Ward Roberta J, Lallemand Frédéric, de Witte Philippe
Biologie du Comportement, Université Catholique de Louvain, Louvain-la-Neuve, Belgium.
Alcohol Alcohol. 2009 Mar-Apr;44(2):128-35. doi: 10.1093/alcalc/agn100. Epub 2009 Jan 20.
The brain damage, which occurs after either chronic alcoholization or binge drinking regimes, shows distinct biochemical and neurotransmitter differences. An excessive amount of glutamate is released into specific brain regions during binge drinking (in excess of 4- to 5-fold of the normal basal concentration) that is not evident during periods of excessive alcohol consumption in chronic alcohol abusers. Increases in glutamate release are only observed during the initial stages of withdrawal from chronic alcoholism ( approximately 2- to 3-fold) due to alterations in the sensitivities of the NMDA receptors. Such changes in either density or sensitivity of these receptors are reported to be unaltered by binge drinking. When such excesses of glutamate are released in these two different models of alcohol abuse, a wide range of biochemical changes occur, mediated in part by increased fluxes of calcium ions and/or activation of various G-protein-associated signalling pathways. Cellular studies of alveolar macrophages isolated from these two animal models of alcohol abuse showed enhanced (binge drinking) or reduced (chronic alcoholization) lipopolysaccharide (LPS)-stimulated NO release. Such studies could suggest that neuroadaptation occurs with the development of tolerance to alcohol's effects in both neurotransmitter function and cellular processes during chronic alcoholization that delay the occurrence of brain damage. In contrast, 'binge drinking' induces immediate and toxic effects and there is no evidence of an increased preference for alcohol as seen after withdrawal from chronic alcoholization.
在长期酗酒或暴饮模式后发生的脑损伤，表现出明显的生化和神经递质差异。在暴饮期间，过量的谷氨酸会释放到特定脑区（超过正常基础浓度的4至5倍），而在慢性酗酒者过量饮酒期间则不明显。由于NMDA受体敏感性的改变，谷氨酸释放增加仅在慢性酒精中毒戒断的初始阶段观察到（约2至3倍）。据报道，暴饮不会改变这些受体的密度或敏感性。当在这两种不同的酒精滥用模型中释放过量的谷氨酸时，会发生广泛的生化变化，部分由钙离子通量增加和/或各种G蛋白相关信号通路的激活介导。对从这两种酒精滥用动物模型中分离出的肺泡巨噬细胞进行的细胞研究表明，脂多糖（LPS）刺激的一氧化氮（NO）释放增强（暴饮）或减少（长期酗酒）。这些研究可能表明，在慢性酗酒过程中，神经适应随着对酒精作用在神经递质功能和细胞过程中的耐受性发展而发生，从而延迟脑损伤的发生。相比之下，“暴饮”会立即产生毒性作用，并且没有证据表明像从慢性酗酒中戒断后那样对酒精的偏好增加。
