Blindsight depends on the lateral geniculate nucleus

Injury to the primary visual cortex (V1) leads to the loss of visual experience. Nonetheless, careful testing shows that certain visually guided behaviors can persist even in the absence of visual awareness1–5. The neural circuits supporting this phenomenon, often termed blindsight, remain uncertain5. Here we demonstrate a causal role of the thalamic lateral geniculate nucleus (LGN) in V1-independent processing of visual information. By comparing fMRI and behavioral measures with and without temporary LGN inactivation, we assessed the contribution of the LGN to visual functions of macaque monkeys with chronic V1 lesions. Prior to LGN inactivation, high contrast stimuli presented to the lesion-affected visual field (scotoma) produced significant V1 independent fMRI activation in extrastriate cortical areas V2, V3, V4, V5/MT, FST, and LIP, and were correctly located by the animals in a detection task. However, following reversible inactivation of the LGN in the V1-lesioned hemisphere both fMRI responses and behavioral detection were abolished. Taken together, these results demonstrate a critical functional contribution of the direct LGN projections to extrastriate cortex in blindsight, and suggest a viable pathway mediating fast detection during normal vision.