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pubmed-article:12184992pubmed:abstractTextSeveral conditions that inhibit female sexual behavior are thought to be associated with altered corticotropin-releasing hormone (CRH) activity in the brain. The present experiments examined the hypothesis that endogenous CRH receptor signaling mediates the inhibition of estrous behavior by undernutrition and in other instances of sexual dysfunction. Intracerebroventricular (ICV) infusion of CRH or urocortin inhibited estrous behavior in ovariectomized steroid-primed hamsters. Conversely, ICV infusion of the CRH receptor antagonist astressin prevented the suppression of estrous behavior by food deprivation or by ICV administration of neuropeptide Y. Astressin treatment also induced sexual receptivity in nonresponders, animals that do not normally come into heat when treated with hormones, and this effect persisted in subsequent weekly tests in the absence of any further astressin treatment. Activation of the hypothalamo-pituitary-adrenocortical axis was neither necessary nor sufficient to inhibit estrous behavior, indicating that this phenomenon is due to other central actions of CRH receptor agonists. This is the first direct evidence that CRH receptor signaling may be a final common pathway by which undernutrition and other conditions inhibit female sexual behavior.lld:pubmed
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pubmed-article:12184992pubmed:authorpubmed-author:JonesJuli EJElld:pubmed
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pubmed-article:12184992pubmed:dateRevised2008-11-21lld:pubmed
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pubmed-article:12184992pubmed:articleTitleDisinhibition of female sexual behavior by a CRH receptor antagonist in Syrian hamsters.lld:pubmed
pubmed-article:12184992pubmed:affiliationCenter for Neuroendocrine Studies, University of Massachusetts, Amherst, Massachusetts 01003, USA. jones@cns.umass.edulld:pubmed
pubmed-article:12184992pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:12184992pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed