Sharma V K, Banerjee S P
Eur J Pharmacol. 1979 Jul 1;56(4):297-304. doi: 10.1016/0014-2999(79)90259-0.
Chronic ethanol administration to cats increased specific [3H]ouabain binding by 63% in cerebral cortex, 47% in cerebellum, 84% in amygdala, and 100% in hippocampus when the binding assays were performed in the presence of 160 nM [3H]ouabain. There was no significant change in specific [3H]ouabain binding in hypothalamus, thalamus, corpus striatum, and brain stem following chronic ethanol ingestion. Scatchard analysis revealed that enhancement of specific [3H]ouabain binding following chronic ethanol treatment in some areas of cat brain is primarily due to changes in densities of ouabain binding sites. Since ouabain is a specific inhibitor of (Na+ + K+)-ATPase the present observations suggest that the molecular mechanism for the enhancement of (Na+ + K+)-ATPase activity after chronic ethanol ingestion may be due to increased net rate of synthesis of (Na+ + K+)-ATPase molecules or exposure of non-functional enzyme system following conformational change of plasma membrane.
当在160 nM [³H]哇巴因存在的情况下进行结合测定时，对猫长期给予乙醇，可使大脑皮层的特异性[³H]哇巴因结合增加63%，小脑增加47%，杏仁核增加84%，海马体增加100%。长期摄入乙醇后，下丘脑、丘脑、纹状体和脑干中的特异性[³H]哇巴因结合没有显著变化。Scatchard分析表明，猫脑某些区域长期乙醇处理后特异性[³H]哇巴因结合的增强主要是由于哇巴因结合位点密度的变化。由于哇巴因是(Na⁺ + K⁺)-ATP酶的特异性抑制剂，目前的观察结果表明，长期摄入乙醇后(Na⁺ + K⁺)-ATP酶活性增强的分子机制可能是由于(Na⁺ + K⁺)-ATP酶分子合成净速率增加，或细胞膜构象变化后非功能性酶系统的暴露。
