Citation

Stromberg MF, Meister SC, Volpicelli JR, Ulm RR. Alcohol 1997; 14(5): 463-468.

Affiliation

University of Pennsylvania, Center for Studies of Addiction, Philadelphia 19104, USA. stromberg@research.trc.upenn.edu

Copyright

(Copyright © 1997, Elsevier Publishing)

DOI

unavailable

PMID

9305461

Abstract

The influence of a low dose of morphine was investigated on the acquisition and maintenance of consumption of a sweetened ethanol solution with water as the alternative in a two-bottle choice procedure. During acquisition in Experiment 1, morphine failed to significantly increase the consumption of a sweetened ethanol solution compared to either a postinjection period in the same animals or a no-treatment control group. Although morphine significantly increased sweetened ethanol consumption when compared to a saline control group, this appears to be due to a stress response to the injections, which suppressed ethanol consumption in the saline animals. During maintenance in Experiment 2, morphine significantly increased consumption of sweetened ethanol in all groups compared to consumption following saline control injections. There was no difference in this effect among the three groups, suggesting that prior history with morphine was not a factor. In addition, rats that were exposed to morphine during both experiments drank significantly more sweetened ethanol following injections in Experiment 2 than in Experiment 1. This suggests that morphine's potentiation of ethanol consumption is due to its interaction with endogenous opioid receptors that modulate the reward value of ethanol rather than more general mechanisms affecting satiety or taste. The results of these experiments provide support for both the Deficit and Surfeit Hypotheses of ethanol consumption, both of which suggest that endogenous opioid receptors are responsible, in part, for ethanol's reinforcing properties.

Language: en