Rats treated with PRS reacted positively to entering the light-dark box, which shows that agomelatine and fluoxetine eradicated variations in anxiety between the controls and treated rats (Maccari et al., 2003). Findings further support the postulated hypothesis because biological dysfunctions seen in the rats, after exposing them to PRNS are similar to those exhibited by depressed patients (Morley-Fletcher et al.; 2003: Maccari et al., 2003). In stress-related ailments, empirical evidence has proven that the disorders result in changes in the hippocampus, which further, supports the postulated hypothesis (Henry et al., 994). Overall, the use of anti-depressants reverses the changes in synaptic vesicle proteins and the resulting defect in the hippocampus that produce glutamate in the PRS rats (Morley-Fletcher et al., 2003).
The degree of glutamate secretion had an inverse relation to anxiety, but a positive relation to memory performance in the PRS rats (Luo and Zhang, 2008). This is one of the empirical evidence from the study because the use of antidepressant treatment led to improved social memory. Therefore, it is conclusive that the article provides a validation for the glutamatergic hypothesis of stress-associated ailments (Marrocco et al., 2014). Overall, the article provides a framework for the investigation in the hippocampus of humans with such disorders. In addition, the glutamatergic transmission in the hippocampus puts forward an approach, which scholars can refer to develop therapeutic strategies (Marrocco et al., 2014).
This review has borrowed greatly from prior studies, but of which most are empirical. The aim of the study is in line with the problem, and the study employs the studies to get hold of information in connection with the postulated hypothesis (Henry et al., 994). This review presents information from actual studies, which use evidence-based approaches. This is apparent because many of the prior studies the followed an experimental approach (Luo and Zhang, 2008).
Darnaudery, M et al. (2007). Impact of an intense stress on ethanol consumption in female rats characterized by their pre-stress preference: modulation by prenatal stress. Brain Research,1131 (1), pp. 181–186.
Henry, C. et al. (1994). Prenatal stress increases the hypothalamo-pituitary–adrenal axis response in young and adult rats. J. Neuroendocrinol, 6 (3), pp. 341–345.
Luo, D, D., &Zhang, X. (2008). Involvement of hippocampal serotonin and neuropeptide Y in depression induced by chronic unpredicted mild stress. Brain Res Bull, 77 (1), pp. 8–12.
Maccari S et al. (2003). Prenatal stress and long-term consequences: implications of glucocorticoid hormones. Neuroscience and biobehavioral reviews, 27 (1-2), pp. 119-127.
Marrocco, J et al. (2014). The Effects of Antidepressant Treatment in Prenatally Stressed Rats
Support the Glutamatergic Hypothesis of Stress-Related Disorders. The Journal of Neuroscience, 34(6), pp. 2014-2024.
Morley-Fletcher, S. et al. (2003). Prenatal stress in rats predicts immobility behavior in the forced swim Test Effects of a chronic treatment with tianeptine. Brain research, 989 (2), pp. 246-251.
Nestler, E. J.,& Hyman, S. E. (2010).Animal models of neuropsychiatric disorders.Natural Neuroscience, 13 (10), pp. 1161–1169.
Richardson, H. N. et al. (2008). Alcohol self-administration acutely stimulates the hypothalamic–pituitary–adrenal axis, but alcohol dependence leads to a dampened neuroendocrine state. Eur J Neuroscience, 28 (8), pp. 1641–1653.
Vallee, M. et al. (1999). Prenatal stress induces high anxiety and postnatal handling induces low anxiety in low offspring: Correlation with stress-induced corticosterone secretion. Journal of neuroscience, 17 (7), pp. 2626-2636.
Van, V. W et al. (2011).Impact of early life stress on alcohol consumption and on the short- and long-term responses to alcohol in adolescent female rats. Behavioral brain research, 221 (1), pp. 43-49.
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