ETHANOL DEPRESSION OF CEREBELLAR PURKINJE NEURON FIRING INVOLVES NICOTINIC ACETYLCHOLINE-RECEPTORS

Local application of ethanol (EtOH) has been reported to inhibit Purki nje neuron firing. EtOH-induced depressions can be antagonized by bicu culline, suggesting involvement of GABA(A) receptors. Since there is e vidence from other studies indicating that nicotine may interact with EtOH responses, in this study we investigated whether nicotinic acetyl choline receptors (nAChR's) might be also involved in EtOH-induced dep ressions of these neurons in urethane-anesthetized Sprague-Dawley rats . Using local application (micropressure ejection) of drugs onto cereb ellar Purkinje neurons while recording extracellular firing rates, we found that depressant responses to EtOH could be potentiated by subdep ressant doses of nicotine. Furthermore, EtOH-induced depressions of fi ring could be antagonized by mecamylamine, a nicotinic acetylcholine r eceptor (nAChR) antagonist. Results from the present study indicate th at EtOH-induced depressions may involve nAChRs in the cerebellum. (C) 1997 Academic Press.