Ethanol inhibits voltage-gated sodium channels in cultured superior cervical ganglion neurons

Ethanol inhibits voltage-gated sodium channels in cultured superior cervical ganglion neurons
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乙醇抑制培养的颈上神经节神经元的电压门控钠通道

DOI:
10.1097/wnr.0b013e328318ed9a
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发表时间:
2008-12
期刊:
影响因子:
1.7
通讯作者:
Liu, Wanhong
Liu, Wanhong
中科院分区:
医学4区
文献类型:
--
作者:
Lu, Zuneng;Yin, Shijin;Dong, Hongjuan;Liu, Zhongchun;Yu, Shaozu;Xiao, Zheman;Li, Lijun;Zhu, Fan;Liu, Wanhong

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为确定钠通道的作用是否参与乙醇对自主神经系统的抑制作用,采用全细胞膜片钳记录方法,观察了乙醇对原代培养的颈上神经节Na+电流的急性影响。乙醇呈浓度依赖性地抑制Na+电流,并使动作电位放电减少。乙醇(100 mM)对失活曲线无影响,但使失活曲线左移,使失活恢复时间延长。这一发现表明,处于失活状态的通道比处于静息状态的通道更容易受到乙醇的影响。本研究首次证实了乙醇对交感神经元钠通道门控的急性抑制作用。
To determine whether actions on sodium channels contribute to ethanol's depressant effects on the autonomic nervous system, the acute effects of ethanol on Na+ currents in primary cultured superior cervical ganglion were examined by whole-cell patch clamp recordings. Ethanol inhibited Na+ currents concentration dependently, and decreased action potential firing. Ethanol (100 mM) did not affect activation curve, but resulted in a left shift of the inactivation curve and prolonged the recovery from inactivation. This finding indicates that the channels in the inactivated state are more susceptible to ethanol than those in the resting state. For the first time, this study demonstrates acute inhibitory effects of ethanol on sodium channel gating in sympathetic neurons.
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