Kril J J, Dodd P R, Gundlach A L, Davies N, Watson W E, Johnston G A, Harper C G
Department of Pathology, University of Sydney, NSW.
Clin Exp Neurol. 1988;25:135-41.
Neurological and cognitive deficits occur in many chronic alcoholic patients. Quantitative studies reveal a significant reduction in the number of neurons in the superior frontal gyrus of chronic alcoholics, with no change in the motor cortex. Our studies are aimed at delineating which neurotransmitter systems are altered in alcoholics and to correlate these alterations with morphometry and, where possible, clinical signs. Much evidence suggests both short- and long-term effects of ethanol on GABA-mediated neurotransmission. GABA and benzodiazepines bind to distinct, but allosterically linked, sites on the GABA/benzodiazepine receptor complex. In the absence of any detected difference in the number of benzodiazepine receptors in both the frontal and motor cortex from alcoholic and control patients, a significant increase in the amount of GABA enhancement of [3H]diazepam binding was measured in frontal cortex membranes from patients with Wernicke's encephalopathy relative to non-alcoholic controls. This finding suggests an increased coupling of the GABA and benzodiazepine recognition sites in this area, which may be due to ethanol-induced conformational changes in the receptor complex.
许多慢性酒精中毒患者会出现神经和认知缺陷。定量研究显示，慢性酒精中毒患者额上回的神经元数量显著减少，而运动皮层则无变化。我们的研究旨在确定酒精中毒患者哪些神经递质系统发生了改变，并将这些改变与形态学以及可能的临床体征联系起来。许多证据表明，乙醇对γ-氨基丁酸（GABA）介导的神经传递具有短期和长期影响。GABA和苯二氮䓬类药物结合于GABA/苯二氮䓬受体复合物上不同但变构连接的位点。在酒精中毒患者和对照患者的额叶和运动皮层中，未检测到苯二氮䓬受体数量存在差异，但相对于非酒精中毒对照，韦尼克脑病患者额叶皮层膜中[³H]地西泮结合的GABA增强量显著增加。这一发现表明该区域GABA和苯二氮䓬识别位点的偶联增加，这可能是由于乙醇诱导受体复合物构象变化所致。
