Leslie S W, Woodward J J, Wilcox R E, Farrar R P
Brain Res. 1986 Mar 12;368(1):174-7. doi: 10.1016/0006-8993(86)91058-9.
Chronic ethanol treatment resulted in a marked reduction in the release of dopamine from striatal synaptosomes in response to depolarization. Calcium entry into the same synaptosomal preparations was not altered. Calculation of the ratio of calcium entry vs dopamine release showed that, under control conditions, approximately 15 calcium ions were required to cause the release of 1 dopamine molecule. Chronic ethanol treatment increased this ratio to more than 80:1, suggesting that chronic ethanol administration altered the coupling between calcium entry and dopamine release. Addition of ethanol in vitro to synaptosomes isolated from chronic ethanol-treated rats returned this ratio to approximately 20:1. These results suggest that chronic ethanol treatment results in dependence which is reflected biochemically in striatum through changes in the coupling between voltage-dependent calcium entry into nerve endings and subsequent neurotransmitter release.
慢性乙醇处理导致纹状体突触体在去极化时多巴胺释放显著减少。相同突触体制剂中的钙内流未发生改变。钙内流与多巴胺释放的比率计算表明，在对照条件下，约15个钙离子才能引起1个多巴胺分子的释放。慢性乙醇处理使该比率增加至超过80:1，表明慢性乙醇给药改变了钙内流与多巴胺释放之间的偶联。在体外将乙醇添加到从慢性乙醇处理大鼠分离的突触体中，该比率恢复至约20:1。这些结果表明，慢性乙醇处理导致依赖性，这在纹状体中通过电压依赖性钙进入神经末梢与随后神经递质释放之间偶联的变化而在生化上得到反映。
