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Mechanisms through which alcohol affects the human central nervous system have remained unclear. Studies in rodents have shown that ethanol results in release of endogenous opioids and suggest that naltrexone, a nonselective opioid antagonist, reduces alcohol consumption via antagonism at µ-opioid receptors. Investigators used positron emission tomography to examine endogenous opioid release after consumption of a standardized drink of alcohol in 13 heavy drinkers (in men, 14–20 drinks per week) and 12 age-, sex-, and ethnicity-matched light drinkers.
In both groups, ligand-binding studies using an opioid agonist indicated that the drink led to release of an endogenous opioid acting at µ-opioid receptors in the left orbitofrontal cortex (OFC…