ACTIVATION OF NICOTINIC CHOLINERGIC RECEPTORS MODULATES THE SOMATOSTATINERGIC SYSTEM IN THE RAT HYPOTHALAMUS

Abstract

Acetylcholine potentiates the excitatory effect of somatostatin (SS) on brain neurons and nicotine, a cholinergic drug, modifies catecholamine turnover in the hypothalamus. The hypothalamus shows a high concentration of nicotinic cholinergic receptors and a dense innervation of SS-positive nerve terminals. In light of these findings, we studied the effect of intravenous (i.v.) nicotine injection (0.3 mg/kg) on SS peptide levels and receptor binding in the hypothalamus of male Sprague-Dawley rats. A second experimental group was pretreated with mecamylamine (5 mg/kg), a centrally acting antagonist of nicotinic cholinergic receptors, in order to evaluate whether the effects of nicotine on the studied system involved the activation of these receptors. Control rats received an i.v. saline injection. The rats were killed 4 min after i.v. administration, and the hypothalamus was dissected to isolate SS and its membrane receptors.Results: Nicotine produced an increase in somatostatin-like immunoreactivity (SLI) and in SS receptors. When the rats were pretreated with mecamylamine, the effects of nicotine were inhibited. Mecamylamine alone did not influence either parameter.Conclusions: 1. These results suggest that the rat hypothalamic somatostatinergic system is regulated by nicotine-like acetylcholine receptors. 2. The somatostatinergic system may be involved in some of the neuroendocrine effects of nicotine.