Effects of acetylcholine analogues and ethanol on the respiration of brain cortex tissue in vitro

Abstract

Unstimulated and electrically stimulated brain cortex slices were exposed to compounds related to acetylcnoline, and to Triton, with or without 1.96 × 10 −1 M (0.9 per cent) ethanol. The lipid-insoluble substances acetylcholine, curare, deca- and suxa-methonium were inactive on the brain tissue respiration. In unstimulated tissue, the lipid-soluble acetylcholine analogues pyridine-2-aldoximedodecyl iodide (PAD) and cetyltrimethyl-ammonium bromide (Cetavlon), like ethanol, caused a transient increase in respiration. Cetavlon, cetylpyridine chloride (CPC) and Triton reduced the respiration of both stir ulated and unstimulated tissue at approximately identical concentrations, the relative effect on unstimulated tissue being smaller. 10 −4 M PAD and 1.8 × 10 −3 M atrepine abolished the response to stimulation almost completely leaving unstimulated tissue unaffected. Ethanol significantly increased the effect of atropine, PAD, Cetavlon and CPC on stimulated tissue. The non-ionized detergent Triton was not synergistic with ethanol. In intact rats, PAD potentiated ethanol action on the CNS Cetavlon acted similarly, but caused strong haemolysis when injected with ethanol. In vitro, haemolysis caused by Cetavlon was not increased by low ethanol concentrations. The results are consistent with the hypothesis that the acetylcholine system is involved in the reaction of brain slices to electrical stimulation, and indicate that ethanol may depress the functional response to stimulation by unspecific action on this system.