Alteration of ethanol-induced sleep latency by physostigmine in animals.

One of the presumed effects of ethanol is the suppression of acetylcholine release at presynaptic sites. If these neuronal effects are associated with CNS depression, then administration of a cholinesterase inhibitor (physostigmine) with ethanol should result in antagonism of this CNS depression. In the present study electrophysiological measures of sleep were used to assess the degree of CNS depression in response to ethanol alone (2.0 g/kg), physostigmine (1.0 mg/kg) alone, and the combination of both drugs administered together. These results were evaluated with respect to a saline control. Our findings indicate an antagonism between ethanol and physostigmine; the shortened sleep latency observed in animals receiving ethanol was reversed to control levels with administration of physostigmine.