OBJECTIVE: To determine whether actions on nicotine acetylcholine receptors (nAChRs) contribute to ethanol's depressant effects on the autonomic nervous system. METHODS: The acute effects of ethanol on nAChRs were examined in primary cultured superior cervical ganglion (SCGs) by whole-cell patch clamp recordings. After the whole-cell configuration was formed, drugs diluted to various concentrations with extracellular solution were applied directly to single neurons. RESULTS: Held at -70 mV, ethanol significantly and reversibly inhibited nicotine-evoked currents (INic) with a maximum inhibition rate of ~80% and an IC50 of 232.88±40.66 mM. At 50 mM, ethanol accelerated the slow decay, but did not affect the quick decay and rising time of INic. There was neither use-dependence nor voltage-dependence of ethanol on suppressing INic in SCGs. CONCLUSION: Ethanol inhibited the whole-cell INic significantly,probably through noncompetitive inhibition at the binding sites outside of the cell membrane.
OBJECTIVE: To determine whether actions on nicotine acetylcholine receptors (nAChRs) contribute to ethanol's depressant effects on the autonomic nervous system. METHODS: The acute effects of ethanol on nAChRs were examined in primary cultured superior cervical ganglion (SCGs) by whole-cell patch clamp recordings. After the whole-cell configuration was formed, drugs diluted to various concentrations with extracellular solution were applied directly to single neurons. RESULTS: Held at -70 mV, ethanol significantly and reversibly inhibited nicotine-evoked currents (INic) with a maximum inhibition rate of ~80% and an IC50 of 232.88±40.66 mM. At 50 mM, ethanol accelerated the slow decay, but did not affect the quick decay and rising time of INic. There was neither use-dependence nor voltage-dependence of ethanol on suppressing INic in SCGs. CONCLUSION:Ethanol inhibited the whole-cell INic significantly,probably through noncompetitive inhibition at the binding sites outside of the cell membrane.
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Keywords:
Ethanol; desensitization; nicotine; nicotine acetylcholine receptors; superior cervical ganglion