Gan Gabriela, Guevara Alvaro, Marxen Michael, Neumann Maike, Jünger Elisabeth, Kobiella Andrea, Mennigen Eva, Pilhatsch Maximilian, Schwarz Daniel, Zimmermann Ulrich S, Smolka Michael N
Department of Psychiatry and Neuroimaging Center, Technische Universität Dresden, Dresden, Germany.
Escuela de Matemática, Universidad de Costa Rica, San José, Costa Rica.
Biol Psychiatry. 2014 Nov 1;76(9):698-707. doi: 10.1016/j.biopsych.2013.12.017. Epub 2014 Jan 15.
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 50 young adults with a stop-signal task during functional magnetic resonance imaging. In a single-blind placebo-controlled cross-over design, all participants performed the stop-signal task once under alcohol with a breath alcohol concentration of .6 g/kg and once under placebo. In addition, alcohol consumption was assessed with a free-access alcohol self-administration paradigm in the same participants.
Inhibitory control was robustly decreased under alcohol compared with placebo, indicated by longer stop-signal reaction times. 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 might enhance alcohol consumption in young adults, which might promote future alcohol problems.
酒精作用下抑制控制受损与酒精消费之间的自我增强循环被认为是易感人群饮酒功能失调的一种潜在机制。然而,酒精导致抑制控制受损的神经基础仍广泛未知。
我们在功能磁共振成像期间,使用停止信号任务对50名年轻成年人的抑制控制进行了测量。在单盲安慰剂对照交叉设计中,所有参与者在呼气酒精浓度为0.6 g/kg的酒精条件下和安慰剂条件下各进行一次停止信号任务。此外,使用自由获取酒精自我给药范式对相同参与者的酒精消费情况进行了评估。
与安慰剂相比,酒精作用下抑制控制显著降低,表现为更长的停止信号反应时间。在神经层面,酒精作用下抑制控制受损与抑制网络右额颞部脑反应减弱有关,该网络支持对罕见停止信号的注意力捕捉以及随后从反应执行到抑制的行动计划更新。此外,酒精导致的抑制控制受损程度可预测自由获取酒精的消费量。
我们认为在抑制控制过程中,酒精会影响实际运动抑制之前的认知过程。在酒精作用下,右额颞区脑反应减弱可能会减缓对罕见停止信号的注意力捕捉以及随后行动计划的更新,从而导致抑制控制受损。反过来,酒精导致的显著抑制控制受损可能会增加年轻人的酒精消费量,这可能会引发未来的酒精问题。