Galizio M, Smaltz S C, Spencer B A
Pharmacol Biochem Behav. 1984 Sep;21(3):423-9. doi: 10.1016/s0091-3057(84)80105-7.
Several recent studies have suggested that some effects of ethanol may be mediated by the opioid receptor systems. The present study examined the possibility of a common link between ethanol and opiates by determining whether the effects of ethanol on rat's free operant avoidance behavior could be reversed by the opiate antagonist naltrexone. In Experiment 1 ethanol produced a dose-dependent impairment of avoidance performance (characterized by a decrease in response rate and/or an increase in shock rate) in all three subjects. Naltrexone (3 mg/kg) alone suppressed avoidance rates, but failed to reverse or reduce the effects of ethanol. In contrast to the expectations of the "common-link" hypothesis, the greatest impairment of performance was observed after high doses of ethanol in combination with naltrexone. In Experiment 2 the effects of chronic naltrexone administration were examined. Since previous research has suggested that chronic treatment with opiate antagonists produces a heightened sensitivity to opiate agonists and antagonists, Experiment 2 addressed the issue of whether sensitization to naltrexone would transfer to ethanol. Although increased sensitivity to the rate-decreasing effects of naltrexone was observed, there was no evidence of heightened sensitivity to ethanol. Taken together the results provided little support for the hypothesis that the effects of ethanol on avoidance performance are mediated by the opiate receptor system.
