Hoffman P L, Tabakoff B
J Neurochem. 1986 Mar;46(3):812-6. doi: 10.1111/j.1471-4159.1986.tb13044.x.
Ethanol increases the activity of "basal," guanine nucleotide- and dopamine-stimulated adenylate cyclase in mouse striatum. In contrast, ethanol, in vitro, did not modify the inhibition of striatal adenylate cyclase activity by opiates (morphine or [D-Ala2,D-Leu5] enkephalin). Following chronic in vivo ethanol treatment of mice, there was also no change in the character of opiate inhibition of striatal adenylate cyclase activity. Since ethanol, in vitro, does decrease striatal opiate receptor binding, the results suggest that the changes in affinity detected by ligand binding studies are not relevant for receptor-coupled adenylate cyclase activity, or that opiate receptor binding and opiate regulation of adenylate cyclase can be modulated independently. The selective effects of ethanol on systems that modulate adenylate cyclase activity may produce imbalances in neuronal function during in vivo ethanol exposure.
乙醇可增强小鼠纹状体中“基础”的、鸟嘌呤核苷酸和多巴胺刺激的腺苷酸环化酶的活性。相比之下，在体外，乙醇不会改变阿片类药物（吗啡或[D-丙氨酸2，D-亮氨酸5]脑啡肽）对纹状体腺苷酸环化酶活性的抑制作用。对小鼠进行慢性体内乙醇处理后，阿片类药物对纹状体腺苷酸环化酶活性的抑制特性也没有变化。由于在体外乙醇确实会降低纹状体阿片受体结合，结果表明，配体结合研究检测到的亲和力变化与受体偶联的腺苷酸环化酶活性无关，或者阿片受体结合和阿片对腺苷酸环化酶的调节可以独立调节。乙醇对调节腺苷酸环化酶活性系统的选择性作用可能会在体内乙醇暴露期间导致神经元功能失衡。
