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Immobilization Induces Acute Nitric Oxide Production in the Rat Hypothalamus: A Role of Ionotropic Glutamate Receptors in the Paraventricular Nucleus

Center for Advanced Oral Medicine (T.S.), Hokkaido University Hospital, Sapporo 060-8586, Japan; and Departments of Oral Functional Science (M.M., T.K., W.N., S.O., T.H., H.O.) and Oral Pathobiological Science (M.S.), Graduate School of Dental Medicine, Hokkaido University, Sapporo 060-8586, Japan

Address all correspondence and requests for reprints to: Tetsuo Shirakawa, Ph.D., Center for Advanced Oral Medicine, Hokkaido University Hospital, N13W6 Kita-ku, Sapporo, 060-8586, Japan. E-mail: tshira{at}den.hokudai.ac.jp.

Abstract

Production of nitric oxide (NO) in the hypothalamic paraventricular nucleus (PVN) was examined by microdialysis in rats subjected to immobilization (IMO) stress. A dialysis probe was implanted in the posterior magnocellular subdivision of the PVN and nitrite (NO₂^–), an oxidized product of NO, was measured continuously. NO₂^– concentration in dialysate was enhanced to 156% after 30 min of IMO compared with the NO₂^– level before IMO. Intraperitoneal administration of N^G-monomethyl-L-arginine (10 mg/kg), a NO synthase inhibitor, before IMO completely inhibited the increase of NO production that IMO was to induce. Depletion of catecholamines innervating the PVN by an injection of 6-hydroxydopamine into the lateral ventricle before the microdialysis had no suppressive effect on the increase of NO production by IMO. In contrast, NO₂^– levels in the PVN were lowered by continuous perfusion of the solution containing the ionotropic glutamate receptor antagonists 2-amino-5-phosphonovaleric acid (500 µM) and 6-cyano-7-nitroquinoxaline-2, 3 dione (50 µM) through the dialysis probe, and the IMO-induced increase of NO production was attenuated by the treatment. These results suggest that catecholaminergic drive to the hypothalamus is not necessary for the IMO-induced increase of NO production and that ionotropic glutamate receptors play a role in the basal and IMO-induced NO production.

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