Effect of acute administration of ethanol on beta-endorphin plasma level in ethanol preferring and non-preferring rats chronically treated with naltrexone.

An ample support can be found in professional literature for the hypothesis that the endogenous opioid system plays an important role in developing a craving for alcohol. It is well established that people with a genetic deficit of beta-endorphin are particularly susceptible to alcoholism. In our study, we looked into the beta-endorphin plasma level of animals with high- and low-risk of alcohol dependency after repeated treatment with naltrexone, the opioid antagonist known to be effective in the treatment of alcoholism. We used the Warsaw High Preferring (WHP) and Warsaw Low Preferring (WLP) rats and treated them for 10 days with naltrexone in a dose of 2 mg/kg i.p. One hour before blood collection the rats were injected with a single dose of ethanol. A prolonged naltrexone treatment or a single application of ethanol resulted in the increase of the beta-endorphin plasma level. In the WLP rats repeated naltrexone treatment prevents the ethanol-induced increase in beta-endorphin plasma level. In the WHP rats the level of this peptide was similar to it while they were undergoing the naltrexone treatment or had received a single alcohol injection. This finding supports the proposition that the endogenous opioid system plays an important role in developing a craving for alcohol. It is likely that effectiveness of naltrexone in reducing craving for alcohol results from the attenuation of the rewarding properties of ethanol and restoring the beta-endorphin deficit in reward system.