|About the Book|
Acute activation of the hypothalamic-pituitary-adrenal (HPA) axis releases glucocorticoids to maintain homeostasis, whereas prolonged exposure to elevated glucocorticoids has deleterious effects. Due to the potential benefits of limitingMoreAcute activation of the hypothalamic-pituitary-adrenal (HPA) axis releases glucocorticoids to maintain homeostasis, whereas prolonged exposure to elevated glucocorticoids has deleterious effects. Due to the potential benefits of limiting stress-induced glucocorticoid secretion, this thesis used drinking in dehydrated rats as a model to delineate mechanisms mobilized to rapidly inhibit HPA activity during stress. Initial experiments were designed to test the hypothesis that repeated episodes, but not a single episode of restriction-induced drinking, inhibits parvocellular neurons in the paraventricular nucleus of the hypothalamus (PVN). In the first experiment, we used double-label immunohistochemistry for Fos and corticotropin releasing hormone or Fos and vasopressin to examine subpopulations of PVN neurons following a single or a repeated episode of drinking. The next experiments were designed to define visceral stimuli that contribute to differential inhibition of the HPA axis when rats drink and to delineate peripheral receptors that differentially inhibit parvocellular PVN neurons versus magnocellular PVN neurons. The first experiment examined the effect of a single and repeated episode of water restriction on the HPA response to drinking an isotonic solution. This experiment tested the hypothesis that drinking isotonic saline reduces plasma corticosterone after a repeated but not a single episode of dehydration. The following experiment further isolated specific stimuli associated with restriction induced drinking. This experiment examined the hypothesis that gastric distension inhibits the HPA axis following repeated water restriction. The final group of experiments were designed to test the overall hypothesis that rapid decreases in HPA activity that occur following water restriction-induced drinking are mediated in part by changes in vagal nerve activity. The first experiment used Fos expression to examine the activity of nucleus tractus solitarious neurons in response to single and repeated episodes of dehydration-induced drinking. The second experiment examined the role of the vagus nerve in reducing HPA activity following restriction-induced drinking by assessing hormonal responses after subdiaphragmatic vagotomy. Collectively, data from this thesis indicate that the rapid reduction in plasma glucocorticoids involves multiple factors including a reduction in magnocellular release of vasopressin, a reduction in parvocellular neuronal activity, and increased vagal activity when a stressor is removed.