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首页> 外文期刊>Alcohol >Is an alpha-conotoxin MII-sensitive mechanism involved in the neurochemical, stimulatory, and rewarding effects of ethanol?
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Is an alpha-conotoxin MII-sensitive mechanism involved in the neurochemical, stimulatory, and rewarding effects of ethanol?

机译：α-芋螺毒素MII敏感机制是否参与乙醇的神经化学，刺激和奖励作用？

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Ethanol and nicotine are the most commonly abused drugs among human beings, and a large body of evidence, from both epidemiologic and preclinical studies, indicates that there is a positive correlation between intake of both drugs. Findings of studies from our research group have demonstrated that nicotinic acetylcholine receptors, especially those located in the ventral tegmental area, are important for the stimulatory, rewarding, and dopamine-enhancing effects of ethanol. Furthermore, results of recent work indicate that the alpha4beta2* and the alpha7* receptor subunits of the nicotinic acetylcholine receptors do not seem to be involved in the neurochemical and behavioral effects of ethanol in rodents. The aim of the current study was to investigate further the role of different nicotinic acetylcholine receptor subunits in the stimulatory, dopamine-enhancing, and rewarding effects of ethanol in rodents by using the peptide alpha-conotoxin MII (5 nmol; an antagonist of the alpha3beta2*, beta3*, and alpha6* subunits of the nicotinic acetylcholine receptor) administered locally into the ventral tegmental area. A significant reduction of ethanol-induced accumbal dopamine overflow, measured by means of in vivo microdialysis, and of locomotor stimulation was observed in mice. Furthermore, alpha-conotoxin MII was demonstrated to reduce voluntary ethanol intake significantly in both rats and mice. These results indicate that alpha-conotoxin MU-sensitive receptors may be important in mediating the stimulatory, dopamine-enhancing, and rewarding effects of ethanol, and that alpha-conotoxin MII-sensitive receptors may constitute targets for development of new adjuvant for treatment of ethanol dependence.
机译：乙醇和尼古丁是人类中最常滥用的药物，流行病学和临床前研究的大量证据表明，两种药物的摄入之间存在正相关。我们研究小组的研究结果表明，烟碱乙酰胆碱受体，尤其是位于腹侧被盖区的受体，对于乙醇的刺激，奖励和多巴胺增强作用很重要。此外，最近的工作结果表明，烟碱乙酰胆碱受体的alpha4beta2 *和alpha7 *受体亚基似乎与啮齿类动物乙醇的神经化学和行为效应无关。本研究的目的是进一步研究不同烟碱型乙酰胆碱受体亚基在鼠类动物中的刺激，多巴胺增强和奖励作用，方法是使用肽α-芋螺毒素MII（5 nmol;α3beta2的拮抗剂）烟碱乙酰胆碱受体的*，beta3 *和alpha6 *亚基）局部施入腹侧被盖区。在体内观察到乙醇诱导的多巴胺累积多巴胺溢出的显着降低，这是通过体内微透析和运动刺激来测量的。此外，在大鼠和小鼠中，α-芋螺毒素MII均可显着减少自愿摄入的乙醇。这些结果表明，α-芋螺毒素MU敏感受体可能在介导乙醇的刺激，多巴胺增强和奖励作用中很重要，并且α-芋螺毒素MII敏感受体可能构成开发用于治疗乙醇的新佐剂的目标依赖。

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