Effect of acute ethanol administration on the extracellular concentrations of the opioid peptides [beta]-endorphin, met-enkephalin and dynorphin A₁-₈ at the level of ventral tegmental area in the rat

There is experimental evidence suggesting that ethanol alters the activity of the endogenous opioid peptide systems in a dose and brain region dependent manner. These ethanol-induced alterations in opioid activity may influence the processes of ethanol reward and reinforcement. However, the precise nature of the link between ethanol-opioid interactions influencing reward and reinforcement is not clearly understood. Thus, it was the objective of the present study to investigate the response of the three major opioid peptide systems (endorphins, enkephalins, and dynorphins) to acute ethanol administration, at the level of the ventral tegmental area (VTA), a brain region important for drug, including ethanol, reinforcement. Using the in vivo microdialysis technique coupled with specific solid-phase radioimmunoassays for beta-endorphin, met-enkephalin, and dynorphin A1-8, changes of the extracellular concentration of theses peptides at the level of VTA were determined at distinct time points following the administration of 0.0 (saline), 0.8, 1.6, and 2.4 g ethanol/kg B/Wt. Results demonstrated a biphasic effect of ethanol on beta-endorphin release with 1.6, but not 0.8 or 2.4, g ethanol/kg B.Wt. enhancing beta-endorphin release. None of the ethanol doses used altered the extracellular levels of met-enkephalin, and dynorphin A1-8 peptides. In conclusion, the present findings suggest that at the level of VTA interactions of beta-endorphin with the mu and/or delta opioid receptors on GABA interneurons may contribute to the ethanol induced augmentation in the activity of the mesolimbic dopaminergic system, and influence ethanol reinforcement