期刊
ADDICTION BIOLOGY
卷 16, 期 3, 页码 440-449出版社
WILEY
DOI: 10.1111/j.1369-1600.2010.00309.x
关键词
Ethanol; nicotine; nicotinic receptors; self-administration; Sprague-Dawley; varenicline
资金
- NIH [1RO1AA017924-01]
- State of California for Medical Research through UCSF
- Department of Defense [W81XWH-07-1-0075]
Alcohol and nicotine use disorders are often treated as separate diseases, despite evidence that approximately 80-90% of alcohol dependent individuals are also heavy smokers. Both nicotine and ethanol have been shown to interact with neuronal nicotinic acetylcholine receptors (nAChRs), suggesting these receptors are a common biological target for the effects of nicotine and ethanol in the brain. There are few studies that have examined the effects of co-administered nicotine and ethanol on the activity of nAChRs in rodents. In the present study, we show that Sprague-Dawley rats, a strain often used for nicotine studies but not as often for voluntary ethanol intake studies, will consume 20% ethanol using both the intermittent-access two-bottle-choice and operant self-administration models without the need for sucrose fading. We show that nicotine (0.2 mg/kg and 0.8 mg/kg, s.c.) significantly increases operant 20% ethanol self-administration and varenicline (2 mg/kg, s.c), a partial agonist at nAChRs, significantly decreases operant ethanol self-administration and nicotine-induced increases in ethanol self-administration. This suggests that nAChRs play an important role in increasing ethanol self-administration and that varenicline may be an efficacious treatment for alcohol and nicotine co-dependencies.
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