Dissecting the circuit for blindsight to reveal the critical role of pulvinar and superior colliculus

Masaharu Kinoshita,Kazuto Kobayashi,Kaoru Isa,Rikako Kato,Tadashi Isa,Kenta Kobayashi,Hirotaka Onoe

doi:10.1038/s41467-018-08058-0

Abstract

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.

Highlights

In patients with damage to the primary visual cortex (V1), residual vision can guide goaldirected movements to targets in the blind field without awareness
The above results showed that ventrolateral pulvinar (vlPul) and the direct pathway from the superior colliculus (SC) to vlPul is, at least partly, involved in mediating the residual vision for execution of visually guided saccades (VGS) in the V1-lesioned monkeys
The electrophysiological recordings showed that a considerable number of neurons in the vlPul are responsive to the inputs from the SC, and inactivation of the area containing these neurons resulted in impairment of VGS in the blindsight monkeys

Summary

Introduction

In patients with damage to the primary visual cortex (V1), residual vision can guide goaldirected movements to targets in the blind field without awareness. This phenomenon has been termed blindsight, and its neural mechanisms are controversial. Cowey and Stoerig[13] showed that there are surviving neurons in the dorsal lateral geniculate nucleus (dLGN), which project to the extrastriate cortex, after the V1 lesion and suggested that they would mediate the visual inputs directly to the extrastriate cortex in blindsight monkeys. In this study, to reveal a role of the SC–Pul pathway in blindsight, we first inactivated the ventrolateral Pul (vlPul) and tested the performance of VGS in unilateral V1-lesioned monkeys. The results will be discussed in line with a recent proposition that blindsight is not a unitary phenomenon but is a constellation of functions mediated by multiple pathways remaining after the V1 lesion[28]

Methods

Results

Conclusion