Charness M E, Gordon A S, Diamond I
Ciba Found Symp. 1984;105:73-84. doi: 10.1002/9780470720868.ch5.
The interaction of ethanol with the nervous system produces acute intoxication, tolerance and withdrawal phenomena. Additionally, there are several alcohol-related neurological disorders which develop in alcoholic patients. Current evidence suggests that ethanol produces some of these changes by altering the structure and function of neural membranes. Therefore, neurotransmitter receptors and receptor-dependent molecular events in the nervous system may be highly sensitive to ethanol. The murine neuroblastoma X glioma hybrid cell line NG108-15 was used to study the acute and chronic interactions of ethanol with intact cells. Ethanol acutely inhibited opiate receptor binding, but after chronic exposure the cells exhibited an apparent adaptive increase in the number of opiate binding sites; this was reversible when ethanol was withdrawn. High levels of ethanol (200 mM) increased opiate binding after 18-24 hours; lower concentrations (25-50 mM) produced similar changes after two weeks. This model system has great potential for exploring the cellular and molecular mechanisms which underlie ethanol intoxication, tolerance and withdrawal.
乙醇与神经系统的相互作用会产生急性中毒、耐受性和戒断现象。此外，酒精性患者会出现几种与酒精相关的神经障碍。目前的证据表明，乙醇通过改变神经膜的结构和功能产生其中一些变化。因此，神经系统中的神经递质受体和受体依赖性分子事件可能对乙醇高度敏感。小鼠神经母细胞瘤X胶质瘤杂交细胞系NG108-15被用于研究乙醇与完整细胞的急性和慢性相互作用。乙醇急性抑制阿片受体结合，但在慢性暴露后，细胞表现出阿片结合位点数量明显的适应性增加；当撤去乙醇时，这种增加是可逆的。高浓度乙醇（200 mM）在18 - 24小时后增加阿片结合；较低浓度（25 - 50 mM）在两周后产生类似变化。这个模型系统在探索乙醇中毒、耐受性和戒断背后的细胞和分子机制方面具有巨大潜力。
