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Vol. 284, Issue 3, 1188-1196, March 1998

Nicotine-Induced Norepinephrine Release in the Rat Amygdala and Hippocampus is Mediated through Brainstem Nicotinic Cholinergic Receptors1

Yitong Fu, Shannon G. Matta , Tressa J. James and Burt M. Sharp

Institute for Brain and Immune Disorders, Minneapolis Medical Research Foundation (Y.F., S.G.M., T.J.J., B.M.S.) and the Departments of Medicine, Hennepin County Medical Center and the University of Minnesota, Minneapolis (S.G.M., B.M.S.), Minnesota

Previous studies have shown that nicotine stimulates norepinephrine (NE) release in the rat hypothalamic paraventricular nucleus, which in turn activates the hypothalamo-pituitary-adrenal axis. In the present study, nicotine induced NE release in the amygdala (AMYG) and the hippocampus (HP) of the same rat in vivo. Nicotine (0.065-0.135 mg/kg i.v. at a rate of 0.09 mg/kg/60 sec) dose-dependently increased NE release at both sites with similar potencies. To determine whether the site of action of nicotine is in the brainstem, which contains the noradrenergic cell bodies projecting to AMYG and HP, nicotinic cholinergic receptor (NAchR) antagonists were injected into the cerebral aqueduct before i.v. nicotine. Use of the following antagonists enabled partial characterization of the NAchRs mediating NE secretion: mecamylamine (Mec), dihydro-beta -erythroidine (DHbeta E), methyllycaconitine (MLA) and alpha -bungarotoxin (alpha -BTX). Mec inhibited 80% of NE release in AMYG and 87% in HP (IC50 = 6 nmol for both regions). DHbeta E blocked 62% of NE release in AMYG (IC50 = 8 nmol) and 63% in HP (IC50 = 15 nmol). Similar to DHbeta E, MLA inhibited 60% of NE release in AMYG and 66% in HP (IC50 = 5 nmol for both regions). In contrast, alpha -BTX had no effect on NE release in either region. These results indicate that brainstem NAchRs accessible from the fourth ventricle mediate nicotine-stimulated NE secretion in AMYG and HP. Taken together with prior investigations showing the brainstem expression of mRNAs encoding NAchR subtypes and the selectivity of antagonists for NAchR subtypes, the present studies suggest that brainstem alpha-3 subunits may be involved.

0022-3565/98/2843-1188$03.00/0
THE JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
Copyright © 1998 by The American Society for Pharmacology and Experimental Therapeutics


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