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Am J Physiol Regul Integr Comp Physiol (February 20, 2003). doi:10.1152/ajpregu.00554.2002
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Submitted on September 9, 2002
Accepted on February 6, 2003

Effect of peptide histidine isoleucine on consummatory behavior in rats

Pawel K Olszewski1*, Michelle M Wirth2, Timothy J Shaw3, Martha K Grace2, and Allen S Levine4

1 Research Service (151), VA Medical Center, Minneapolis, MN, USA; College of Veterinary Medicine, Minneapolis, MN, USA; Department of Medicine, University of Minnesota, Minneapolis, MN, USA
2 Research Service (151), VA Medical Center, Minneapolis, MN, USA
3 Bethel College, Arden Hills, MN, USA
4 Research Service (151), VA Medical Center, Minneapolis, MN, USA; Department of Psychiatry, University of Minnesota, Minneapolis, MN, USA

* To whom correspondence should be addressed. E-mail: olsze005{at}tc.umn.edu.

Peptide histidine isoleucine (PHI) and vasoactive intestinal polypeptide (VIP) are derived from the same precursor. While central VIP decreases food intake, potential effects of PHI on feeding have not been studied. In the current study, we found that PHI administered intracerebroventricularly (ICV) or into the hypothalamic paraventricular nucleus (PVN) or central nucleus of the amygdala (CeA) decreased food consumption in overnight-deprived rats. The magnitude of an anorexigenic response to PHI differed depending on the injection route: ICV-infused peptide evoked the most potent effect. We determined that only PVN- and CeA-injected PHI did not have aversive consequences. In addition, we infused anorexigenic doses of PHI via the same routes and assessed Fos immunoreactivity of PVN oxytocin (OT) and vasopressin (VP) neurons using double immunohistochemistry. OT and VP are thought to promote feeding termination. PHI increased the percentage of Fos-positive OT neurons regardless of the injection route. ICV- and PVN-infused PHI induced activation of VP cells. We conclude that central PHI has an inhibitory influence on food intake in rats. The PVN, with OT and VP neurons, and CeA may be involved in the mediation of anorexigenic effects of PHI.




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