Characterization of the effects of acute ethanol administration on the release of beta-endorphin peptides by the rat hypothalamus.

In the present studies the direct effect of ethanol on the release of beta-endorphin by the rat hypothalamus was investigated. When various concentrations of ethanol (10-120 mM) were added into the incubation medium, it was noticed that though low concentrations of ethanol (10, 20 and 30 mM) induced a pronounced increase in the release of beta-endorphin-like peptides from the hypothalamus, high concentrations of ethanol (40, 60 and 120 mM) induced a less pronounced increase. Exposure of hypothalamus to depolarizing concentrations of potassium chloride (following washing of the ethanol), provoked a significant release of beta-endorphin-like peptides, regardless of the ethanol concentration the tissues were exposed prior to the stimulation with the potassium chloride. Chromatographic analysis of the incubation media with Sephadex-G-75 revealed that the hypothalamus released mainly beta-endorphin-sized peptides. Analysis of the beta-endorphin-sized peptides with reverse-phase high performance liquid chromatography indicated the presence of beta-endorphin-(1-31) as well as non-acetyl and acetyl beta-endorphin-(1-27). Thus ethanol exerts a biphasic effect on the release of beta-endorphin-like peptides by the rat hypothalamus, with low concentrations inducing a dose-dependent increase, reaching maximum at 20 mM ethanol, and with higher concentrations of ethanol inducing a less pronounced increase in the release of beta-endorphin-like peptides, leading to an inverted U-shaped dose response relationship of ethanol and release of beta-endorphin-like peptides from the rat hypothalamus.