The Effects of Antidepressant Treatment in Prenatally Stressed Rats - Literature review Example

Review: The Effects of Antidepressant Treatment in Prenatally Stressed Rats Support the Glutamatergic Hypothesis of Stress-Related Disorders Course Date Abstract Introduction: Evidence suggests that abnormalities in hippocampal glutamatergic transmission contribute in the pathophysiology of mood and anxiety conditions. Conversely, exposure to chronic stress in adults leads to the production of enhanced glutamate in the hippocampus. This suggests that for adolescents, the effect of chronic stress on glutamatergic transmission will vary in comparison to adults. This explains why some of the prior studies use both male and female rats in their investigation. Therefore, age plays an influential role on the effect of chronic stress on the release of glutamate. Purpose: The interest of this paper is to provide a review, “The Effects of Antidepressant Treatment in Prenatally Stressed Rats Support the Glutamatergic Hypothesis of Stress-Related Disorders.” In so doing, the paper will provide an analysis, which will establish the empirical evidence behind the hypothesis. Methods: This paper relies on prior literatures to achieve the objective of the study. In this context, the paper relied on databases, for instance, Google Scholar to retrieve the studies, and other prior literatures that touch on the subject matter. This paper does not impose restriction on any paper, but includes all papers that show relevance to the topic of study. Conclusion: Findings from the different literaturesrevealed a direct relationship between production of hippocampal glutamate and anxiety in the pregnant rats exposed to prenatal restraint stress. Adult rats that the investigators exposed to chronic stress represent depression, or post-traumatic disorders, and anti-depressants result to improved glutamate secretion. Owing to this, it is apparent that it is possible to restore cognitive roles because of such improvements. The utilization of anti-depressants in the treatment of stress and anxiety disorders is central to either increase or decrease in glutamate secretion. The Effects of Antidepressant Treatment in Prenatally Stressed Rats Support the Glutamatergic Hypothesis of Stress-Related Disorders Prior studies suggest that abnormalities in the transmission of hippocampal glutamate play a vital role in the pathophysiology of mood and anxiety ailments. Apparently, many of the studies borrowed greatly from prior studies on the same line, but other studies present actual studies to provide empirical evidence on the same (Marrocco et al., 2014). Alternatively, there is empirical evidence in regards to a model of depression and anxiety, which is central to the hypo-function hippocampus, and many of the studies utilize female rats because of their high incidence of major depression in women (Van et al., 2011). Exposure to chronic stress in adulthood leads to the improvement of production of glutamate in the hippocampus. In this regard, there are other treatments for anxiety noted from the cited articles. The evidence asserts that a portion of the hippocampus, which specifically encodes memories of stress, emotions and anxiety, is in line with the postulated hypothesis of stress-related disorders (Marrocco et al., 2014). In addition, chronic stress can result in long-term physiological and behavioral disorders such as low birth weight, infant morbidity, anxiety, and lack of sleep and cognition retardation (Maccari et al., 2003). Other scholars have aimed to establish a link between PRS exposure, and alcohol consumption (Richardson et al., 2008). In this perspective, there is a variance between male and female consumption of alcohol, and research suggests that males show reduced activation to acute alcohol administration (Richardson et al., 2008). Recently, evidence has come up showing that PRS has can prevent reduction in the consumption of alcohol induced by chronic stress in adult alcohol-preferring female rats (Darnaudery et al., 2007). Many of the scholars have utilized rats, as subjects, in their studies, to show how mood disorders can be stable throughout the life of a human being (Vallee et al., 1999). This is because it is possible to notice the ailments early and later as they develop (Henry et al., 994). The methods utilized by many of the studies follow an evidence-based approach, whereby the aim was to test the evidence (Darnaudery et. al., 2007). In scientific research, the objective is to achieve empirical evidence and because most of the studies identified followed experimental approaches (Nestle and Hyman, 2010). This approach is effective, and it utilizes randomized trials, including a control group and experimental group. The two groups help investigators to compare results, or findings appropriately (Richardson et al., 2008). In other cases, the investigators further, classify the control and experimental groups in terms of sex, age to find out the variations in the provided context. The most important advantage of this approach is to increase internal validity (Henry et al., 994). This means that in the event of subsequent studies on the same subject will amount to similar findings (Morley-Fletcher et al., 2003). Chronic treatment of the PRS rats using antidepressants had a positive outcome, in that it resulted to normal levels of synaptic vesicle-associated proteins in rats (Maccari et al., 2003). In this context, the use of anxiolytics and tranquilizers escalate the rigidity in the animal models of depression (Moley-Fletcher et al., 2003). Alternatively, depolarization-evoked the production of glutamate was in high PRS rats. 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 to 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 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 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). The use of control groups helps in maintaining internal and external validity, such that subsequent investigations in the same line will lead to similar results (Richardson et al., 2008). Nevertheless, there is potential biases because the control group of rats used could have self-induced emotions, anxiety and memories of stress. In such a situation, the investigators could make assumptions when comparing the two groups of rats (Van et al., 2011). Nevertheless, such cases are negligible, and the article under review; therefore, provides an empirical study. Studies used in the reviews help in achieving empirical evidence, and it shows that fluoxetine and agolematine had the capacity to bring secretion of glutamate to normal levels (Marrocco et al., 2014). The information in this paper provides a framework, which can help in improving the therapeutic strategies applied in managing and treating abnormal stress-related disorders (Nestle and Hyman, 2010). The findings from the studies confirm that the use of antidepressants in the PRS rats improved secretion of glutamate. This is significant as it can help in the correction of imbalance between excitatory and inhibitory neurotransmission of the glutamate in the hippocampus (Marrocco et al., 2014). In so doing, it will further help in restoring initially impaired cognitive functions. PRS rats represent the biological aspects that depression, and other patients suffering from stress-related illnesses go through, and this is in line with the postulated hypothesis (Maccari et al., 2003). Bibliography 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. Read More