| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 1907107 | Experimental Gerontology | 2011 | 6 Pages |
The major neuroendocrine response mediating stress adaptation is activation of the hypothalamic pituitary adrenal axis, with stimulation of corticotropin releasing hormone (CRH) and vasopressin (VP) from parvocellular neurons of the hypothalamic paraventricular nucleus, leading to stimulation of pituitary ACTH secretion and increases in glucocorticoid secretion from the adrenal cortex. Basal production and transient increases during stress of glucocorticoids and its hypothalamic regulators are essential for neuronal plasticity and normal brain function. While activation of the HPA axis is essential for survival during stress, chronic exposure to stress hormones can predispose to psychological, metabolic and immune alterations. Thus, prompt termination of the stress response is essential to prevent negative effects of inappropriate levels of CRH and glucocorticoids. This review addresses the regulation of HPA axis activity with emphasis on the mechanisms of termination of CRH transcription, which is a critical step in this process. In addition, the actions by which glucocorticoids, CRH and VP can affect the aging process will be discussed.
Research highlights► Transient activation of the HPA axis is necessary for survival during increasing demand, but similarly prompt termination of the stress response is essential to prevent negative effects of excessive CRH and glucocorticoids. ► The mechanisms contributing to curbing stress responses involve coordinated regulation of stimulatory and inhibitory neurocircuitry regulating HPA axis activity, neuronal sensitivity to glucocorticoids and intracellular feedback mechanisms. ► Ageing leads to changes in HPA axis activity depending on the genetic background. ► Increases in glucocorticoid activity and central levels of CRH during aging can have damaging effects and contribute to pathology associated with advancing.
