[Neural mechanism of blindsight].

"Blindsight" is a phenomenon whereby hemianopic patients with damage in the primary visual cortex (V1) are able to process visual information in their blind visual field. Two pathways that bypass the V1 may be responsible for this residual vision. The first pathway is the retinotectal pathway in which the superior colliculus in the midbrain receives direct retinal signals and sends them to the extrastriate cortex via the pulvinar. The second pathway is the geniculo-extrastriate pathway in which direct retinal input to the lateral geniculate nucleus is sent straight to the extrastriate cortex. Herein, I summarize evidence supporting the involvement of either pathway. The evidence was obtained from anatomical, neurophysiological, imaging, and behavioral studies carried out on macaque monkeys and humans. I emphasize three points: 1) crosstalk exists between the retinotectal pathway and the geniculo-extrastriate pathway, that is, the projection from the superficial layer of the superior colliculus to the koniocellular layer of the lateral geniculate nucleus; 2) three visual channels (the luminance in the magnocellular pathway, the red-green opponency in the parvocellular pathway, and the blue-yellow opponency in the koniocellular pathway) are not independent, as previously assumed; and 3) a global reorganization in the brain circuit occurs following the lesions of the V1 and subsequent recovery. Finally, I introduce a recent study that employed a saliency computational model to quantitatively evaluate the residual visual channels in blindsight monkeys during free-viewing behavior. Their findings suggest that plastic changes occur in the color-processing pathways.