As we have so diligently studied this semester, the stress response yields a number of physiological changes. Sterrenburg et al. (2004) and Horstmann & Binder (2011) studied the effects of stress. Both female and male rats were exposed to chronic variable mild stress (CVMS) for a period of two weeks in a controlled environment. In Sterrenburg's et al. study and Horstmann & Binder's review determined increased levels of corticotropin-releasing factor (CRF) in the hypothalamic paraventricular nucleus (PVN) directly after CVMS exposure.
The PVN releases corticotropin-releasing factor (CRF) which controls the hypothalamic pituitary adrenal axis (HPA). CVMS overstimulates the HPA-axis to release CRF. There are two types of glucocorticoid receptors: 1)the high affinity mineralocorticoid receptor and 2)the low affinity glucocorticoid receptor. Once the high affinity mineralocorticoid receptors are saturated, glucocorticoids begin binding to the low affinity glucocorticoid receptors. These glucocorticoid receptors trigger the negative feedback mechanism of the stress response. Horstmann & Binder note that prolonged depression is chronic stress, and so also triggers overstimulation of the HPA-axis. They also note that antidepressants actually suppress the overstimulation of the HPA-axis so that CRF release is decreased and the stress response is also decreased.
Horstmann, S & Binder, E. (2011). Glucocorticoids as predictors of treatment response in depression. Harv Rev Psychiatry. pages 125-139.
Sterrenburg, L.; Gaszner, B.; Boerrigter, J.; Santbergen, L.; Bramini, M.; Chen, A.; Peeters, B.W.M.M.; Roubos, E.; Kozicz, T. (2011). Chronic stress induces sex-specific alterations in methylation and expression of corticotropin-releasing factor gene in the rat. PLoS ONE. 6(11).
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