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低剂量的乙醇增强了在海马神经元细胞内测量的钙介导机制。

Ethanol in low doses augments calcium-mediated mechanisms measured intracellularly in hippocampal neurons.

作者信息

Carlen P L, Gurevich N, Durand D

出版信息

Science. 1982 Jan 15;215(4530):306-9. doi: 10.1126/science.7053581.

DOI:10.1126/science.7053581
PMID:7053581
Abstract

The electrophysiological effects of ethanol in low doses (5 to 20 millimoles per liter or 23 to 92 milligrams per 100 milliliters) were examined intracellularly in CA1 cells of rat hippocampus in vitro. Inhibitory and excitatory postsynaptic potentials were increased when ethanol was applied to the respective synaptic terminal regions. Postsynaptically, ethanol caused a moderate hyperpolarization with increased membrane conductance, even when synaptic transmission was blocked. Ethanol augmented the hyperpolarization that followed repetitive firing or that followed the eliciting of calcium spikes in the presence of tetrodotoxin, but not the rapid afterhyperpolarization in calcium-free medium. Ethanol appears to augment calcium-mediated mechanisms both pre- and postsynaptically.

摘要

在体外对大鼠海马体CA1细胞进行细胞内研究,检测低剂量乙醇(5至20毫摩尔/升或23至92毫克/100毫升)的电生理效应。当乙醇作用于相应的突触终末区域时,抑制性和兴奋性突触后电位均增强。在突触后,即使突触传递被阻断,乙醇也会导致适度的超极化并伴有膜电导增加。乙醇增强了重复放电后或在存在河豚毒素的情况下诱发钙峰后出现的超极化,但不增强无钙培养基中的快速超极化后电位。乙醇似乎在突触前和突触后均增强钙介导的机制。

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Science. 1982 Jan 15;215(4530):306-9. doi: 10.1126/science.7053581.
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