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A Novel Role for Endogenous Pituitary Adenylate Cyclase Activating Polypeptide in the Magnocellular Neuroendocrine System

Department of Cell Biology and Neuroscience (E.R.G., A.d.L., H.M., M.C.C.-C.) and Environmental Toxicology Program (C.G.C.), University of California at Riverside, Riverside, California 92521; Laboratorio de Histología y Microscopía Electrónica (M.L.-O., S.M.-R., E.S.-I.), Dirección de Neurociencias, Instituto Nacional de Psiquiatría "Ramón de la Fuente," Colonia San Lorenzo Huipulco, Mexico Distrito Federal 14370, Mexico; and Hotchkiss Brain Institute and Department of Physiology and Biophysics (L.G.B., Q.J.P.) University of Calgary, Calgary, Alberta, Canada T2N 4N1

Address all correspondence and requests for reprints to: E. R. Gillard, Department of Cell Biology and Neuroscience, 1208 Spieth Hall, University of California, Riverside, Riverside, California 92521. E-mail: erachelgillard{at}yahoo.com.

Central release of vasopressin (VP) by the magnocellular neuroendocrine cells (MNCs) responsible for systemic VP release is believed to be important in modulating the activity of these neurons during dehydration. Central VP release from MNC somata and dendrites is stimulated by both dehydration and pituitary adenylate cyclase activating polypeptide (PACAP). Although PACAP is expressed in MNCs, its potential role in the magnocellular response to dehydration is unexplored. The current study demonstrates that prolonged dehydration increases immunoreactivity for PACAP-27, PACAP-38, and the type I PACAP receptor in the supraoptic nucleus (SON) of the rat. In addition, PACAP stimulates local VP release in the euhydrated rat SON in vitro, and this effect is reduced by the PACAP receptor antagonist PAC_6–27 (100 nM), suggesting the participation of PACAP receptors. Concomitant with its effects on local VP release, PACAP also reduces basal glutamate and aspartate release in the euhydrated rat SON. Furthermore, somatodendritic VP release elicited by acute dehydration is blocked by PAC_6–27, suggesting that endogenous PACAP participates in this response. Consistent with this, RIA revealed that local PACAP-38 release within the SON is significantly elevated during acute dehydration. These results suggest that prolonged activation of hypothalamic MNCs is accompanied by up-regulation of PACAP and the type I PACAP receptor in these cells and that somatodendritic VP release in response to acute dehydration is mediated by activation of PACAP receptors by endogenous PACAP released within the SON. A potential role for PACAP in promoting efficient, but not exhaustive, systemic release of VP from MNCs during physiological challenge is discussed.

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