Department of Neurology, University Hospital of Giessen and Marburg, Baldingerstrasse, 35043 Marburg, Germany.
Department of Epileptology, University of Bonn, Sigmund-Freud-Strasse 25, 53127 Bonn, Germany.
Curr Biol. 2018 Sep 24;28(18):3016-3022.e4. doi: 10.1016/j.cub.2018.07.042. Epub 2018 Sep 6.
Forgetting does not necessarily reflect failure to encode information but can, to some extent, also be voluntarily controlled. Previous studies have suggested that voluntary forgetting relies on active inhibition of encoding processes in the hippocampus by the dorsolateral prefrontal cortex (DLPFC) [1-4]. During attentional and sensorimotor processing, enhanced DLPFC theta power alongside increased alpha/beta oscillations are a neural signature of an inhibitory top-down mechanism, with theta oscillations reflecting prefrontal control and alpha/beta oscillations occurring in areas targeted by inhibition [5-12]. Here, we used intracranial EEG recordings in presurgical epilepsy patients implanted in DLPFC (n = 13) and hippocampus (n = 15) during an item-method directed forgetting paradigm. We found that voluntary forgetting is associated with increased neural oscillations in the low theta band (3-5 Hz) in DLPFC and in a broad theta/alpha/beta (6-18 Hz) frequency range in hippocampus. Combining time-lagged correlation analysis, phase synchronization, and Granger causality in 6 patients with electrodes in both DLPFC and hippocampus, we obtained converging evidence for a top-down control of hippocampal activity by the DLPFC. Together, our results provide strong support for a model in which voluntary forgetting relies on enhanced inhibition of the hippocampus by the DLPFC.
遗忘并不一定反映信息编码的失败，但在某种程度上也可以被主动控制。先前的研究表明，主动遗忘依赖于背外侧前额叶皮层（DLPFC）对海马体编码过程的主动抑制[1-4]。在注意和感觉运动处理过程中，增强的 DLPFC θ 功率伴随着增加的α/β 振荡是抑制性自上而下机制的神经特征，其中θ 振荡反映了前额叶控制，α/β 振荡发生在抑制作用的目标区域[5-12]。在这里，我们在接受手术前癫痫患者的 DLPFC（n=13）和海马体（n=15）中使用颅内 EEG 记录，进行项目方法定向遗忘范式。我们发现，主动遗忘与 DLPFC 中低 theta 波段（3-5 Hz）的神经振荡增加以及海马体中广泛的 theta/alpha/beta（6-18 Hz）频率范围内的神经振荡增加有关。在 6 名患者中结合时间滞后相关分析、相位同步和 Granger 因果关系，这些患者的电极位于 DLPFC 和海马体中，我们获得了一致的证据，证明 DLPFC 对海马体活动的自上而下控制。总的来说，我们的研究结果为主动遗忘依赖于 DLPFC 对海马体的增强抑制的模型提供了有力的支持。
