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Am J Physiol Regul Integr Comp Physiol 280: R473-R480, 2001;
0363-6119/01 $5.00
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Vol. 280, Issue 2, R473-R480, February 2001

Feeding inhibition by urocortin in the rat hypothalamic paraventricular nucleus

Chuanfeng Wang1, Mary A. Mullet2, Michael J. Glass1, Charles J. Billington1,2,3, Allen S. Levine1,2,3,4,5, and Catherine M. Kotz1,3,4

1 Veterans Affairs Medical Center and 3 Minnesota Obesity Center, Minneapolis 55417, and 4 Departments of Food Science and Nutrition, 5 Psychiatry, and 2 Medicine, University of Minnesota, Saint Paul, Minnesota 55108

Ventricular administration of urocortin (UCN) inhibits feeding, but specific site(s) of UCN action are unknown. In the current studies we examined the effect of UCN in the hypothalamic paraventricular nucleus (PVN) on feeding. We tested UCN administered into the PVN in several paradigms: deprivation-induced, nocturnal, and neuropeptide Y (NPY)-induced feeding. We compared the effect of equimolar doses of UCN and corticotrophin releasing hormone (CRH) on NPY-induced and nocturnal feeding, determined whether UCN in the PVN produced a conditioned taste aversion (CTA) and induced changes in c-Fos immunoreactivity (c-Fos-ir) after UCN and NPY administration in the PVN. UCN in the PVN significantly decreased NPY and nocturnal and deprivation-induced feeding at doses of 1, 10, and 100 pmol, respectively. UCN anorectic effects lasted longer than those attributed to CRH. Ten and thirty picomoles UCN did not induce a CTA, whereas 100 pmol UCN produced a CTA. UCN (100 pmol) in the PVN neither increased c-Fos-ir in any brain region assayed nor altered c-Fos-ir patterns resulting from PVN NPY administration. These data suggest the hypothalamic PVN as a site of UCN action.

energy balance; neuropeptide Y; feeding behavior; brain sites


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