Erwin C W, Linnoila M
Alcohol Clin Exp Res. 1981 Jan;5(1):49-55. doi: 10.1111/j.1530-0277.1981.tb04864.x.
Effects of ethyl alcohol evoked potentials were studied in 12 healthy volunteers. Alcohol significantly reduced the amplitude and prolonged the latency of the N2-P2 components of the centrally derived flash evoked potential. Amplitude attenuation was positively correlated with alcohol doses of 0.8 and 1.2 g/kg. Analysis of subsets of data revealed the amplitude attenuation to be time related and not present in the initial five responses after alcohol. Possible neurochemical mechanisms related to the amplitude attenuation are discussed.
对12名健康志愿者研究了乙醇诱发电位的影响。酒精显著降低了中央源性闪光诱发电位N2-P2成分的波幅并延长了潜伏期。波幅衰减与0.8和1.2 g/kg的酒精剂量呈正相关。数据分析子集显示波幅衰减与时间相关，且在饮酒后的最初五次反应中不存在。讨论了与波幅衰减相关的可能神经化学机制。
