Ethanol reinforcement in nondeprived mice: Effects of abstinence and naltrexone

Citation
Ld. Middaugh et al., Ethanol reinforcement in nondeprived mice: Effects of abstinence and naltrexone, ALC CLIN EX, 24(8), 2000, pp. 1172-1179
Citations number
42
Categorie Soggetti
Clinical Psycology & Psychiatry","Neurosciences & Behavoir
Journal title
ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH
ISSN journal
01456008 → ACNP
Volume
24
Issue
8
Year of publication
2000
Pages
1172 - 1179
Database
ISI
SICI code
0145-6008(200008)24:8<1172:ERINME>2.0.ZU;2-N
Abstract
Background: Operant experiments which indicate that ethanol can serve as a reinforcer to maintain lever responding during limited periods of access ha ve not been conducted on non-food-deprived mice, as they have for rats and monkeys. Furthermore, there are no reports of the effects of chronic ethano l and subsequent abstinence on ethanol reward in mice. Finally, although na ltrexone reduces responding for ethanol in food-deprived mice, the effects of the drug on ethanol reward for non-food-deprived mice have not been repo rted. Methods: In three experiments, lever responding for ethanol (10-12%) was es tablished in C57BL/6 (B6) mice by using either sucrose or saccharin fading procedures commonly used for rats. Experiment 1 examined both appetitive an d consummatory responses while sucrose was faded from the ethanol solutions . Experiment 2 examined lever responding and ethanol intake (1) during sacc harin fading; (2) when reinforcement schedules, reward availability, and pr imary conditioned reinforcers were manipulated; and (3) when mice were allo wed chronic ethanol consumption followed by forced abstinence. Experiment 3 examined the effects of low doses of naltrexone on ethanol reward. Results: Lever responding for ethanol can be established in non-food-depriv ed mice with the sucrose and saccharin fading procedures commonly used for rats. Lever responses increased with decreases in the reinforcer and increa ses in schedule demand, which indicated the reward value of the ethanol sol ution. Removal of ethanol from the solution reduced consumption with no cha nge in the appetitive, instrumental response, which indicated that the two responses were under control of different stimuli, perhaps mediated by diff erent neural mechanisms. Forced abstinence after chronic ethanol exposure i ncreased responding for the drug, which suggested increased reward value. N altrexone reduced responding as previously reported for food-deprived B6 mi ce. Conclusions: Ethanol appears to serve as a reinforcer for non-food-deprived or non-water-deprived B6 mice. Its reinforcing effects are increased by fo rced abstinence after chronic exposure and are decreased by naltrexone.