axon terminals (Fig. 6.1) B. Sequence of information flow (electrical signals) across neurons C. Myelination (Fig. 6.2) D. Axon transport (Fig. 6.3) ©2017 by McGraw-Hill Education. This is proprietary material solely for authorized instructor use. Not authorized for sale or distribution in any manner. This document may not be copied, scanned, duplicated, forwarded, distributed, or posted on a website, in whole or part.

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III. Functional classes of neurons (Fig. 6.4, Table 6.1) IV. Neuronal communication: the synapse (Fig. 6.5) V. Glial cells (Fig. 6.6) VI. Neuronal growth A. Undifferentiated precursor/stem cells B. Migration C. Growth cone D. Neurotrophic factors E. Plasticity VII. Neuronal regeneration

LECTURE OUTLINE SECTION B: Membrane Potentials I. Basic principles of electricity A. Interaction of positive and negative charges (Fig. 6.7) B. Physical principles: potential, current, resistance, Ohm’s Law (Fig. 6.8) C. Applications to the fluid compartments of the human body (Fig. 6.8) II. Resting membrane potential A. Definition and measurement (Fig. 6.8) B. Determinants 1. Ion concentration differences (Fig. 6.9, Fig. 6.10, Fig. 6.11, Fig. 6.12, Table 6.2) 2. Ion permeabilities and leak channels (Fig. 6.12) 3. Ion pumps: the Na+/K+-ATPase pump (Fig. 6.13) III. Membrane potentials in excitable cells A. Terminology (see Fig. 6.14 and Table 6.3) 1. Deplarization (Fig. 6.15, Fig. 6.18) 2. Repolarization (Fig. 6.18) 3. Overshoot and Repolarization B. Properties of graded potentials (Figs. 6.16, Fig. 6.17, Table 6.4) 1. Graded response to increasing stimulus intensity 2. Decremental conduction of signal 3. Summation of responses to two or more stimuli C. Action potentials (Fig. 6.19, Table 6.4) 1. Changes in membrane potential (Fig 6.21) 2. Changes in ion permeability and properties of involved ion channels (Fig. 6.18) 3. Properties of action potentials a. Threshold potential i. Ionic basis for reaching the threshold potential ii. Voltage-gated channels and positive feedback (Fig. 6.20) b. All-or-none response ©2017 by McGraw-Hill Education. This is proprietary material solely for authorized instructor use. Not authorized for sale or distribution in any manner. This document may not be copied, scanned, duplicated, forwarded, distributed, or posted on a website, in whole or part.

c. Refractory periods: absolute and relative (Fig. 6.22) 4. Propagation of action potentials a. Unidirectional, nondecremental propagation (Fig. 6.23) b. Myelinated axons (Fig. 6.4) LECTURE OUTLINE SECTION C: Synapses I. Transmission of neural signals from neuron to neuron: the synapse (Fig. 6.26) A. Convergence and divergence in synaptic pathways (Fig. 6.25) B. Mechanisms of neurotransmitter release (Fig. 6.27) C. Excitatory and inhibitory postsynaptic potentials (Fig. 6.28, Fig. 6.29, Fig. 6.30, Fig. 6.32) D. Synaptic integration (Fig. 6.31) 1. Temporal summation 2. Spatial summation E. Regulation of synaptic strength (see Table 6.5) 1. Presynaptic mechanisms (Fig. 6.33) 2. Postsynaptic mechanisms 3. Modulation by drugs and disease (Fig. 6.34) II. Classes of neurotransmitters or neuromodulators (see Table 6.6) A. Acetylcholine (ACh) and cholinergic receptors B. Biogenic amines 1. Catecholamines (Fig. 6.35) a. Dopamine (DA) b. Norepinephrine (NE) c. Epinephrine (Epi) 2. Serotonin (5-hydroxytryptamine, 5-HT) C. Amino acids 1. Excitatory: glutamate (Fig. 6.36) 2. Inhibitory a. GABA (gamma-aminobutyric acid) b. Glycine D. Neuropeptides: endogenous opioids E. Gases 1. Nitric oxide 2. Carbon monoxide 3. Hydrogen sulfide F. Purines 1. ATP 2. Adenosine G. Neuroeffector communication

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LECTURE OUTLINE SECTION D: Structure of the Nervous System I. Overview of the structures and general functions of the Nervous System (Fig. 6.37) II. The Central Nervous System, CNS (see Fig. 6.37) A. The Brain (Fig. 6.38, Table 6.7) 1. Cerebrum (see Fig. 6.38, Fig. 6.39) a. Gray matter i. Cerebral cortex ii. Subcortical nuclei b. White matter—fiber tracts and corpus callosum 2. Limbic system (Fig. 6.40) 3. Diencephalon—thalamus, hypothalamus, and epithalamus (Fig. 6.38) 4. Hindbrain: cerebellum (Fig. 6.38) 5. Brainstem—midbrain, pons, and medulla oblongata (Fig. 6.38) B. Spinal cord (Fig. 6.41, 6-42) 1. Gray matter a. Dorsal horns b. Ventral horns 2. White matter—ascending and descending tracts III. The Peripheral Nervous System, PNS: structure and general functions (see Fig. 6.7, Fig. 6.45, Fig. 6.46, Table 6.9) A. Cranial and spinal nerves (Table 6.8, Fig. 6.42) B. Somatic nervous system B. Autonomic nervous system (Fig. 6.43, Fig. 6.44, Table 6.11) 1. Sympathetic division 2. Parasympathetic division III. Protection of the brain A. Cerebrospinal fluid (Fig. 6.47) B. The blood-brain barrier

TEACHING/LEARNING OBJECTIVES BY SECTION SECTION A: Cells of the Nervous System 6.1 Structure and Maintenance of Neurons Students should be able to: explain that the nervous system is composed of Central Nervous System (CNS) and Peripheral Nervous System (PNS) divisions: the brain and spinal cord comprise the CNS and the cranial and spinal nerves comprise the PNS. ©2017 by McGraw-Hill Education. This is proprietary material solely for authorized instructor use. Not authorized for sale or distribution in any manner. This document may not be copied, scanned, duplicated, forwarded, distributed, or posted on a website, in whole or part.

identify that the basic unit of the nervous system is a nerve cell or neuron, which is capable of transmitting electrical signals that lead to the release of chemical neurotransmitters. identify the structures—cell body, dendrites, and axon—found on most neurons. describe the general sequence of information flow via electrical signals across the different regions of a neuron. name the myelin-forming cells in the CNS and PNS. Explain how myelin is formed, and what its general function is. define axonal transport, describe its general function, and identify two motor proteins associated with this process.

6.2 Functional Classes of Neurons Students should be able to: identify the three functional classes of neurons—afferent, efferent, and interneurons— and identify the direction of information flow relative to the CNS and/or PNS. know the ratio of 1 afferent neuron to 10 efferent neurons to 200,000 interneurons. state where the cell bodies and axons for each class of neuron are located, and generally what type of information each class of neurons relays. distinguish between a nerve fiber and a nerve. describe the relationship of one neuron to another at a synapse. Understand that all interneurons are both postsynaptic cells and presynaptic cells.

6.3 Glial Cells Students should be able to: describe the general functions of glial cells with regard to Nervous System function. list types of glial cells and generally describe their functions. explain the functional role of the blood-brain barrier. identify the structures associated with the blood-brain barrier. recognize that some glial cells play a role in immune function in the CNS. 6.4 Neural Growth and Regeneration understand that neurons develop from precursor cells, migrate to their final location, and send out processes to their target cells. describe the importance of plasticity during the first few years following birth. recognize that recent research suggests that new neurons can be produced in some brain regions throughout life. explain that after damage to an axon, a peripheral neuron may regrow that axon to its target organ, but that damaged neurons in the CNS do not regenerate (yet—but scientists are working on how to promote axonal regeneration in the CNS).

SECTION B: Membrane Potentials

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6.5 Basic Principles of Electricity Students should be able to: identify the major positive and negative ions in the intracellular and extracellular fluids. describe how positive and negative charges interact with each other. recognize that a separation of charges results in an electrical potential, which has the capacity to do biological work. understand how current, voltage, and resistance are related (Ohm’s law). explain why water is a good conductor of electricity.

6.6 The Resting Membrane Potential Students should be able to: recognize that in all body cells under resting conditions there is a potential difference across the membrane such that the inside is negative with respect to the outside. understand that the membrane potential is a result of two factors: (1) the uneven distribution of (primarily) Na+ and K+ across the plasma membrane and (2) the unequal permeabilities of membranes to those ions. describe how a two-compartment model of solutions of NaCl and KCl separated by a selectively permeable membrane demonstrates how a membrane potential can be generated by having the membrane first permeable only to K +, and then permeable only to Na+. define equilibrium potential as the membrane potential needed to oppose the diffusion of ions based upon a given concentration gradient, and at this point there is no net flux of the ion. Recognize that each type of ion has its own equilibrium potential. state the Nernst equation, and understand that it is used to determine the equilibrium potential for a particular type of ion. recognize that the Goldman-Hodgkin-Katz (GHK) equation can be used to calculate the resting membrane potential of a cell by taking into consideration relative membrane permeabilites to different ions. understand why the resting membrane potential of cells is much closer to the equilibrium potential for K+ than to the equilibrium potential for Na+. define the term leak channel and describe how it influences membrane potential. recognize that at the resting membrane potential, the driving force for Na + diffusion is much greater than that for K+. discuss the importance of the Na+/K+-ATPase in maintaining the concentration gradients for Na+ and K+ and establishing the resting membrane potential. describe how the movement of the Cl- is affected by the membrane potential.

6.7 Graded Potentials and Action Potentials Students should be able to: define the terms depolarize, repolarize, and hyperpolarize. understand that depolarizing a membrane causes it to have a lesser potential difference across (i.e. it becomes more positive). ©2017 by McGraw-Hill Education. This is proprietary material solely for authorized instructor use. Not authorized for sale or distribution in any manner. This document may not be copied, scanned, duplicated, forwarded, distributed, or posted on a website, in whole or part.

define graded potential and describe how local current surrounding the depolarized region produces depolarization of adjacent regions. describe how the magnitude of the graded potential is affected by the magnitude of the stimulus, the distance the potential has traveled, and summation. describe an action potential and identify the types of cells with excitable membranes capable of generating action potentials. compare and contrast graded potentials and action potentials. discuss the importance of ligand-gated channels and mechanically-gated channels to the initiation of an action potential and the importance of voltage-gated channels to the excitability of the membrane. reproduce an action potential as membrane potential vs. time and label its various parts in terms of being depolarized, repolarizing, and after-hyperpolarized. Superimpose the changing patterns of Na+ and K+ permeabilities on the action potential. describe the mechanism of ion channel changes that generate and terminate action potentials. Appreciate that the action potential is a good example of a physiologically important positive feedback mechanism. explain why the threshold potential must be reached in order for a neuron to generate an action potential. explain why action potentials are said to be “all-or-none.” understand the ionic basis of relative and absolute refractory periods. differentiate between action potential propagation in myelinated axons and in unmyelinated ones. provide a physiological description of three different ways that action potentials can be initiated.

SECTION C: Synapses 6.8 Functional Anatomy of Synapses Students should be able to: differentiate between excitatory and inhibitory synapses. discuss how the functional anatomy of a synapse can account for the one-way conduction of action potentials in a neural circuit. draw a model illustrating convergence and divergens of neural inputs and discuss the implications of these processes for synaptic transmission of information. compare the structural and functional similarities and differences between electrical and chemical synapses. recognize that electrical synapses have recently been described in widespread locations in the adult mammalian nervous system. diagram a typical chemical synapse.

6.9 Mechanisms of Neurotransmitter Release Students should be able to: ©2017 by McGraw-Hill Education. This is proprietary material solely for authorized instructor use. Not authorized for sale or distribution in any manner. This document may not be copied, scanned, duplicated, forwarded, distributed, or posted on a website, in whole or part.

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understand that neurotransmitters are stored in vesicles within the axon terminal. outline the sequence of events that links action potential propagation to neurotransmitter release. discuss the role of Ca2+ in stimulating neurotransmitter exocytosis from synaptic vesicles.

6.10 Activation of the Postsynaptic Cell Students should be able to: describe the general ways in which neurotransmitters can directly or indirectly affect ion channels on the postsynaptic membrane. describe the three ways that unbound neurotransmitters can be removed from a synaptic cleft. distinguish between an excitatory postsynaptic potentials (EPSPs) and an inhibitory postsynaptic potentials (IPSPs), discuss which ions are typically responsible for each, and identify whether the membrane potential is increased or decreased.

6.11 Synaptic Integration Students should be able to: recognize that the membrane potential of a postsynaptic cell reflects the effects of possibly hundreds of different, simultaneous synaptic inputs, both excitatory and inhibitory. understand how spatial and temporal summation interact to influence membrane potential and may bring a postsynaptic cell to threshold. discuss the significance of the initial segment of a postsynaptic cell’s axon and why synapses near the initial segment have greater influence on the cell’s activation than do synapses far removed from it.

6.12 Synaptic Strength Students should be able to: appreciate that the amount of neurotransmitter released following an action potential’s arrival at the axon terminal is variable. discuss the effects of greater or lesser amounts of neurotransmitter on the postsynaptic cell. appreciate the importance of presynaptic (axo-axonic) synapses and autoreceptors in altering synaptic effectiveness. differentiate presynaptic inhibition from presynaptic facilitation. propose postsynaptic mechanisms that could varying synaptic effectiveness. define receptor desensitization and explain how it influences the postsynaptic response. identify eight mechanisms by which certain diseases and drugs can alter synaptic effectiveness, and explain whether each mechanism affects pre- or post- synaptic neural transmission.

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6.13 Neurotransmitters and Neuromodulators Students should be able to: differentiate between neurotransmitters and neuromodulators. list the six major classes of neurotransmitters and neuromodulators. describe how and where acetylcholine is synthesized and metabolized. discuss what is meant by the terms cholinergic neurons and cholinergic receptors; identify nicotinic and muscarinic receptors as cholinergic receptors. explain the link between Alzheimer’s Disease and cholinergic neuron function. list five common biogenic amines. describe the synthetic pathway for the catecholamines and how and where they are metabolized. Understand why neurons that secrete norepinephrine or epinephrine are called adrenergic neurons.

Identify the two major classes of adrenergic receptors. describe the general functions/actions of the biogenic amine serotonin and the amino acid neurotransmitters glutamate, GABA, and glycine. discuss the role of glutamate in long-term potentiation and exitotoxicity. discuss how the synthesis of neuropeptide neurotransmitters differs from that of other types of neurotransmitters. describe the general role of the opioid family of neurotransmitters. (The first one of these to be discovered, beta-endorphin, was given its name because it resembled “endogenous morphine” in relieving pain.) discuss how gases such as nitric oxide, carbon monoxide, and hydrogen sulfide can act as neurotransmitters. recognize that the purines, ATP and adenosine, act principally as neuromodulators.

6.13 Neuroeffector Communication Students should be able to: understand what is meant by the term neuroeffector communication and neuroeffector junctions. understand the functional similarities for neuron-to-neuron communication and neuron-effector communication.

SECTION D: Structure of the Nervous System Introduction Students should be able to: describe the organization of the central and peripheral nervous systems. define the following terms: nerve, pathway/tract, commissure, ganglia, and (nervous system) nuclei 6.15 Central Nervous System: Brain Students should be able to: ©2017 by McGraw-Hill Education. This is proprietary material solely for authorized instructor use. Not authorized for sale or distribution in any manner. This document may not be copied, scanned, duplicated, forwarded, distributed, or posted on a website, in whole or part.

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describe the general structural organization of the brain. identify the structures and general functions associated with the cerebrum, limbic system, diencephalon, cerebellum, and the brainstem. differentiate between white matter and gray matter.

6.16 Central Nervous System: Spinal Cord Students should be able to: describe the basic anatomy of the spinal cord and its associated nerves. Differentiate between the dorsal and ventral horns, and the dorsal and ventral roots. explain the significance of the dorsal root ganglia.

6.17 Peripheral Nervous System Students should be able to: distinguish between the afferent and efferent divisions of the peripheral nervous system. recognize that the efferent division is divided into the somatic and autonomic nervous systems and that the autonomic division is divided into the parasympathetic, sympathetic, and enteric divisions. summarize the flow of information from the central nervous system to the somatic nervous system. Identify the primary neurotransmitter associated with the somatic motor system and its effector.

6.16 Autonomic Nervous System Students should be able to: describe the structural organization of the autonomic nervous system, and recognize that autonomic efferents consist of two neurons: a preganglionic and postganglionic neuron. identify similarities and differences between sympathetic and parasympathetic neurons, paying particular attention to neurotransmitters and postsynaptic receptors. explain how dual innervation of autonomic effectors contributes to regulation of body function. Appreciate the importance of dual innervation of organs to allow for finetuned control of organ function (akin to having both an accelerator and a brake). provide examples of autonomic effectors that exhibit dual innervation and effectors that do not. discuss the basic functions of the somatic and autonomic nervous systems (and appreciate that they are not actually separate nervous systems but are members or divisions of the peripheral nervous system). Understand how the two systems differ anatomically and functionally.

6.19 Protective Elements Associated with the Brain Students should be able to: define and discuss the importance of cerebrospinal fluid.

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recognize meningitis and hydrocephalus as examples of disease conditions related to cerebrospinal fluid. recognize that the brain is dependent upon a continuous supply of glucose and oxygen. understand the importance of the blood-brain barrier in regulating the composition of the brain’s extracellular fluid.

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CHAPTER 6 REVIEW QUESTIONS & ANSWERS

SECTION A: Cells of the Nervous System 1.

Describe the direction of information flow through a neuron in response to input from another neuron. What is the relationship between the presynaptic neuron and the postsynaptic neuron?

3.

Afferent neurons have dendrites and axonal projections that originate near the skin or organs.

Their cell bodies are located outside the CNS in the dorsal root ganglia. They also contain central processes, which is the part of the axon that projects into the CNS. Efferent neurons have cell bodies that lie within the CNS and axons that project out to muscles, glands, or other neurons. Interneurons lie entirely within the CNS. The enteric nervous system contains all three types of neurons, and the CNS contains parts of all three types of neurons - the central processes of afferent neurons, the interneurons, and the cell bodies and first part of the axon of efferent neurons.

Information flows into the dendrites and cell body regions of most neurons, and out from axons and axon terminals. The presynaptic neuron releases neurotransmitters into the synaptic cleft which then bind to receptors on the postsynaptic neuron to cause an effect.

2.

Where are afferent neurons, efferent neurons, and interneurons located in the nervous system? Are there places where all three could be found?

Contrast the two uses of the word receptor.

“Receptor” refers both to structures at the peripheral endings of afferent neurons that respond to physical or chemical changes in their environment by causing electrical signals to be generated in the neuron, and to the proteins within cells or on the plasma membrane of cells that are activated by an intercellular messenger.

SECTION B: Membrane Potentials 1.

Negative charges repel negative charges, positive charges repel positive charges, and negative and positive charges are mutually attractive. The electrical force of attraction between positive and negative charges increases with the quantity of charge and with a decrease in distance between them.

2.

carry the current. Thus, the ion-containing intracellular and extracellular fluids are relatively good conductors of electrical current, but membrane lipids contain very few charged groups and are very poor conductors (they have high electrical resistance).

Describe how negative and positive charges interact.

Contrast the abilities of intracellular and extracellular fluids and membrane lipids to conduct electrical current.

3.

Draw a simple cell; indicate where the concentrations of Na+, K+, and Cl- are high and low and the electric potential difference across the membrane when the cell is at rest.

Water that contains dissolved ions is a relatively good conductor of electricity because the ions can

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15 As stated above, (1) the relative ion concentrations on either side of the membrane and (2) the relative permeabilities of the membrane to the ions.

6.

4.

Explain the conditions that give rise to the resting membrane potential. What effect does membrane permeability have on this potential?

What role do Na+/K+-ATPase membrane pumps play in the membrane potential? Are these functions direct or indirect?

The resting membrane potential of neurons is close to but not equal to the K+ equilibrium potential because the membrane is not completely impermeable to Na+. Therefore, at rest, Na+ diffuses into the cell constantly along its electrochemical gradient as K+ diffuses out. (The diffusion force for Na+ is much greater than that for K+.) Thus, the Na+/K+-ATPase pumps must work constantly to maintain the concentration gradients of the ions. (The fact that the membrane at rest is much more permeable to K+ than to Na+ is reflected in the fact that the resting membrane potential is much closer to the equilibrium potential of K+ than to that of Na+.)

7.

Membrane potentials are generated by the diffusion of ions and are determined by the ionic concentration differences across the membrane and the membrane’s relative permeabilities to different ions. In a neuron at rest, the intracellular concentration of K+ is thirty times greater than its extracellular concentration.

Conversely, the extracellular concentrations of Na+ and Cl- are about ten times greater than their intracellular concentrations. Moreover, the permeability of the membrane to K+ at rest is much greater (50-75 fold) than its permeability to Na+, and thus the resting membrane potential is much closer to the equilibrium potential for K+ than for Na+. The Na+/K+-ATPase membrane pumps maintain the membrane potential indirectly by pumping K+ in and Na+ out, thereby maintaining the concentration gradients across the cell membrane. Because the pumps eject three Na+ for every two K+ they bring into the cell, they also have a small direct electrogenic effect on the membrane potential.

5.

Which two factors involving ion diffusion determine the magnitude of the resting membrane potential?

Explain why the resting membrane potential is not equal to the K+ equilibrium potential.

Draw a graded potential and an action potential on a graph of membrane potential versus time.

Indicate zero membrane potential, resting membrane potential, and threshold potential; indicate when the membrane is depolarized, repolarizing, and hyperpolarized.

Overshoot

+30

Depolarized Repolarizing

0 Resting membrane potential

Threshold potential

1

-70 Graded potential

2 Hyperpolarized TIME (milliseconds)

8.

List the differences between graded potentials and action potentials.

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16 (1) Graded potentials (GPs) have variable amplitude; action potentials (APs) are all-or-none once threshold depolarization is reached. AP amplitude is independent of the initiating event.

(2) GPs can be summed; APs cannot be summed.

(3) GPs have no threshold; APs have a threshold that is usually about 15 mV depolarized relative to the resting potential.

(4) GPs have no refractory period; APs have both an absolute and a relative refractory period.

(5) GPs are conducted passively and decrementally; APs are conducted actively and without decrement; the depolarization is amplified to a constant value at each point along the membrane.

(6) The duration of GPs varies with the initiating conditions; the duration of APs is constant for a given cell type under constant conditions.

(7) A GP can be a depolarization or a hyperpolarization; an AP is always a depolarization, with an overshoot (the cell becomes positive, inside with respect to outside) and an afterhyperpolarization phase in neurons.

(8) GPs are initiated by environmental stimuli (receptors), neurotransmitters (synapses), or spontaneously; APs are initiated by membrane depolarization (i.e., GPs that depolarize to threshold).

(9) The mechanism for eliciting GPs depends on ligand-gated channels or other chemical or physical changes; the mechanism for APs depends on voltagegated channels.

9.

Describe how ion movement generates the action potential.

Depolarization by a graded potential opens voltagegated Na+ channels. The higher extracellular Na+ concentration and the negative membrane potential favor the influx of Na+, which carries a positive charge into the cell. This depolarizes the cell further which opens more Na+ channels which allows more Na+ to enter. This positive feedback mechanism accounts for the "spike" or upstroke of the action potential. Na+ channel inactivation prevents further influx of Na+. As the slower, voltage-gated K+ channels open, the efflux of K+ begins. K+ efflux is

favored by the positive membrane potential and the higher intracellular K+ concentration. K+ efflux repolarizes the cell.

10. What determines the activity of the voltagegated Na+ channel?

The Na+ channel is said to be voltage-gated because it possesses charged amino acid residues that make it open and close in response to changes in the membrane potential. Negative membrane potentials tend to close the channel and depolarization opens the channel. Additionally, the channel can be closed by an inactivation gate that physically blocks the channel shortly after it is opened by depolarization.

11. Explain threshold and the relative and absolute refractory periods in terms of the ionic basis of the action potential.

The threshold is the level of depolarization at which Na+ influx just exceeds K+ outflux, so that there is a net flux of positive charge into the cell. The driving force for K+ out of the cell increases as the membrane depolarizes, but at threshold the increased permeability of the membrane for Na+ assures that the positive-feedback cycle can be sustained.

The absolute refractory period corresponds to the period when voltage-gated Na+ channels are already opened or are inactivated (roughly the first part of the repolarizing phase of the action potential). The relative refractory period corresponds to the period of increased K+ permeability after the first repolarizing phase, and this is also the timing when some of the voltage-gated Na+ channels have returned to their closed state. The reason that a suprathreshold stimulus (i.e., greater depolarization than at rest) is necessary for an action potential to be initiated during the relative refractory period is because some K+ channels are still open during this time, and net K+ efflux favors membrane hyperpolarization. Thus, Na+ influx resulting from a new stimulus must exceed K+ efflux, which is occurring simultaneously.

12. Describe the propagation of an action potential.

Contrast this event in myelinated and unmyelinated axons.

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17 In unmyelinated axons, action potentials are propagated by local current flow from the site of one action potential to an adjacent part of the axon membrane. Positive charge flows from the depolarized area in both directions along the intracellular membrane (and negative charges do the same along the outside of the membrane). In the “forward” direction, this current flow depolarizes the adjacent membrane to threshold, and an action potential is generated. In the “backward” direction, the membrane is still in the absolute refractory period, so it cannot be stimulated to generate another action potential.

saltatory conduction, and it is considerably faster than action potential propagation in unmyelinated axons.

13. List three ways in which action potentials can be initiated in neurons.

(1) receptor potentials (2) synaptic potentials (3) pacemaker potentials

In myelinated axons the same process occurs, except that current cannot flow across the membrane where there is myelin because myelin has a very high resistance to flow. Instead, the current flows along the membrane from one interruption in the myelin (a node of Ranvier) to the next. At the nodes, the current flow causes depolarization to threshold and an action potential is generated. This is called

SECTION C: Synapses 1.

At inhibitory synapses, the binding of neurotransmitter to its receptor results in a hyperpolarizing graded potential (an inhibitory postsynaptic potential—IPSP) or a stabilization of the membrane potential at (or below) its existing value. The activated receptor at such synapses causes ligand-sensitive channels for Cl- and/or K+ to open.

(In the cases where only Cl- channels open, a hyperpolarizing potential is not recorded but the membrane is more stabilized at its resting level than normal, because the increased membrane permeability to Cl- makes it more difficult for other ion types to change the membrane potential.)

Increasing the permeability to K+ causes the postsynaptic membrane potential to become more negative and closer to the K+ equilibrium potential.

Describe the structure of presynaptic axon terminals and the mechanism of neurotransmitter release.

See Figure 6.27 and accompanying text for a description of the structure of presynaptic axon terminals and the detailed mechanism of neurotransmitter release.

2.

Contrast the postsynaptic mechanisms of excitatory and inhibitory synapses.

At an excitatory synapse, the postsynaptic response to the released neurotransmitter is a depolarization (an excitatory postsynaptic potential—EPSP) because binding of neurotransmitter to its receptor causes ligand-sensitive channels for small, positively charged ions to open. Even though the permeability of the postsynaptic membrane is increased to both Na+ and K+, both the electrical and concentration gradients favor Na+ influx, while the electrical gradient opposes the concentration gradient for K+.

Therefore, there is net influx of Na+ and an increase in membrane potential.

3.

Explain how synapses allow neurons to act as integrators; include the concepts of facilitation, temporal and spatial summation, and convergence in your explanation.

Neurons act as integrators because they receive information in the form of synaptic activity from more (often many, many more) than one presynaptic

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18 cell, a property known as convergence. The amount of depolarization caused by the discharge of neurotransmitter from a single excitatory synapse is only about 0.5 mV, much less than the ~15 mV depolarization needed to reach threshold. Thus, activation of a postsynaptic neuron to the point that it will generate action potentials requires summation of many excitatory synaptic events. This occurs in two ways: The same synapse continues to be repeatedly activated before the previous EPSPs or IPSPs have died away—temporal summation; and more than one synapse may be activated simultaneously or within a short time of the first synapse—spatial summation. The postsynaptic cell integrates IPSPs as well as EPSPs. In order for the postsynaptic cell to become activated to threshold, excitatory synaptic activity must be considerably greater than inhibitory synaptic activity.

and desensitization of receptors. (9) Certain drugs and diseases can affect both the presynaptic and postsynaptic factors listed above. General factors include: (10) the area of synaptic contact; (11) enzymatic destruction of the neurotransmitter; (12) the geometry of the diffusion path, and (13) the rate of neurotransmitter reuptake.

5.

Neurotransmitters cause the postsynaptic events described above, i.e., they elicit EPSPs or IPSPs when they bind to receptors in the postsynaptic membrane. Neuromodulators have more complex effects, including influencing the postsynaptic cell’s response to specific neurotransmitters, or changing the rate of synthesis, release, reuptake, or metabolism of a transmitter by the presynaptic cell. In other words, they alter the effectiveness of the synapse.

Facilitation refers to one presynaptic cell’s (cell A) positive influence on another presynaptic cell (cell B) through an axo-axonic synapse. If the neurotransmitter from cell A causes cell B to release more neurotransmitter to postsynaptic cell C when an action potential reaches cell B’s axon terminal, then cell A has increased cell B’s synaptic effectiveness by presynaptic facilitation. (Another presynaptic cell with an axo-axonic synapse with cell B could decrease the amount of neurotransmitter released by cell B. This is presynaptic inhibition.)

4.

The two kinds of messengers also have different time courses: neurotransmitters initiate events that occur within milliseconds and are short-lived. The activation of receptors for neuromodulators often brings about changes in the metabolic processes in neurons via G proteins coupled to second-messenger systems. Such changes can occur over minutes, hours, or even days. Neuromodulators can be synthesized by the presynaptic cell and co-released with the neurotransmitter at synapses, or they can be hormones, paracrine substances, or immune-system messengers.

List at least eight ways in which the effectiveness of synapses may be altered.

(1) The presynaptic facilitation and inhibition described above is one way. Other presynaptic factors include: (2) availability of neurotransmitter, which is in turn dependent upon the availability of precursor molecules and the amount or activity of the rate-limiting enzyme in the pathway for neurotransmitter synthesis; (3) the axon terminal membrane potential—the more depolarized the terminals are, the more voltage-gated Ca2+ channels open; (4) the residual Ca2+ in the terminal from previous action potentials; and (5) the presence of autoreceptors. Postsynaptic factors include: (6) the immediate past history of the postsynaptic membrane; (7) effects of other neurotransmitters or neuromodulators; and (8) up- or down-regulation

Discuss differences between neurotransmitters and neuromodulators.

6.

List the major classes of neurotransmitters and give examples of each.

(1) Acetylcholine, (2) biogenic amines: the catecholamines dopamine, norepinephrine, and epinephrine; serotonin; 5-HT; and histamine, (3) amino acids: glutamate, GABA, and glycine, (4) neuropeptides: endogenous opioids and morphine, (5) gases: nitric oxide, carbon monoxide, and hydrogen sulfide, and (6) purines: adenosine and ATP.

7.

Detail the mechanism of long-term potentiation, and explain what function it might have in in learning and memory. See Figure 6.36 and accompanying text description for a detailed

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19 mechanism of long-term potentiation. This mechanism might be central to learning and memory, because it provides a way to strengthen synapses that receive frequent, strong activation.

SECTION D: Structure of the Nervous System 1.

Make an organizational chart showing the CNS, PNS, brain, spinal cord, spinal nerves, cranial nerves, forebrain, brainstem, cerebrum, diencephalon, midbrain, pons, medulla oblongata, and cerebellum.

Central nervous system A. Brain 1. Forebrain a. Cerebrum b. Diencephalon 2. Brainstem a. Midbrain b. Pons c. Medulla oblongata 3. Cerebellum B. Spinal cord II. Peripheral nervous system A. Cranial nerves B. Spinal nerves

3.

The thalamus is an important relay station for sensory pathways on their way to the cerebral cortex.

It also participates in control of body movement and skeletal muscle coordination, and it plays a key role in awareness.

I.

2.

List two functions of the thalamus.

4.

List the functions of the hypothalamus, and discuss how they relate to homeostatic control.

(1) The hypothalamus is the “master gland” of the endocrine system and regulates the secretions of the pituitary gland. It also: (2) regulates water balance; (3) participates in the regulation of the autonomic nervous system; (4) regulates eating and drinking behavior; (5) regulates the reproductive system and reproductive behavior; (6) reinforces certain behaviors; (7) generates and regulates circadian rhythms; (8) regulates body temperature; and (9) participates in generation of emotional behavior.

The hypothalamus is the master command center for neural and endocrine coordination. It is the single most important control area for homeostatic regulation of the internal environment.

Draw a cross section of the spinal cord showing the gray and white matter, dorsal and ventral roots, dorsal root ganglion, and spinal nerve.

Indicate the general location of pathways.

5.

Make a PNS chart indicating the relationships among afferent and efferent divisions, somatic and autonomic nervous systems, and sympathetic and parasympathetic divisions.

The peripheral nervous system I.

Afferent division

II. Efferent division A. Somatic nervous system B. Autonomic nervous system a.

Sympathetic division

b.

Parasympathetic division

Fig. 6.41

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6.

superior mesenteric, and inferior mesenteric ganglia—are in the abdominal cavity, closer to the innervated organ. The parasympathetic ganglia all lie within the organs innervated by the postganglionic fibers or close to them, and so the postganglionic parasympathetic fibers are quite short.

Contrast the somatic and autonomic divisions of the efferent nervous system; mention at least three characteristics of each.

The neurons of the somatic nervous system innervate skeletal muscle, whereas autonomic neurons innervate smooth and cardiac muscle, glands, and neurons in the gastrointestinal tract. The somatic system consists of single neurons between the CNS and skeletal muscle cells, whereas the autonomic system has two-neuron chains (connected by a synapse in a ganglion) between the CNS and the effector organ. The output of the somatic system is always excitatory, whereas the autonomic output can be excitatory or inhibitory.

7.

Name the neurotransmitter released at each synapse or neuroeffector junction in the somatic and autonomic systems.

Acetylcholine is the neurotransmitter released by: (1) the somatic motor neurons at neuromuscular junctions; (2) the preganglionic fibers of both the parasympathetic and sympathetic divisions; and (3) postganglionic, parasympathetic fibers.

Norepinephrine is released by postganglionic sympathetic fibers. The adrenal medulla releases epinephrine into the blood; it is considered a neurohormone.

8.

The two divisions differ functionally as well. To some extent the sympathetic division acts as a single unit, whereas the parasympathetic division is made up of relatively independent components. Perhaps most importantly, the two divisions often innervate the same organ and usually have opposite effects. In general, the sympathetic division is activated in situations requiring physical action—the fight-orflight response—and also when one is under psychological stress. The parasympathetic system is more dominant in times of rest-ordigest.

Contrast the sympathetic and parasympathetic components of the autonomic nervous system; mention at least four characteristics of each.

The first difference is mentioned above: the postganglionic fibers of each division secrete different neurotransmitters.

The two divisions also differ anatomically: the nerve fibers of the two divisions leave the CNS from different levels—the sympathetic fibers from the thoracic and lumbar areas of the spinal cord, and the parasympathetic fibers from the brain and the sacral portion of the spinal cord. The locations of ganglia also differ for the two divisions: most of the sympathetic ganglia lie close to the spinal cord and form two chains of ganglia, the sympathetic trunks.

The postsynaptic fibers from these ganglia can be quite long. Other sympathetic ganglia—the celiac,

9.

Explain how the adrenal medulla can affect receptors on various effector organs despite the fact that its cells have no axons.

The adrenal medulla is essentially a sympathetic ganglion. The postsynaptic cells within the adrenal medulla secrete their chemical messengers— primarily epinephrine with some norepinephrine and small amounts of dopamine—into the blood; therefore, the substances released by the adrenal medulla are considered neurohormones. The neurohormones are transported via the blood to effector cells having receptors sensitive to them.

10. The chemical composition of the CNS extracellular fluid is different from that of blood. Explain how this difference is achieved.

A complex group of blood-brain barrier mechanisms closely controls the kinds of substances that enter the extracellular fluid of the brain and the rate at which they enter. The blood-brain barrier comprises the cells that line the smallest blood vessels in the brain (the capillaries), and has both anatomical features such as tight junctions and physiological transport systems that handle different classes of substances in different ways.

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21

SUMMARY OF INSTRUCTOR RESOURCES: CHAPTER 6

Topics

Nervous System Cells

Section (pages)

6.1-6.5 (pp. 137-143)

Figures & Tables (* denotes Physiological Inquiry)

Fig. 6.1, 6.2, 6.3, 6.4, 6.5

Chapter Review Questions

Section A p. 143

Chapter Test Questions

Recall and Comprehend: #2

Table 6.1

Membrane Potentials

6.5-6.7 (pp. 143-158)

Fig. 6.7, 6.8, 6.9, 6.10*, 6.11*, 6.12*, 6.13, 6.14, 6.15*, 6.16, 6.17, 6.18, 6.19*, 6.20, 6.21, 6.22, 6.23*, 6.24*

Table 6.2, 6.3, 6.4

Recall and Comprehend: #3, 4, 5, 6, 7,

Section B pp. 157-158

Apply, Anayze, and Evaluate: # 1, 2, 5, 7, 8 General Principles Assessment: #2

CONNECT Question Bank 2. Neuron structure 3. Structure and maintenance of neurons 4. Functional classes of neurons 5. Anatomy of efferent, afferent, and interneurons 6. Glial cells 7. The truth about glial cells 8. Neural growth and regeneration 9. The truth about neural plasticity 1. General principles of physiology 10. Basic principles of electricity 11. Potential, current, and resistance 12. Electrical properties of membranes 13. Ion distribution 14. Nerst equation 15. Resting membrane potential 16. Equilibrium potentials and ion flux 17. Membrane potential terminology 18. Membrane potential glossary 19. Action potential 20. Feedback control of voltage-gated channels 21. Action potentials and refractory periods 22. Graded vs. action potentials 23. Voltage clamp experiment 24. Voltage clamp toxin 51. Charge movement during an action potential 52. Adjacent to an action potential 53. One-way action potential propagation 54. Directionality of action potentials 55. Threshold definition

CONNECT Animations

Action potential propagation in an unmyelinated axon

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Chapter 6

Synapses

6.8-6.14 (pp. 66-171)

22

Fig. 6.25, 6.26, 6.27, 6.28, 6.29, 6.30, 6.31*, 6.32, 6.33, 6.34, 6.35, 6.36

Recall and Comprehend: #8, 9

Section C p. 170

General Principles Assessment: #3

Table 6.5, 6.6

Structure of the Nervous System

6.15-6.19 (pp. 171-185)

Fig. 6.37*, 6.38, 6.39, 6.40, 6.41, 6.42, 6.43, 6.44, 6.45, 6.46*, 6.47

Recall and Comprehend: #1, 10

Section D p. 182

Table 6.7, 6.8, 6.9, 6.10, 6.11

Apply, Anayze, and Evaluate: #6

Apply, Anayze, and Evaluate: #3, 4, General Principles Assessment: #1, 3

1. General principles of physiology 25. Functional anatomy of synapses 26. Label the synapse 27. Neurotransmitter release 28. Steps of neurotransmitter signaling 29. Excitatory chemical synapses 30. Inhibitory chemical synapses 31. Synaptic modification 32. EPSP vs. IPSP 33. Synaptic integration 34. Synaptic facilitation 35. Long-term potentiation 36. Specific neurotransmitters 37. Neuroeffector communication 1. General principles of physiology 37. Neuroeffector communication 38. Brain anatomy 39. Nervous system terms 40. Brain region functions 41. Spinal cord 42. Spinal cord injuries 43. Cranial nerves 44. Spinal nerves 45. Somatic vs. autonomic nervous system 46. Divisions of the ANS 47. Autonomic drugs 48. Ventricles of the brain 49. The truth about the blood-brain barrier 50. Clinical case study

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