Visually Driven Activation in Macaque Areas V2 and V3 without Input from the Primary Visual Cortex

摘要: Creating focal lesions in primary visual cortex (V1) provides an opportunity to study the role of extra-geniculo-striate pathways for activating extrastriate cortex. Previous studies have shown that more than 95% neurons macaque area V2 and V3 stop firing after reversibly cooling V1 [1], [2], [3]. However, no on long term recovery areas V2, following permanent been reported macaque. Here we use fMRI activity patterns from 1 22 months lesioning V1. We find visually driven BOLD responses persist inside V1-lesion projection zones (LPZ) V3, but are reduced strength by ∼70%, average, compared pre-lesion levels. Monitoring LPZ over time starting one month lesion did not reveal systematic changes signal amplitude. Surprisingly, retinotopic organization remained similar non-lesioned hemisphere, suggesting activation is result input arising nearby (non-lesioned) Electrophysiology recordings multi-unit corroborated observations: could be elicited LPZ, even when stimulus was entirely contained within scotoma induced lesion. Restricting intact hemi-field produced significant modulation LPZs. conclude observed largely mediated parallel, V1-bypassing, subcortical can activate absence input. Such may contribute behavioral phenomenon blindsight.