Ethanol exposure selectively alters beta-endorphin content but not [3H]-DAMGO binding in discrete regions of the rat brain.

The dopaminergic mesocorticolimbic system plays an important role in the reinforcing effects of ethanol. Opioid peptides modulate the activity of this system and have been suggested to mediate, at least in part, the reinforcing properties of ethanol. Thus, beta-endorphin (beta-END) could participate in the development of ethanol reinforcement and addiction. The aim of this work was to investigate the acute and chronic ethanol effects on beta-END content in regions of the mesolimbic system and to examine if chronic ethanol treatment alters ligand binding to mu opioid receptor (muOR). Male Wistar rats received a single acute ethanol dose of 2.5 g/kg or water by intra-gastric administration. For chronic ethanol treatment experiments, one group of rats was given ethanol (10% v/v solution) to drink, two groups were given equivalent volumes of sucrose (14.14% isocaloric solution) or water, respectively, and a fourth group had ad libitum access to food and water. Treatment was followed for 4 weeks. Beta-endorphin content in brain regions was quantified by radioimmunoassay and ligand binding studies to muOR were performed by quantitative autoradiography using 8 nM [(3)H]-DAMGO as radioligand. Acute ethanol decreased beta-END content in the hypothalamus (26%) 1h after administration. No ethanol effects were observed in the midbrain, ventral tegmental area, substantia nigra, nucleus accumbens, nucleus accumbens-septum and prefrontal cortex. Chronic ethanol treatment neither changed beta-END levels nor [(3)H]-DAMGO binding to mu opioid receptors in any of the regions studied. However, beta-END levels in the sucrose group were significantly increased in the nucleus accumbens and substantia nigra, in comparison to all other groups. These findings suggest that different neural mechanisms and specific brain regions may be involved in the reinforcing effects of ethanol and sucrose.