Regulation of histamine turnover via muscarinic and nicotinic receptors in the brain

• Published in: Japanese Journal of Pharmacology Vol. 52; no. suppl-1.1; p. 160
• Main Authors: Oishi, Ryozo, Adachi, Naoto, Okada, Keishi, Muroi, Nobuyuki, Saeki, Kiyomi
• Format: Journal Article
• Language: English; Japanese
• Published: The Japanese Pharmacological Society 1990
• ISSN: 0021-5198; 1347-3506
• DOI: 10.1016/S0021-5198(19)55308-2

The effects of cholinergic stimulants on brain histamine(HA) turnover were examined, based upon the accumulation of tele-methylhistamine(t-MH) after administration of pargyline. In the mouse brain, oxotremorine (>0.05mg/kg, s.c.) significantly inhibited the HA turnover, this effect being completely antagonized by atropine but not by methylatropine. A large dose of nicotine produced a significant inhibition of the HA turnover, which was antagonized by mecamylamine but not by atropine or hexamethonium. Physostigmine (>0.1mg/kg, s.c.) also significantly inhibited the HA turnover. This effect was antagonized by atropine but not by mecamylamine. None of these antagonists used affected the t-MH level or HA turnover by themselves. In the rat brain, physostigmine decreased the HA turnover markedly in the striatum and cerebral cortex where muscarinic receptors are present in high density. These results suggest that the stimulation of central muscarinic receptors potently inhibits the histaminergic activity in the brain and that strong stimulation of central nicotinic receptors can also induce a similar effect.