RESUMO
Ethanol's actions in brain have been suggested to be partially mediated by a mechanism involving the ethanol-induced activation of the endogenous opioid system. Opioid systems, which are closely linked with dopamine transmission, are thought to be affected by ethanol through alterations in the processing, release, and/or receptor binding of opioid peptides. We studied the effects of a single acute dose of ethanol on rat nigrostriatal mu opioid receptors by quantitative receptor autoradiography, using [3H] [D-Ala(2),MePhe(4),Gly-ol(5)]-enkephalin ([3H]-DAMGO) as radioligand. [3H]-DAMGO binding was significantly decreased in the pars reticulata of the substantia nigra 1 h after ethanol administration. Ethanol exposure did not affect [3H]-DAMGO binding neither in the pars compacta of the substantia nigra nor in the caudate-putamen at any time tested after drug administration. The observed effects may reflect ethanol-induced changes in ligand binding affinity (Kd) or in receptor density (Bmax). Early and transitory ethanol-induced changes of mu receptors in the substantia nigra pars reticulata may be related to regulation of dopaminergic nigrostriatal transmission and contribute to determine brain sensitivity to the drug.