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Inhibition of Neuropeptide Y (NPY)-Induced Feeding and c-Fos Response in Magnocellular Paraventricular Nucleus by a NPY Receptor Antagonist: A Site of NPY Action¹

Departments of Neuroscience (S.P.K.) and Physiology (P.S.K.), University of Florida Brain Institute, University of Florida College of Medicine, Gainesville, Florida 32610

Address all correspondence and requests for reprints to: Satya P. Kalra, Ph.D., Department of Neuroscience, University of Florida Brain Institute, University of Florida College of Medicine, 100 South Newell Drive, Box 100244, Gainesville, Florida 32610-0244. E-mail: skalra{at}ufbi.ufl.edu

Neuropeptide Y (NPY) is one of the important endogenous orexigenic peptides. In these studies we employed c-Fos immunostaining and a selective NPY Y₁ receptor antagonist to identify the site of action of NPY in the hypothalamus. The results showed that intracerebroventricular administration of NPY stimulated feeding and increased immunostaining of c-Fos, a product of the immediate early gene c-fos, in several hypothalamic sites, including the dorsomedial nucleus, the supraoptic nucleus, and the two subdivisions of the paraventricular nucleus (PVN), the parvocellular PVN, and magnocellular PVN (mPVN). Intracerebroventricular administration of 1229U91, a selective NPY Y₁ receptor antagonist, affected neither food intake nor c-Fos-like immunoreactivity (FLI) in these hypothalamic sites. Coadministration of NPY and NPY Y₁ receptor antagonist inhibited NPY-induced food intake by 48%, but failed to affect NPY-induced FLI in the supraoptic nucleus, dorsomedial nucleus, and parvocellular PVN. However, this combined treatment decreased FLI by 46% in the mPVN (P < 0.05). These results showed that whereas NPY can stimulate FLI in several hypothalamic sites, the selective NPY Y₁ antagonist suppressed NPY-induced FLI only in the mPVN. Thus, these findings lend credence to the view that a subpopulation of Y₁ receptor-containing neurons in the mPVN in part mediate stimulation of feeding by NPY.

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