Alcohol releases beta-endorphin: a mechanism for LDN interaction

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Alcohol Clin Exp Res. 2009 Jun;33(6):1033-43. Epub 2009 Mar 19.

Effect of acute ethanol administration on the release of opioid

peptides from the midbrain including the ventral tegmental area.

Jarjour S, Bai L, Gianoulakis C.

Department of Psychiatry, McGill University, Montréal, Québec, Canada.

BACKGROUND: Experimental evidence suggests that ethanol alters the

activity of the endogenous opioid peptide systems in a dose and brain-

region dependent manner. These alterations may influence the processes

of ethanol reward and reinforcement. Thus, it was the objective of

this study to investigate the response of the 3 major opioid peptide

systems (endorphins, enkephalins, and dynorphins) to acute ethanol

administration, at the level of the midbrain including the ventral

tegmental area (midbrain/VTA), a region important for drug, including

ethanol reinforcement. METHODS: Using the in vivo microdialysis

technique coupled with specific solid-phase radioimmunoassay for beta-

endorphin, met-enkephalin, and dynorphin A(1-8,) changes in the

extracellular concentration of theses peptides at the level of

midbrain/VTA were determined at distinct time points following the

administration of 0.0 (saline), 0.8, 1.2, 1.6, 2.0, and 2.4 g ethanol/

kg B.Wt. RESULTS: A biphasic effect of ethanol on beta-endorphin

release was found, with low to medium (1.2, 1.6, and 2.0 g) but not

high (2.4 g) doses of ethanol, inducing a significant increase in the

dialysate content of beta-endorphin. A late increase in the dialysate

content of dynorphin A(1-8) was observed in response to the 1.2 g

ethanol dose. However, none of the ethanol doses tested significantly

altered the content of met-enkephalin in the dialysate. CONCLUSIONS:

The present findings suggest that the ethanol-induced increase of beta-

endorphin release at the level of midbrain/VTA may influence alcohol

reinforcement.

PMID: 19302084