Negro M, Fernández A, Calvo P
Department of Biochemistry and Molecular Biology, University of León, Spain.
Neurochem Res. 1992 Apr;17(4):381-5. doi: 10.1007/BF00974581.
Ethanol alters almost all membrane functions, but it behaves essentially like a benzodiazepine-type GABAergic agonist. The mechanism by which ethanol affects the GABA/benzodiazepine complex is not clear. We studied the possible changes in [3H]flunitrazepam binding induced by chronic ethanol treatment, using light microscopic autoradiography, to try to elucidate the controversy underlying this topic. This technique allows us to measure densities of benzodiazepine receptors in different anatomical brain areas--visual cortex and hippocampus--which seem to constitute the anatomical support for the behavioral and physiological responses affected by ethanol. Autoradiographic studies on the visual cortex and hippocampus from rats chronically treated with ethanol do not show statistically significant differences in the binding of [3H]flunitrazepam with respect to control animals. Furthermore, we did not find either rostro-caudal or medio-lateral differences in benzodiazepine receptor densities in each layer of the visual cortex.
乙醇几乎会改变所有的膜功能，但它的作用本质上类似于苯二氮䓬类GABA能激动剂。乙醇影响GABA/苯二氮䓬复合物的机制尚不清楚。我们使用光学显微镜放射自显影技术，研究了慢性乙醇处理对[³H]氟硝西泮结合的可能影响，试图阐明这一话题背后的争议。该技术使我们能够测量不同脑区——视觉皮层和海马体——中苯二氮䓬受体的密度，这些脑区似乎构成了乙醇影响行为和生理反应的解剖学基础。对慢性乙醇处理大鼠的视觉皮层和海马体进行的放射自显影研究表明，与对照动物相比，[³H]氟硝西泮的结合没有统计学上的显著差异。此外，我们在视觉皮层各层的苯二氮䓬受体密度中未发现前后或中外侧差异。
