Xiao Zheman, Zhu Fan, Lu Zuneng, Pan Songqing, Liang Jingjing, Zheng Jiangquan, Liu Zhongchun
Department of Neurology, Institution of Neuropsychiatry Research, Renmin Hospital of Wuhan University Jiefang Road 238, Wuhan 430060, Hubei, PR China.
Int J Physiol Pathophysiol Pharmacol. 2013 Sep 10;5(3):161-8. eCollection 2013.
To determine whether actions on nicotine acetylcholine receptors (nAChRs) contribute to ethanol's depressant effects on the autonomic nervous system.
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.
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.
Ethanol inhibited the whole-cell INic significantly,probably through noncompetitive inhibition at the binding sites outside of the cell membrane.
确定对烟碱型乙酰胆碱受体（nAChRs）的作用是否有助于乙醇对自主神经系统的抑制作用。
通过全细胞膜片钳记录，在原代培养的颈上神经节（SCGs）中检测乙醇对nAChRs的急性作用。形成全细胞模式后，将用细胞外溶液稀释至不同浓度的药物直接施加于单个神经元。
在-70 mV钳制下，乙醇显著且可逆地抑制烟碱诱发电流（INic），最大抑制率约为80%，IC50为232.88±40.66 mM。在50 mM时，乙醇加速了INic的缓慢衰减，但不影响其快速衰减和上升时间。乙醇对SCGs中INic的抑制既无使用依赖性也无电压依赖性。
乙醇显著抑制全细胞INic，可能是通过对细胞膜外结合位点的非竞争性抑制。
