It has been described a b-endorphin deficiency in alcoholic patients or in men with a family history of alcoholism. It is well known that alcohol consumption release b-endorphin from hypothalamus; therefore, it has been hypothesized that high alcohol intake in alcoholics could be due to a compensatory strategy with the purpose of increase the b-endorphin levels. There are two opioid pathways that apparently are involved in the rewarding effects of alcohol. The main one is characterized for the projections from arcuate nucleus to ventral tegmental area (VTA). In VTA there are interneurons GABA that have an inhibitory action on dopamine (DA) neurons; this GABA neurons contain m-opioid receptors (MOR); therefore, when b-endorphin binding these receptors, GABA neurons are inhibited and DA release is facilitated, increasing this way the rewarding effects of alcohol. In the other pathway DA is no directly involved; in this case, when alcohol release b-endorphin from arcuate nucleus its action is directly on nucleus accumbens (NAc), afterwards, the disinhibition of projections to structures as ventral pallidum seems to be an additional mechanism of alcohol rewarding. Besides the activation or inhibition of opioid receptors, the density and probable a differential sensitivity of MORs seems to play an important role in rewarding effects of alcohol. It has been described higher density of MOR in rats selected genetically for its alcohol preference when compared with no-preference rats, mainly in structures of mesolimbic-cortical system, which is intimately related to rewarding perception. The questions are, this difference is the result of the inbreeding after several generations? is consequence of chronic alcohol exposure? or this molecular difference is an intrinsic characteristic of organisms with high liking for alcohol? Recent studies in our laboratory suggest that differences in MOR density may depend on high vs. low liking for alcohol in wild type rats, and that chronic alcohol consumption also produces adaptive changes in MOR expression. Therefore, evidence supports adaptive changes as a result chronic alcohol consumption as well as intrinsic characteristics related to proclivity for high alcohol consumption.
The findings from the study and the clinic use of opioid antagonists have an additional support of the participation of the opioid system in the rewarding effects of alcohol; therefore, several pharmacological strategies have been used as therapy in alcoholic patients. There is no doubt concerning the important role of the opioid system in the rewarding effects of alcohol; however, is evident that other neurotransmission systems are involved in this phenomenon; therefore, it is necessary to make a comprehensive analysis of the neurophysiological and molecular mechanisms underlaying to alcohol abuse as an addictive behaviour.