Cholinergic involvement in ethanol intoxication and withdrawal-induced seizure susceptibility.
The enzymes of the cholinergic system have been investigated in discrete brain areas in alcohol-dependent rats, which were still intoxicated or were undergoing withdrawal. The ethanol intoxication resulted in a slight, but significant increase in choline acetyltransferase (CAT) activity in the caudate nucleus both 1 and 7 h after the last dose of ethanol. We also found a significant decrease in CAT activity in the temporal limbic cortex while rats were highly intoxicated. All other brain regions investigated, e.g., cerebellum, pons-medulla, frontoparietal cortex, hypothalamus and septum showed unchanged CAT activity. Rats were also analysed immediately following the onset of a withdrawal-induced audiogenic convulsive seizure where, in addition to the striatum, depressed CAT activity was observed in the hippocampus. In all the analysed situations acetylcholinesterase activity remained unchanged. These results show that ethanol intoxication leads to a perturbation in the synthetic capacity of acetylcholine in certain defined brain structures and that this may have some correlation to the observed behavioural impairments.
D000110:Acetylcholinesterase / Q000378:metabolism; D000161:Acoustic Stimulation; D000435:Alcoholic Intoxication; D000437:Alcoholism / Q000503:physiopathology*; D000818:Animals; D001921:Brain / Q000201:enzymology; D002795:Choline O-Acetyltransferase / Q000378:metabolism; D006801:Humans; D008297:Male; D010275:Parasympathetic Nervous System / Q000502:physiology*; D051381:Rats; D012640:Seizures / Q000503:physiopathology*; D013375:Substance Withdrawal Syndrome / Q000503:physiopathology*; D013997:Time Factors
D002795:Choline O-Acetyltransferase; D000110:Acetylcholinesterase