Effect of chronic ethanol treatment on adenylate cyclase activity in rat striatum

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.