乙醇抑制成年哺乳动物离体神经元中NMDA激活电流，但不改变GABA激活电流。

Ethanol inhibits NMDA-activated current but does not alter GABA-activated current in an isolated adult mammalian neuron.

作者信息

White G, Lovinger D M, Weight F F

机构信息

Section of Electrophysiology, National Institute on Alcohol Abuse and Alcoholism, Rockville, MD 20852.

出版信息

Brain Res. 1990 Jan 22;507(2):332-6. doi: 10.1016/0006-8993(90)90292-j.

DOI:10.1016/0006-8993(90)90292-j

PMID:2186844

Abstract

The effects of ethanol (EtOH) on membrane ion currents activated by N-methyl-D-aspartate (NMDA) and gamma-aminobutyric acid (GABA) were studied under voltage-clamp conditions in isolated sensory neurons within hours of being dissociated from adult rats. The amplitude of the ion current activated by NMDA was decreased in the presence of 2.5-100 mM EtOH (IC50, 10 mM or 0.05% EtOH), a concentration range that produces intoxication. The amplitude of the GABA-activated Cl- current, on the other hand, was not significantly affected by this concentration range of EtOH. The observations suggest that some of the neural and cognitive impairments associated with EtOH intoxication may result from inhibition of the NMDA-activated ion current.

摘要

在从成年大鼠分离后的数小时内，在电压钳条件下，研究了乙醇（EtOH）对N-甲基-D-天冬氨酸（NMDA）和γ-氨基丁酸（GABA）激活的膜离子电流的影响。在存在2.5 - 100 mM乙醇（IC50为10 mM或0.05%乙醇）的情况下，NMDA激活的离子电流幅度降低，该浓度范围会导致中毒。另一方面，GABA激活的Cl-电流幅度不受该乙醇浓度范围的显著影响。这些观察结果表明，与乙醇中毒相关的一些神经和认知障碍可能是由于NMDA激活的离子电流受到抑制所致。