Davidson M, Wilce P A, Shanley B C
Department of Biochemistry, University of Queensland, St. Lucia, Australia.
Alcohol Alcohol Suppl. 1993;2:365-9.
The hyperexcitability observed following ethanol withdrawal in dependent animals is thought to be related to increased sensitivity of glutamate receptors. This may predispose to 'excitotoxic' neural damage. The aim of this study was to test this hypothesis by intrahippocampal injection of N-methyl-D-aspartic acid (NMDA) in ethanol-dependent rats and to quantify brain damage using enzymic neuronal markers, viz. choline acetyltransferase (ChAT) and glutamate decarboxylase (GAD). Specific activity of GAD but not ChAT was found to be significantly decreased in hippocampi of ethanol-dependent animals following injection of NMDA, suggesting that chronic ethanol administration sensitizes GABAergic neurons to the toxic effects of excitatory amino acid transmitters.
在依赖酒精的动物体内，戒酒后观察到的过度兴奋性被认为与谷氨酸受体敏感性增加有关。这可能易导致“兴奋性毒性”神经损伤。本研究的目的是通过向酒精依赖大鼠海马内注射N-甲基-D-天冬氨酸（NMDA）来验证这一假设，并使用酶促神经元标记物，即胆碱乙酰转移酶（ChAT）和谷氨酸脱羧酶（GAD）来量化脑损伤。结果发现，注射NMDA后，酒精依赖动物海马中GAD的比活性显著降低，而ChAT的比活性未降低，这表明长期给予酒精会使GABA能神经元对兴奋性氨基酸递质的毒性作用更加敏感。
