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首页> 外文期刊>Brain research bulletin >Exposure to nicotine increases nicotinic acetylcholine receptor density in the reward pathway and binge ethanol consumption in C57BL/6J adolescent female mice
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Exposure to nicotine increases nicotinic acetylcholine receptor density in the reward pathway and binge ethanol consumption in C57BL/6J adolescent female mice

机译：暴露于尼古丁可增加C57BL / 6J青春期雌性小鼠奖励途径中的烟碱型乙酰胆碱受体密度，并大量饮酒

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Nearly 80% of adult smokers begin smoking during adolescence. Binge alcohol consumption is also common during adolescence. Past studies report that nicotine and ethanol activate dopamine neurons in the reward pathway and may increase synaptic levels of dopamine in the nucleus accumbens through nicotinic acetylcholine receptor (nAChR) stimulation. Activation of the reward pathway during adolescence through drug use may produce neural alterations affecting subsequent drug consumption. Consequently, the effect of nicotine exposure on binge alcohol consumption was examined along with an assessment of the neurobiological underpinnings that drive adolescent use of these drugs. Adolescent C57BL/6J mice (postnatal days 35-44) were exposed to either water or nicotine (200 mu g/ml) for ten days. On the final four days, ethanol intake was examined using the drinking-in-the-dark paradigm. Nicotine-exposed mice consumed significantly more ethanol and displayed higher blood ethanol concentrations than did control mice. Autoradiographic analysis of nAChR density revealed higher epibatidine binding in frontal cortical regions in mice exposed to nicotine and ethanol compared to mice exposed to ethanol only. These data show that nicotine exposure during adolescence increases subsequent binge ethanol consumption, and may affect the number of nAChRs in regions of the brain reward pathway, specifically the frontal cortex. Published by Elsevier Inc.
机译：将近80％的成年吸烟者在青春期开始吸烟。在青春期期间，酗酒也很常见。过去的研究报告说，尼古丁和乙醇会激活奖励途径中的多巴胺神经元，并可能通过烟碱乙酰胆碱受体（nAChR）刺激来增加伏隔核中多巴胺的突触水平。在青春期通过吸毒激活奖励途径可能会产生神经改变，从而影响随后的药物消费。因此，检查了尼古丁暴露对暴饮酒的影响，并评估了推动青少年使用这些药物的神经生物学基础。将青春期的C57BL / 6J小鼠（出生后35-44天）暴露于水或尼古丁（200微克/毫升）中放置10天。在最后四天，使用暗饮范例检查了乙醇摄入量。暴露于尼古丁的小鼠比对照组的小鼠消耗更多的乙醇，并且血液中的乙醇浓度更高。放射自显影的nAChR密度分析显示，与仅暴露于乙醇的小鼠相比，暴露于尼古丁和乙醇的小鼠的额叶皮层区域具有更高的依巴替丁结合。这些数据表明，青春期暴露于尼古丁会增加随后的狂饮乙醇消耗，并可能影响大脑奖励途径（特别是额叶皮层）区域中nAChR的数量。由Elsevier Inc.发布

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