Recruitment of a Neuronal Ensemble in the Central Nucleus of the Amygdala Is Required for Alcohol Dependence
Recruitment of a Neuronal Ensemble in the Central Nucleus of the Amygdala Is Required for Alcohol Dependence
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DOI：
10.1523/jneurosci.1395-16.2016
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发表时间：
2016-09-07
影响因子：
5.3
通讯作者：
George, Olivier
中科院分区：
文献类型：
--
作者：
de Guglielmo, Giordano;Crawford, Elena;George, Olivier
在酗酒的非酒精依赖大鼠和酒精依赖大鼠中，戒酒与杏仁核中央核（CeA）神经元的募集有关。然而，这种神经元集合在cea中的募集是否与过量饮酒有因果关系，或者它是否代表过量饮酒的后果，仍然未知。我们测试了一个假设，即在不依赖酒精的大鼠和酒精依赖的大鼠中，戒酒期间CeA中神经元集合的募集是过量饮酒所必需的。我们发现戒酒期间CeA神经元群失活显著减少了两组的饮酒。在非依赖性大鼠中，酒精摄入量的减少是短暂的，并在注射后的第二天恢复正常。在依赖的大鼠中，Daun02使神经元群失活导致长期饮酒减少。此外，我们观察到在CeA中注射Daun02的依赖动物的躯体戒断症状显着减少。这些结果表明，在酒精依赖的大鼠中，戒酒期间CeA中神经元集合的募集与过量饮酒有因果关系，而在非酒精依赖的大鼠中，类似的神经元集合仅部分促成了酗酒样饮酒。这些结果确定了过渡到酒精依赖可能需要的关键神经生物学机制，表明关注CeA中的神经元集合可能导致更好地了解酒精使用障碍的病因并改善药物开发。
Abstinence from alcohol is associated with the recruitment of neurons in the central nucleus of the amygdala (CeA) in nondependent rats that binge drink alcohol and in alcohol-dependent rats. However, whether the recruitment of this neuronal ensemble in the CeAis causally related to excessive alcohol drinking or if it represents a consequence of excessive drinking remains unknown. We tested the hypothesis that the recruitment of a neuronal ensemble in the CeA during abstinence is required for excessive alcohol drinking in nondependent rats that binge drink alcohol and in alcohol-dependent rats. We found that inactivation of the CeA neuronal ensemble during abstinence significantly decreased alcohol drinking in both groups. In nondependent rats, the decrease in alcohol intake was transient and returned to normal the day after the injection. In dependent rats, inactivation of the neuronal ensemble with Daun02 produced a long-term decrease in alcohol drinking. Moreover, we observed a significant reduction of somatic withdrawal signs in dependent animals that were injected with Daun02 in the CeA. These results indicate that the recruitment of a neuronal ensemble in the CeA during abstinence from alcohol is causally related to excessive alcohol drinking in alcohol-dependent rats, whereas a similar neuronal ensemble only partially contributed to alcohol-binge-like drinking in nondependent rats. These results identify a critical neurobiological mechanism that may be required for the transition to alcohol dependence, suggesting that focusing on the neuronal ensemble in the CeA may lead to a better understanding of the etiology of alcohol use disorders and improve medication development.