Werner Reichardt Centre for Integrative Neuroscience, Tübingen University, 72076, Tübingen, Germany.
Hertie Institute for Clinical Brain Research, Tübingen University, 72076, Tübingen, Germany.
Nat Commun. 2020 Apr 24;11(1):1977. doi: 10.1038/s41467-020-15890-w.
Visual sensitivity, probed through perceptual detectability of very brief visual stimuli, is strongly impaired around the time of rapid eye movements. This robust perceptual phenomenon, called saccadic suppression, is frequently attributed to active suppressive signals that are directly derived from eye movement commands. Here we show instead that visual-only mechanisms, activated by saccade-induced image shifts, can account for all perceptual properties of saccadic suppression that we have investigated. Such mechanisms start at, but are not necessarily exclusive to, the very first stage of visual processing in the brain, the retina. Critically, neural suppression originating in the retina outlasts perceptual suppression around the time of saccades, suggesting that extra-retinal movement-related signals, rather than causing suppression, may instead act to shorten it. Our results demonstrate a far-reaching contribution of visual processing mechanisms to perceptual saccadic suppression, starting in the retina, without the need to invoke explicit motor-based suppression commands.
视觉敏感性是通过对非常短暂的视觉刺激的感知检测来探测的,在快速眼动时会受到强烈损害。这种强大的感知现象,称为扫视抑制,通常归因于直接源自眼球运动指令的主动抑制信号。相反,我们发现,由扫视引起的图像移位激活的仅视觉机制可以解释我们已经研究过的扫视抑制的所有感知特性。这种机制始于,但其不一定仅限于大脑中视觉处理的最初阶段,即视网膜。关键的是,起源于视网膜的神经抑制在扫视时的感知抑制之后仍然存在,这表明眼球运动相关的神经抑制信号不是引起抑制,而是可能缩短抑制。我们的结果表明,视觉处理机制从视网膜开始,对感知性扫视抑制有深远的贡献,而无需调用明确的基于运动的抑制命令。