The Enkephalinergic System and Maintenance of Ethanol Drinking
Many behavioral and physiological effects of opiates and ethanol are very similar including induction of euphoria, sedation, acquisition of tolerance and development of physical dependence (1). These similarities have led to the hypothesis that the reinforcing properties of ethanol may be due, in part, to an interaction between ethanol and the endogenous opioid system. Specifically, consumption of ethanol may stimulate increased activity in the opioid system which, in turn, leads to further ethanol drinking. If this hypothesis is correct, antagonists which block the action of endogenous opioids might be expected to decrease ethanol intake. Rats of the alcohol-preferring (P) and high alcohol drinking (HAD) lines, which have been genetically selected for oral ethanol preference, were used to determine whether activation of the endogenous opioid system is important for the maintenance of ethanol drinking. Initial experiments explored the effects of nonspecific opioid receptor antagonists, such as naloxone and naltrexone on ethanol drinking. Naloxone, in doses of 0.075–18.0 mg/kg, significantly suppressed ethanol drinking in a dose-dependent manner without altering water intake in rats of the HAD line when ethanol and water were presented concurrently (2,3). These results suggest that the stimulation of the endogenous opioid system and occupation of opioid receptors may be necessary for the maintenance of ethanol drinking.
KeywordsAttenuation Hydrochloride Naloxone Barbiturate Naltrexone
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