ETHANOL INHIBITS NMDA-ACTIVATED ION CURRENT IN HIPPOCAMPAL-NEURONS
ETHANOL INHIBITS NMDA-ACTIVATED ION CURRENT IN HIPPOCAMPAL-NEURONS
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DOI：
10.1126/science.2467382
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发表时间：
1989-03-31
期刊：
影响因子：
56.9
通讯作者：
WEIGHT, FF
中科院分区：
文献类型：
--
作者：
LOVINGER, DM;WHITE, G;WEIGHT, FF
电压钳位海马神经元中谷氨酸受体激动剂 N-甲基-D-天冬氨酸 (NMDA) 诱导的离子电流被乙醇 (EtOH) 抑制。在 5 至 50 mM 范围内，抑制作用以浓度依赖性方式增加，该范围也会产生中毒。 50 mM EtOH 使 NMDA 激活电流的幅度降低 61%；相比之下，这一浓度的乙醇仅使谷氨酸受体激动剂红藻氨酸和使君子氨酸激活的电流幅度分别降低了 18% 和 15%。几种酒精对 NMDA 激活电流的抑制效力与其中毒效力呈线性相关，这表明酒精诱导的对 NMDA 受体激活反应的抑制可能会导致与中毒相关的神经和认知障碍。
The ion current induced by the glutamate receptor agonist N-methyl-D-aspartate (NMDA) in voltage-clamped hippocampal neurons was inhibited by ethanol (EtOH). Inhibition increased in a concentration-dependent manner over the range 5 to 50 mM, a range that also produces intoxication. The amplitude of the NMDA-activated current was reduced 61 percent by 50 mM EtOH; in contrast, this concentration of EtOH reduced the amplitude of current activated by the glutamate receptor agonists kainate and quisqualate by only 18 and 15 percent, respectively. The potency for inhibition of the NMDA-activated current by several alcohols is linearly related to their intoxicating potency, suggesting that alcohol-induced inhibition of responses to NMDA receptor activation may contribute to the neural and cognitive impairments associated with intoxication.