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AJP - Regulatory, Integrative and Comparative Physiology, Vol 260, Issue 2 448-R452, Copyright © 1991 by American Physiological Society
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B. R. Olson, M. D. Drutarosky, E. M. Stricker and J. G. Verbalis
Department of Medicine, University of Pittsburgh, Pennsylvania 15261.
Central administration of corticotropin-releasing hormone (CRH) is known to inhibit food intake and stimulate pituitary oxytocin (OT) secretion in rats. These experiments addressed the possibility that the inhibition of food intake that follows central CRH administration is mediated through oxytocinergic pathways. Male food-deprived rats, with stable baseline food intakes after intracerebroventricular (icv) injections of artificial cerebrospinal fluid, received 150 pmol of CRH icv. Food intake was inhibited by 62 +/- 5% during a 90-min test period. Pretreatment with 9 nmol of the OT antagonist [d(CH2)5, Tyr(Me)2, Orn8]vasotocin icv completely eliminated the inhibition of food intake produced by icv CRH. In contrast, pretreatment with the OT-receptor antagonist did not significantly alter pituitary secretion of adrenocorticotropic hormone and OT stimulated by icv CRH. The results of these experiments implicate OT as a possible central mediator of CRH-induced anorexias in rats, particularly those that are accompanied by stimulation of neurohypophysial OT secretion.
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