Lovinger D M, White G, Weight F F
Section of Electrophysiology, National Institute on Alcohol Abuse and Alcoholism, Rockville, MD 20852.
Science. 1989 Mar 31;243(4899):1721-4. doi: 10.1126/science.2467382.
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.
在电压钳制的海马神经元中，谷氨酸受体激动剂N-甲基-D-天冬氨酸（NMDA）诱导的离子电流受到乙醇（EtOH）的抑制。在5至50 mM的浓度范围内，抑制作用呈浓度依赖性增加，该浓度范围也会产生中毒现象。50 mM乙醇可使NMDA激活电流的幅度降低61%；相比之下，该浓度的乙醇仅使谷氨酸受体激动剂海人藻酸和quisqualate激活电流的幅度分别降低18%和15%。几种醇类对NMDA激活电流的抑制效力与其致毒效力呈线性相关，这表明酒精诱导的对NMDA受体激活反应的抑制可能导致与中毒相关的神经和认知损伤。
