Conclusion
Ethanol inhibited the whole-cell INic significantly,probably through noncompetitive inhibition at the binding sites outside of the cell membrane.
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.
Objective
To determine whether actions on nicotine acetylcholine receptors (nAChRs) contribute to ethanol's depressant effects on the autonomic nervous system.
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.