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• W2086671474 abstract "Reinforcing effects are ascribed to endogenous opioids, particularly to the pro-opiomelanocortin (POMC)-derived beta-endorphin 1-31, the most potent opiate-active substance. Alcohol induces variations in the genetic processing of the precursor POMC and of beta-endorphin at different levels. Studies focused on changes in POMC gene expression (mRNA quantitation) and post-translational processing. Chronic alcohol intake significantly reduces POMC mRNA in the lobes of the pituitary. In inbred strains of mice, genotypic differences are seen in post-translational processing of hypothalamic beta-endorphin, thus inducing differences in alcohol sensitivity. Clinical studies show a disproportion of POMC cleavage products in the CSF of chronic alcoholics (reduced beta-endorphin versus increased ACTH contents), together with remarkable indications for baseline differences in beta-endorphin levels. Errors within the genetic sequence of POMC are suggested to underlie alcohol-seeking behavior." @default.
• W2086671474 created "2016-06-24" @default.
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• W2086671474 date "1988-03-01" @default.
• W2086671474 modified "2023-10-02" @default.
• W2086671474 title "Beta-endorphin genetics in the etiology of alcoholism" @default.
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• W2086671474 doi "https://doi.org/10.1016/0741-8329(88)90014-6" @default.
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