Clinical NeuroImaging Research Core, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, Maryland, United States of America.
Laboratory for Integrative Neuroscience, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Rockville, Maryland, United States of America.
PLoS One. 2020 Mar 26;15(3):e0224906. doi: 10.1371/journal.pone.0224906. eCollection 2020.
Despite the harm caused by binge drinking, the neural mechanisms leading to risky and disinhibited intoxication-related behaviors are not well understood. Evidence suggests that the globus pallidus externus (GPe), a substructure within the basal ganglia, participates in inhibitory control processes, as examined in stop-signaling tasks. In fact, studies in rodents have revealed that alcohol can change GPe activity by decreasing neuronal firing rates, suggesting that the GPe may have a central role in explaining impulsive behaviors and failures of inhibition that occur during binge drinking. In this study, twenty-five healthy volunteers underwent intravenous alcohol infusion to achieve a blood alcohol level of 0.08 g/dl, which is equivalent to a binge drinking episode. A resting state functional magnetic resonance imaging scan was collected prior to the infusion and at binge-level exposure. Functional connectivity analysis was used to investigate the association between alcohol-induced changes in GPe connectivity, drinking behaviors, and impulsivity traits. We found that individuals with greater number of drinks or heavy drinking days in the recent past had greater alcohol-induced deficits in GPe connectivity, particularly to the striatum. Our data also indicated an association between impulsivity and alcohol-induced deficits in GPe-frontal/precentral connectivity. Moreover, alcohol induced changes in GPe-amygdala circuitry suggested greater vulnerabilities to stress-related drinking in some individuals. Taken together, these findings suggest that alcohol may interact with impulsive personality traits and drinking patterns to drive alterations in GPe circuitry associated with behavioral inhibition, possibly indicating a neural mechanism by which binge drinking could lead to impulsive behaviors.
尽管 binge drinking 会造成危害,但导致冒险和抑制解除与醉酒相关的行为的神经机制仍不清楚。有证据表明,苍白球外(GPe)是基底神经节的一个亚结构,参与了抑制控制过程,这在停止信号任务中得到了检验。事实上,啮齿动物研究表明,酒精可以通过降低神经元的放电率来改变 GPe 的活动,这表明 GPe 可能在解释冲动行为和 binge drinking 期间的抑制失败中起着核心作用。在这项研究中,二十五名健康志愿者接受了静脉内酒精输注,以达到 0.08 g/dl 的血液酒精水平,相当于 binge drinking 发作。在输注前和 binge-level 暴露时采集了静息状态功能磁共振成像扫描。功能连接分析用于研究 GPe 连接变化与饮酒行为和冲动特质之间的关系。我们发现,过去有更多饮酒量或更多饮酒日的个体,GPe 连接的酒精诱导缺陷更大,特别是与纹状体的连接。我们的数据还表明,冲动性与 GPe-前额/中央前回连接的酒精诱导缺陷之间存在关联。此外,GPe-杏仁核电路中的酒精诱导变化表明,一些人对与压力相关的饮酒更敏感。总之,这些发现表明,酒精可能与冲动人格特质和饮酒模式相互作用,导致与行为抑制相关的 GPe 电路改变,这可能表明 binge drinking 导致冲动行为的神经机制。