Dissociation of EEG and behavioural effects of ethanol provide evidence for a noncholinergic basis of intoxication
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IN 1957 it was reported that physotigmine, a drug that potentiates brain acetylcholine by inhibiting the enzyme which normally destroys it, could partially antagonise a tranquilliser, such as chlorpomazine1. Many years elapsed before anyone tested physostigmine for possible antagonistic effects against other sedative type drugs, such as ethanol. Physostigmine given before but not after massive doses of ethanol (4.5 g kg-1) did seem to shorten sleeping time and to reduce death of mice, an observation that led to the conclusion that ethanol might inhibit acetylcholine release or function2,3. © 1974 Nature Publishing Group.
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