Review Articles
Prenatally stressed rats exhibit behavior that signals depression when evaluating blood glucose metabolism
Figure 1. Bélanger, Allaman and. Magistrett (2011) illustrated in vitro findings (above) when determining the end product of glycolysis. They found that lactate, not both lactate and pyruvate, resulted from reactions in vitro with glucose-6-phosphate dehydrogenase [1]. The research demonstrated that glutamine synthetase is an astrocyte specific. Glucose is synthesized into glutamate due to processes of the astrocytes [10].
Summary of Major Results
The prenatally stressed rats showed statistically significant higher immobility and lower time spent climbing measurements than the control group. The stressed rats demonstrated behavior that signaled depression. Several processes that are linked to glucose metabolism take place in different cell compartments. The influence of disturbed neuronal and glial function is known with regards to depression. The results were similar to other published research that indicated some increase in glycolysis while at the same time some decrease is observed in the tri-carboxylic cycle during depression. The results demonstrated that elevated brain glucose levels are not caused by glycolysis inhibition. The measurements showing that brain glycolysis inhibition was not evident based on the observation that pyruvate and lactate levels showed no change in concentration. The glycolytic enzyme pyruvate kinase shWowed a decrease in both the frontal cortex and the hippocampus for acute stress. Meanwhile the second glycolytic enzyme observed, hexokinase did not show any change for either the hippocampus or the frontal cortex. The third glycolytic enzyme observed, phosphofructokinases showed the largest number of location activities increased during acute stress in the frontal cortex and the hippocampus. One of the products glycolysis pyruvate showed group dependent change in the frontal cortex and increased change for acute stress in the hippocampus. The other product observed, lactate behaved differently in the frontal cortex with an increase during prenatal stress, and meanwhile lactate showed an increase in glucose treatment in the hippocampus.
Conclusions and Discussion
The research of Detka et al. (2015) added knowledge to topic of using an animal model to evaluate the glucose metabolism enzymes with reference to depression. The only similar research addresses a different stage of the metabolism process [14]. For example, DeVry et al. (2016) evaluated how the TrkB receptor is moderator of behavior from the hippocampus and affects the nucleus accumbens (NAc). Only a few research studies are available perhaps due to the difficulty in identifying changes in the brain when the subjects exhibit distinctive behavior towards vulner-
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able or resistant to stress. The current research under discussion was motivated by the indication that the “brain glucose uptake and glycolysis are rather increased and the Krebs cycle and/or oxidative phosphorylation are rather decreased in depression” [4]. Kurek et al. (2015) also noted the potential of brain glucose metabolism disruption as an impact on pathological depression. The current study demonstrated using the prenatally stressed model of depression with rats as the subject that frontal cortex and hippocampus glucose concentration became elevated [4]. Interestingly no decrease in the key glycolytic enzymes accompanied the increased glucose concentrations indicating no link with a decrease glycolytic process [4]. Therefore the most probable link was with the increased glucose uptake or gluconeogenesis [4]. The findings led to further research by Kurek et al. (2015) to evaluate the degree that permanent changes were caused by prenatal stress. The focus of the research was on glucose transporters (GLUTs) expression to learn about the effect of prenatal stress specifically on the glucose transporter GLUT1, GLUT3 and GLUT4 [7]. During the same experiment a control group of rats and a prenatally stressed group of rats two other factors were evaluated a) acute immobilization stress and b) oral glucose administration [7]. Related to the current research under discussion, the researchers observed that the glucose transporter GLUT1 was identified in higher concentrations [7]. The experimental results indicated that the increased concentration of all three glucose transporters, especially GLUT1 influenced higher levels of glucose in the hippocampus and in the frontal cortex [7]. Kurek et al. (2015) noted that prenatal stress did initiate depression behaviors (long-term) and permanent changes were observed for the glucose transporters concentrations. Human studies on changes in depression behavior were carried out in 2011 on over 480 diabetes patients. The purpose of the experiment was to evaluate the education level of the patient and the effect on glucose monitoring. Interestingly the results demonstrated improved “association with H1bA1c and with glucose” Of particular interest in reference to the current study the experiment demonstrated no depression symptoms dependency on “improved metabolic parameters or glucose” [2]. Other research discussed here showed the independent characteristic of depression behaviors under experimental conditions.
Journal of Undergraduate Life Sciences • Volume 11 • Issue 1 • Spring 2017