Ethanol depression of cerebellar Purkinje neuron firing involves nicotinic acetylcholine receptors.
Local application of ethanol (EtOH) has been reported to inhibit Purkinje neuron firing. EtOH-induced depressions can be antagonized by bicuculline, suggesting involvement of GABAA receptors. Since there is evidence from other studies indicating that nicotine may interact with EtOH responses, in this study we investigated whether nicotinic acetylcholine receptors (nAChR's) might be also involved in EtOH-induced depressions of these neurons in urethane-anesthetized Sprague-Dawley rats. Using local application (micropressure ejection) of drugs onto cerebellar Purkinje neurons while recording extracellular firing rates, we found that depressant responses to EtOH could be potentiated by subdepressant doses of nicotine. Furthermore, EtOH-induced depressions of firing could be antagonized by mecamylamine, a nicotinic acetylcholine receptor (nAChR) antagonist. Results from the present study indicate that EtOH-induced depressions may involve nAChRs in the cerebellum.
Freund
R K
RK
Department of Pharmacology, University of Colorado Health Sciences Center, Denver, Colorado, 80262, USA.
Palmer
M R
MR
D000200:Action Potentials / Q000187:drug effects*; D000818:Animals; D002531:Cerebellum / Q000187:drug effects*; D000431:Ethanol / Q000494:pharmacology*; D008297:Male; D008464:Mecamylamine / Q000494:pharmacology; D009538:Nicotine / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D011978:Receptors, Nicotinic / Q000187:drug effects*
D011978:Receptors, Nicotinic; D000431:Ethanol; D008464:Mecamylamine; D009538:Nicotine