Department of Developmental Physiology, National Institute for Physiological Sciences, Okazaki, 444-8585, Japan.
Department of Physiology, Hirosaki University School of Medicine, Hirosaki, 036-8562, Japan.
Nat Commun. 2019 Jan 11;10(1):135. doi: 10.1038/s41467-018-08058-0.
In patients with damage to the primary visual cortex (V1), residual vision can guide goal-directed movements to targets in the blind field without awareness. This phenomenon has been termed blindsight, and its neural mechanisms are controversial. There should be visual pathways to the higher visual cortices bypassing V1, however some literature propose that the signal is mediated by the superior colliculus (SC) and pulvinar, while others claim the dorsal lateral geniculate nucleus (dLGN) transmits the signal. Here, we directly test the role of SC to ventrolateral pulvinar (vlPul) pathway in blindsight monkeys. Pharmacological inactivation of vlPul impairs visually guided saccades (VGS) in the blind field. Selective and reversible blockade of the SC-vlPul pathway by combining two viral vectors also impairs VGS. With these results we claim the SC-vlPul pathway contributes to blindsight. The discrepancy would be due to the extent of retrograde degeneration of dLGN and task used for assessment.
在初级视皮层（V1）受损的患者中，残留的视觉可以引导目标导向的运动到盲区内的目标，而无需意识。这种现象被称为盲视，其神经机制存在争议。应该有视觉通路绕过 V1 到达高级视觉皮层，但有些文献提出信号是由上丘（SC）和丘脑枕介导的，而另一些则声称背外侧膝状体核（dLGN）传递信号。在这里，我们直接测试 SC 到腹外侧丘脑枕（vlPul）通路在盲视猴中的作用。vlPul 的药理学失活会损害盲区内的视觉引导扫视（VGS）。通过结合两种病毒载体选择性和可逆地阻断 SC-vlPul 通路也会损害 VGS。有了这些结果，我们声称 SC-vlPul 通路有助于盲视。这种差异可能是由于 dLGN 的逆行退化程度和用于评估的任务不同所致。
