Danielmeier Claudia, Allen Elena A, Jocham Gerhard, Onur Oezguer A, Eichele Tom, Ullsperger Markus
Donders Institute for Brain, Cognition and Behaviour, Radboud University Nijmegen, Montessorilaan 3, 6525 HR Nijmegen, the Netherlands; Max Planck Institute for Neurological Research, Gleueler Strasse 50, 50931 Cologne, Germany; Department of Neuropsychology, Otto-von-Guericke-Universität, Universitätsplatz 2, 39106 Magdeburg, Germany.
Department of Biological and Medical Psychology, University of Bergen, Jonas Liesvei 91, 5009 Bergen, Norway; The Mind Research Network, 1101 Yale Boulevard NE, Albuquerque, NM 87106, USA.
Curr Biol. 2015 Jun 1;25(11):1461-8. doi: 10.1016/j.cub.2015.04.022. Epub 2015 May 7.
Humans often commit errors when they are distracted by irrelevant information and no longer focus on what is relevant to the task at hand. Adjustments following errors are essential for optimizing goal achievement. The posterior medial frontal cortex (pMFC), a key area for monitoring errors, has been shown to trigger such post-error adjustments by modulating activity in visual cortical areas. However, the mechanisms by which pMFC controls sensory cortices are unknown. We provide evidence for a mechanism based on pMFC-induced recruitment of cholinergic projections to task-relevant sensory areas. Using fMRI in healthy volunteers, we found that error-related pMFC activity predicted subsequent adjustments in task-relevant visual brain areas. In particular, following an error, activity increased in those visual cortical areas involved in processing task-relevant stimulus features, whereas activity decreased in areas representing irrelevant, distracting features. Following treatment with the muscarinic acetylcholine receptor antagonist biperiden, activity in visual areas was no longer under control of error-related pMFC activity. This was paralleled by abolished post-error behavioral adjustments under biperiden. Our results reveal a prominent role of acetylcholine in cognitive control that has not been recognized thus far. Regaining optimal performance after errors critically depends on top-down control of perception driven by the pMFC and mediated by acetylcholine. This may explain the lack of adaptivity in conditions with reduced availability of cortical acetylcholine, such as Alzheimer's disease.
当人类被无关信息分散注意力，不再专注于手头任务的相关内容时，往往会犯错。犯错后的调整对于优化目标达成至关重要。后内侧额叶皮层（pMFC）是监测错误的关键区域，已被证明可通过调节视觉皮层区域的活动来触发这种犯错后的调整。然而，pMFC控制感觉皮层的机制尚不清楚。我们提供了一种基于pMFC诱导胆碱能投射至与任务相关的感觉区域的机制的证据。在健康志愿者中使用功能磁共振成像（fMRI），我们发现与错误相关的pMFC活动可预测随后与任务相关的视觉脑区的调整。特别是，犯错后，参与处理与任务相关刺激特征的视觉皮层区域的活动增加，而代表无关、分散注意力特征的区域的活动减少。在用毒蕈碱型乙酰胆碱受体拮抗剂安坦治疗后，视觉区域的活动不再受与错误相关的pMFC活动的控制。这与安坦治疗后犯错后行为调整的消失相平行。我们的结果揭示了乙酰胆碱在认知控制中迄今未被认识到的重要作用。犯错后恢复最佳表现关键取决于pMFC驱动并由乙酰胆碱介导的自上而下的感知控制。这可能解释了在皮质乙酰胆碱可用性降低的情况下（如阿尔茨海默病）缺乏适应性的原因。
