Abstract
Neural peptides found in brain and gut tissues modulate the intake of ethanol by animals and humans. Experiments show that injections of sulfated cholecystokinin octapeptide, tetradecapeptide bombesin, angiotensin, and the opioid receptor blockers, naloxone and naltrexone, potently reduce oral consumption of ethanol solutions. Vasoactive intestinal peptide, neuropeptide Y, and galanin increase ethanol intake, and increases in blood levels of the opioid peptide beta endorphin are associated with relapse in alcoholics. Specific neuropeptide receptor blockers increase ethanol intake and prevent injected cholecystokinin and bombesin from inhibiting ethanol intake. Recently, naltrexone (Revia®) has been approved by the FDA for wider clinical use in the treatment of alcoholism. These findings support the hypothesis of neuropeptidergic regulation of alcohol consumption and innovative therapies for alcoholism.