Lucchi L, Covelli V, Anthopoulou H, Spano P F, Trabucchi M
Neurosci Lett. 1983 Sep 30;40(2):187-92. doi: 10.1016/0304-3940(83)90300-2.
Chronic ethanol consumption induces an increase in striatal adenylate cyclase enzymatic activity but is unable to further potentiate the dopamine stimulated production of cyclic-AMP. In striatal membranes obtained from chronic ethanol-treated rats, apomorphine exerts a more potent inhibition of [3H]spiperone binding when compared with controls, demonstrating that ethanol increases the affinity of the dopaminergic receptors associated with adenylate cyclase activity. In addition, GTP is unable to modify the agonist component of dopamine receptor in membrane exposed 'in vivo' to ethanol. Data are discussed in terms of a derangement of receptor-adenylate cyclase coupling system produced by chronic ethanol treatment.
长期摄入乙醇会导致纹状体腺苷酸环化酶的酶活性增加，但无法进一步增强多巴胺刺激的环磷酸腺苷生成。与对照组相比，在从长期乙醇处理的大鼠获得的纹状体膜中，阿扑吗啡对[3H]司哌罗宁结合的抑制作用更强，这表明乙醇增加了与腺苷酸环化酶活性相关的多巴胺能受体的亲和力。此外，GTP无法改变体内暴露于乙醇的膜中多巴胺受体的激动剂成分。根据长期乙醇处理产生的受体-腺苷酸环化酶偶联系统紊乱来讨论这些数据。
