Alcohol-induced impairment of inhibitory control is linked to attenuated brain responses in right fronto-temporal cortex.
Alcohol-induced impairment of inhibitory control is linked to attenuated brain responses in right fronto-temporal cortex.
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DOI：
10.1016/j.biopsych.2013.12.017
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发表时间：
2014-11-01
影响因子：
10.6
通讯作者：
Smolka MN
中科院分区：
文献类型：
--
作者：
Gan G;Guevara A;Marxen M;Neumann M;Jünger E;Kobiella A;Mennigen E;Pilhatsch M;Schwarz D;Zimmermann US;Smolka MN
酒精抑制控制受损和饮酒之间的自我增强循环被认为是易感人群饮酒功能失调的可能机制。然而，酒精引起的抑制控制损伤的神经基础尚不清楚。在功能磁共振成像（fMRI）中，我们用停止信号任务（SST）测量了50名年轻人的抑制控制。在单盲安慰剂对照交叉设计中，所有参与者分别在呼吸酒精浓度（BrAC）为0.6 g/kg的酒精下和安慰剂下进行SST。此外，在同一参与者中，使用自由获取酒精自我管理（ASA）范式评估酒精消费量。与安慰剂相比，酒精组抑制控制明显下降，表现为更长的停止信号反应时间（SSRTs）。在神经层面上，酒精导致的抑制控制受损与抑制网络右侧额颞部分的大脑反应减弱有关，抑制网络支持对不常见的停止信号的注意捕获，以及随后从反应执行到抑制的行动计划的更新。此外，酒精引起的抑制控制损伤的程度预测了自由饮酒。我们认为，在抑制控制期间，酒精会影响实际运动抑制之前的认知过程。在酒精的作用下，大脑右侧额颞区反应的减弱可能会减慢对不常见的停止信号的注意力捕捉和随后的行动计划更新，从而导致抑制控制受损。反过来，酒精引起的抑制控制的明显损伤可能会增加年轻人的酒精消费量，这可能会促进未来的酒精问题。
A self-enhancing loop between impaired inhibitory control under alcohol and alcohol consumption has been proposed as a possible mechanism underlying dysfunctional drinking in susceptible people. However, the neural underpinnings of alcohol-induced impairment of inhibitory control are widely unknown. We measured inhibitory control in fifty young adults with a stop-signal task (SST) during functional magnetic resonance imaging (fMRI). In a single-blind placebo-controlled cross-over design, all participants performed the SST once under alcohol with a breath alcohol concentration (BrAC) of 0.6 g/kg, and once under placebo. In addition, alcohol consumption was assessed using a free-access alcohol self-administration (ASA) paradigm in the same participants. Inhibitory control was robustly decreased under alcohol compared to placebo indicated by longer stop-signal reaction times (SSRTs). On the neural level, impaired inhibitory control under alcohol was associated with attenuated brain responses in the right fronto-temporal portion of the inhibition network that supports the attentional capture of infrequent stop-signals, and subsequent updating of action plans from response execution to inhibition. Furthermore, the extent of alcohol-induced impairment of inhibitory control predicted free-access alcohol consumption. We suggest that during inhibitory control alcohol affects cognitive processes preceding actual motor inhibition. Under alcohol, decreased brain responses in right fronto-temporal areas might slow down the attentional capture of infrequent stop-signals and subsequent updating of action plans which leads to impaired inhibitory control. In turn, pronounced alcohol-induced impairment of inhibitory control may enhance alcohol consumption in young adults which might promote future alcohol problems.