This study was supported by grants from the Department of Veterans Affairs, the Alcoholic Beverage Medical Research Foundation, and the National Institute on Alcohol Abouse and Alcoholism (Grants P01-AA08621 and P50-AA10760).
Naltrexone Effects on Ethanol Drinking Acquisition and on Established Ethanol Consumption in C57BL/6J Mice
Version of Record online: 30 MAY 2006
Alcoholism: Clinical and Experimental Research
Volume 21, Issue 4, pages 691–702, June 1997
How to Cite
Phillips, T. J., Wenger, C. D. and Dorow, J. D. (1997), Naltrexone Effects on Ethanol Drinking Acquisition and on Established Ethanol Consumption in C57BL/6J Mice. Alcoholism: Clinical and Experimental Research, 21: 691–702. doi: 10.1111/j.1530-0277.1997.tb03824.x
- Issue online: 30 MAY 2006
- Version of Record online: 30 MAY 2006
- Received for publication September 3. 1996; accepted January 21, 1997
- Alcohol Intake;
- C57BL/6J Mice;
Naltrexone's success as a treatment agent for alcoholism seems to be due to its ability to reduce craving in abstinent, dependent individuals and to reduce the pleasure associated with subsequent intake. However, more study is needed to establish the optimal amount of time that naltrexone treatment should be continued. Little information seems to have been collected regarding the most effective dosing regimen for reducing alcohol craving and consumption, and the usefulness of opiate antagonists in the prevention of alcohol dependence in nonaddicts, rather than just as a treatment agent in addicted individuals, also deserves further study. The alcohol-preferring C57BL/6J (B6) mice were used to: (1) study naltrexone effects on consumption in established drinkers using an increasing dosing regimen, (2) study naltrexone effects on the acquisition of ethanol drinking, and (3) study the effects of chronic naltrexone from timed-release pellets on drinking in alcohol-naive mice. Naltrexone reduced ethanol preference in established drinkers, but its effects waned at increasing doses. Naltrexone slowed the acquisition of ethanol drinking, but was ineffective when readministered after a phase when ethanol was offered in the absence of naltrexone. Mice with chronic naltrexone pellets consumed greater amounts of ethanol and showed higher ethanol preference than did placebo-pelleted animals. The observed reduced efficacy of naltrexone with increasing dosage and chronic treatment may have been due to naltrexone-induced opiate receptor changes. Such changes are presumably more likely to occur when naltrexone doses remain high or perhaps accumulate. Thus, dose and frequency of administration may be important factors in determining naltrexone's effectiveness in treating alcohol dependence.