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Journal of Pharmacology And Experimental Therapeutics, Vol. 185, Issue 3, 583-593, 1973
Copyright © 1973 by American Society for Pharmacology and Experimental Therapeutics

ALTERATION OF CORTICAL AND RETICULAR ACETYLCHOLINE RELEASE BY ETHANOL IN VIVO

CARLTON K. ERICKSON 1 and DAVID T. GRAHAM 1

1 Department of Pharmacology, Toxicology, School of Pharmacy, University of Kansas, Lawrence, Kansas

The effect of ethanol on spontaneously released acetylcholine (ACh) was studied in rabbits with cortical collecting cups and push-pull cannulas. The investigation was designed to examine the possibility that behavioral depression produced by acute doses of ethanol is the consequence of impaired central cholinergic transmission. Spontaneously released ACh was collected in Locke's solution, containing physostigmine, held in acrylic cups over the parietal cortex of unanesthetized but immobilized rabbits during consecutive 15-minute periods. Ethanol, 0.5, 1.0 and 2.0 g/kg, was injected i. v. after appropriate control collections. Samples were assayed for ACh by comparing the contractions produced by the samples on a dorsal leech muscle with those produced by standard ACh chloride solutions. For subcortical collection of ACh, a push-pull cannula placed in the mesencephalic reticular formation was used in a similar manner. Ethanol, 1.0 and 2.0 g/kg i. v., depressed, in a dose-dependent manner, the amount of ACh that was collected from the parietal cortex and mesencephalic reticular formation. The site of perfusion within the reticular formation was more sensitive to ethanol depression than the parietal cortex, since the 0.5 g/kg dose of ethanol, unlike its effect on the cortex, significantly decreased free ACh in the reticular formation and produced synchrony of the reticular electroencephalogram. In separate experiments in rats, ethanol, 4.5 g/kg p.o., increased total brain ACh and produced blood ethanol concentrations similar to those produced by an oral dose of ethanol that depressed free cortical ACh in rabbits. The results show that ethanol can depress the release of free ACh in selected areas of the cortex and reticular formation in rabbits. The depressed release may contribute to the acute behavioral intoxication produced by ethanol.

Submitted on November 13, 1972
Accepted on January 29, 1973




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Copyright © 1973 by the American Society for Pharmacology and Experimental Therapeutics.