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Endocrinology Vol. 140, No. 2 933-940
Copyright © 1999 by The Endocrine Society

ARTICLES

Interactions between Neuropeptide Y and {gamma}-Aminobutyric Acid in Stimulation of Feeding: A Morphological and Pharmacological Analysis1

Shuye Pu, Mukul R. Jain, Tamas L. Horvath, Sabrina Diano, Pushpa S. Kalra and Satya P. Kalra

Departments of Neuroscience (S.P., S.P.K.) and Physiology (M.R.J., P.S.K.), University of Florida College of Medicine, Gainesville, Florida 32610; and the Department of Obstetrics and Gynecology, Yale University School of Medicine (T.L.H., S.D.), New Haven, Connecticut 06510

Address all correspondence and requests for reprints to: Shuye Pu, M.D., Department of Neuroscience, University of Florida College of Medicine, P.O. Box 100244, Gainesville, Florida 32610. E-mail: pu{at}neocortex.health.ufl.edu

Neuropeptide Y (NPY) produced in neurons in the arcuate nucleus and brain stem and released in the paraventricular nucleus (PVN) and surrounding areas is involved in stimulation of feeding in rats. We recently reported that {gamma}-aminobutyric acid (GABA) is coexpressed in a subpopulation of NPY neurons in the arcuate nucleus. To determine whether GABA is colocalized in NPY terminals in the PVN, the site of NPY action, light and electron microscopic double staining for NPY and GABA using pre- and postembedding immunolabeling was performed on rat brain sections. GABA was detected in NPY-immunopositive axons and axon terminals within both the parvocellular and magnocellular divisions of the PVN. These morphological findings suggested a NPY-GABA interaction in the hypothalamic control of feeding. Therefore, the effects of muscimol (MUS), a GABAA receptor agonist, on NPY-induced food intake were examined in sated rats. When injected intracerebroventricularly, both NPY and MUS elicited dose-dependent feeding responses that were blocked by the administration of 1229U91 (a putative Y1 receptor antagonist) or bicuculline (a GABAA receptor antagonist), respectively. Coadministration of NPY and MUS intracerebroventricularly amplified the feeding response over that evoked by NPY or MUS alone. Similarly, microinjection of either NPY or MUS into the PVN stimulated food intake in a dose-related fashion, and coinjection elicited a significantly higher response than that evoked by either individual treatment. These results suggest that GABA and NPY may coact through distinct receptors and second messenger systems in the PVN to augment food intake.




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