title: Central vasopressin V1A receptor blockade impedes hypothalamic-pituitary-adrenal habituation to repeated restraint stress exposure in adult male rats.
abstract: Previous studies suggest that central arginine vasopressin (AVP) signaling can inhibit the hypothalamic-pituitary-adrenal (HPA) axis. To test a role for the AVP V1A receptor in stress HPA axis habituation, adult male rats were exposed to 5 consecutive days of 3 h restraint with or without continuous intracerebroventricular infusion of the V1A receptor antagonist d(CH2)5Tyr(Me)AVP (10 μg/day). Assessment of neuropeptide expression and HPA output under basal conditions revealed no effects of V1A receptor antagonism in stress naive animals. Between the first and last day of restraint exposure, controls showed marked declines in ACTH and corticosterone responses, and maintained plasma concentrations of testosterone. In contrast, V1A receptor antagonized animals displayed significantly smaller declines in ACTH and corticosterone responses, and a decrease in plasma testosterone. Despite their reduced expression of HPA axis habituation, antagonized animals continued to show stress-induced increases in AVP mRNA in the hypothalamic paraventricular nucleus and bed nucleus of the stria terminalis, and even higher levels of AVP expression in the medial amygdala relative to controls. The data leave open the nature and extent to which these and other AVP-containing pathways are recruited during repeated restraint, but nevertheless reveal a critical role for central V1A receptors in stress adaptation. As the effects of V1A receptor antagonism were restricted to the repeated restraint condition, we conclude that normal adaptation to stress involves a shift toward enhanced AVP utilization and/or V1A receptor signaling.
authors: Neuroscience Program, Department of Cellular and Physiological Sciences, Life Science Centre, University of British Columbia, Vancouver, British Columbia, Canada.
authors: Megan
authors: M
authors: Gray
authors: Leyla
authors: L
authors: Innala
authors: Victor
authors: V
authors: Viau
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000097:blood; D000818:Animals; D065092:Antidiuretic Hormone Receptor Antagonists; D001127:Arginine Vasopressin / Q000031:analogs & derivatives* / Q000378:metabolism / Q000494:pharmacology; D003345:Corticosterone / Q000097:blood; D003346:Corticotropin-Releasing Hormone / Q000096:biosynthesis; D006185:Habituation, Psychophysiologic / Q000187:drug effects*; D006727:Hormone Antagonists / Q000494:pharmacology*; D007030:Hypothalamo-Hypophyseal System / Q000378:metabolism / Q000503:physiopathology*; D007032:Hypothalamus, Anterior / Q000378:metabolism; D017403:In Situ Hybridization; D008297:Male; D010913:Pituitary-Adrenal System / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology*; D011863:Radioimmunoassay; D051381:Rats; D017207:Rats, Sprague-Dawley; D012149:Restraint, Physical; D013315:Stress, Psychological / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology*; D013493:Suprachiasmatic Nucleus / Q000378:metabolism; D013739:Testosterone / Q000097:blood
chemical_list: D065092:Antidiuretic Hormone Receptor Antagonists; D006727:Hormone Antagonists; D001127:Arginine Vasopressin; D013739:Testosterone; C025043:vasopressin, 1-(1-mercaptocyclohexaneacetic acid)-2-(O- methyl-L-tyrosine)-8-L-arginine-; D000324:Adrenocorticotropic Hormone; D003346:Corticotropin-Releasing Hormone; D003345:Corticosterone