J. Broadbent et al., GENETIC-DIFFERENCES IN NALOXONE ENHANCEMENT OF ETHANOL-INDUCED CONDITIONED TASTE-AVERSION, Psychopharmacology, 126(2), 1996, pp. 147-155
The influence of the opioid system on acquisition of an ethanol-induce
d conditioned taste aversion was examined in alcohol-preferring and av
oiding inbred strains of mice (C57BL/6J and DBA/2J). Fluid-deprived mi
ce from each strain received either ethanol alone, naloxone alone, or
both ethanol and naloxone immediately after access to a novel tasting
fluid. Naloxone alone (1 or 3 mg/kg) did not induce a conditioned tast
e aversion in either strain of mice. Administration of ethanol (1.5 g/
kg) to DBA/2J mice produced a moderate taste aversion that was not aff
ected by co-administration of naloxone. Although ethanol administered
alone (3 g/kg) did not cause a taste aversion in C57BL/6J mice, the co
mbination of ethanol and the higher dose of naloxone produced a signif
icant taste aversion that increased across trials. A second experiment
addressed the possibility that naloxone failed to enhance the ethanol
-induced condition taste aversion in DBA/2J mice due to a ''floor'' ef
fect on consumption. A lower ethanol dose (1 g/kg) was given alone or
in combination with naloxone (1 or 3 mg/kg). Again, ethanol produced a
moderate conditioned taste aversion that was not potentiated by nalox
one. Subsequent conditioning with a high ethanol dose produced further
suppression of intake, confirming that naloxone's failure to enhance
aversion on earlier trials was not due to a ''floor'' effect. These da
ta demonstrate a strain specific interaction between the aversive effe
ct of ethanol and naloxone. More specifically, the results indicate th
at blockade of opioid receptors enhances the aversive effect of ethano
l in C57BL/6J but not DBA/2J mice, suggesting that genetically determi
ned differences in the endogenous opioid system of alcohol-preferring
mice may mitigate ethanol's aversive effect.