期刊
PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR
卷 110, 期 -, 页码 161-167出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.pbb.2013.07.009
关键词
Nicotinic receptor; Alcohol; Alcohol deprivation effect; Relapse; Varenicline; Mice
资金
- Juhnke Endowment Research Grant
- SDSU College of Pharmacy
- SDSU Research Foundation
Relapse is a core feature of alcohol addiction and hinders the pharmacotherapy of alcohol use disorders. Pre-clinical and clinical studies have shown that neuronal nicotinic acetylcholine receptor (nAChR) partial agonists such as cytisine and its derivative, varenicline, reduce alcohol (ethanol) consumption and seeking behavior. However, the effects of these ligands on ethanol relapse are little understood. In the present study, we examined the effects of varenicline and cytisine on alcohol deprivation effect (ADE) - a validated model for relapse-like ethanol drinking in C57BL/6J mice. After habituation to 15% (v/v) ethanol intake using a continuous free-choice procedure, mice were exposed to alternating cycles of ethanol deprivation (5 days) and re-exposure (2 days). At the end of third deprivation cycle, animals received repeated intraperitoneal injections of saline, varenicline (0.5 or 3.0 mg/kg) or cytisine (0.5 or 3.0 mg/kg) and fluid intake was measured post 4 h and 24 h ethanol re-exposure. Repeated ethanol deprivation and re-exposure cycles significantly produced a robust and transient increase in ethanol (ADE). Pretreatment with varenicline (0.5 or 3.0 mg/kg) or cytisine (0.5 or 3.0 mg/kg) significantly reduced the expression of ADE at 4 h and 24 h after ethanol re-exposure. The results from this study indicate that nAChR partial agonists reduce the expression of ADE in mice and further suggest the involvement of nAChR mechanisms in ADE, a relapse-like ethanol drinking behavior. (C) 2013 Elsevier Inc. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据