Abstract

Repeated exposure to stressors was reported to increase the expression of arginine-vasopressin (AVP), especially in corticotropin-releasing hormone (CRH) neurons co-expressing AVP, within the hypothalamus. This may increase the potential for subsequent stressor-elicited enhancement of hypothalamic–pituitary–adrenal (HPA) functioning as these peptides synergistically stimulate pituitary ACTH secretion. Likewise, members of the bombesin (BB) family of peptides (including its mammalian analogues gastrin-releasing peptide (GRP) and neuromedin B (NMB)) stimulate the release of ACTH and may play a role in the mediation and/or modulation of the CRH stress response. In the present investigation, chronic stressor exposure (daily restraint over 14 days) was associated with increased co-expression of CRH and AVP at the median eminence. In addition, in vivo interstitial levels of anterior pituitary AVP, GRP and NMB (but not CRH) were elevated following chronic stressor exposure. Basal pituitary corticosterone levels, in contrast, were unaffected by chronic stressor exposure. Following consumption of a highly palatable snack, interstitial levels of CRH, GRP, NMB and corticosterone (but not AVP) were elevated at the pituitary; however, a cross-sensitization was not apparent among rats previously exposed to the stressor and then provided with the snack. As the CRH, AVP and BB-like peptide systems have been associated with altered anxiety and depressive symptoms, the sustained peptidergic alterations observed in the chronically stressed rats may have implications for the development of these stressor-related disorders.

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