Dou Wei, Morrow Audrey, Iemi Luca, Samaha Jason
Psychology Department, University of California, Santa Cruz, CA 95064, USA.
Department of Psychiatry, Columbia University, College of Physicians and Surgeons, New York, NY 10032, USA.
Neuroimage. 2022 Jun;253:119060. doi: 10.1016/j.neuroimage.2022.119060. Epub 2022 Mar 11.
Alpha-band (8-13 Hz) oscillations have been shown to phasically inhibit perceptual reports in human observers, yet the underlying physiological mechanism of this effect is debated. According to contrasting models, based primarily on animal experiments, alpha activity is thought to either originate from specialized cells in the visual thalamus and periodically inhibit the relay of visual information to the primary visual cortex (V1) in a feedforward manner, or to propagate from higher visual areas back to V1 in a feedback manner. Human neurophysiological evidence in favor of either hypothesis, both, or neither, has been limited. To help address this issue, we explored the link between pre-stimulus alpha phase and visual electroencephalography (EEG) responses thought to arise from afferent input onto human V1. Specially-designed visual stimuli were used to elicit large amplitude C1 event-related potentials (ERP), with polarity, topography, and timing indicative of striate genesis. Single-trial circular-linear associations between pre-stimulus phase and post-stimulus global field power (GFP) during the C1 time window revealed significant effects peaking in the alpha frequency band. Control analyses ruling out the potential confound of post-stimulus data bleeding into the pre-stimulus window demonstrated that GFP amplitude decreases as pre-stimulus alpha phase deviates from an individual's preferred phase. These findings demonstrate an early locus - suggesting that the phase of pre-stimulus alpha oscillations could modulate visual processing by gating the feedforward flow of sensory input between the thalamus and V1, although other models are potentially compatible.
α波段(8-13赫兹)振荡已被证明会阶段性地抑制人类观察者的知觉报告,但其潜在的生理机制仍存在争议。根据主要基于动物实验的不同模型,α活动被认为要么起源于视觉丘脑的特殊细胞,并以前馈方式周期性地抑制视觉信息向初级视觉皮层(V1)的传递,要么以反馈方式从更高视觉区域传播回V1。支持这两种假设之一、两者或两者都不成立的人类神经生理学证据一直很有限。为了帮助解决这个问题,我们探索了刺激前α相位与被认为源于传入人类V1的视觉脑电图(EEG)反应之间的联系。使用特别设计的视觉刺激来诱发大振幅C1事件相关电位(ERP),其极性、地形图和时间表明其起源于纹状区。在C1时间窗口期间,刺激前相位与刺激后全局场功率(GFP)之间的单试验圆形-线性关联揭示了在α频段达到峰值的显著效应。排除刺激后数据渗入刺激前窗口的潜在混淆因素的对照分析表明,随着刺激前α相位偏离个体的偏好相位,GFP振幅会降低。这些发现表明了一个早期位点——这表明刺激前α振荡的相位可能通过控制丘脑和V1之间感觉输入的前馈流来调节视觉处理,尽管其他模型也可能与之兼容。