Visuomotor coordination and cognitive capacity in blindsight.

Classical literature on blindsight described that some patients with lesions to the primary visual cortex could respond to visual stimuli without subjective awareness. Recent studies addressed more complex arguments on the conscious state of blindsight subjects such as existence of partial awareness, namely "feeling of something happening" in the lesion-affected visual field, termed 'type II blindsight', and high-level performance in complex cognitive tasks in blindsight model monkeys. Endeavors to clarify the visual pathways for blindsight revealed the parallel thalamic routes mediating the visual inputs from the superior colliculus to extrastriate and frontoparietal cortices, which may underlie the flexible visuomotor association and cognitive control in the blindsight subjects.

Protocol for making an animal model of "blindsight" in macaque monkeys.

Patients with damage to the primary visual cortex (V1) can respond correctly to visual stimuli in their lesion-affected visual field above the chance level, an ability named blindsight. Here, we present a protocol for making an animal model of blindsight in macaque monkeys. We describe the steps to perform pre-lesion training of monkeys on a visual task, followed by lesion surgery, post-lesion training, and evaluation of blindsight.

Contribution of the Pulvinar and Lateral Geniculate Nucleus to the Control of Visually Guided Saccades in Blindsight Monkeys.

After damage to the primary visual cortex (V1), conscious vision is impaired. However, some patients can respond to visual stimuli presented in their lesion-affected visual field using residual visual pathways bypassing V1. This phenomenon is called "blindsight.

Cortical visual processing evokes short-latency reward-predicting cue responses in primate midbrain dopamine neurons.

After classical conditioning dopamine (DA) neurons exhibit short latency responses to reward-predicting visual cues. At least two possible projections could induce such DA responses; the cortical and subcortical visual pathways. Our recent study has shown that after a lesion of the striate cortex (V1), the superior colliculus (SC), a critical node of the subcortical visual pathway, can mediate short latency cue responses in the DA neurons of macaque monkeys.

Emergence of visually-evoked reward expectation signals in dopamine neurons via the superior colliculus in V1 lesioned monkeys.

Responses of midbrain dopamine (DA) neurons reflecting expected reward from sensory cues are critical for reward-based associative learning. However, critical pathways by which reward-related visual information is relayed to DA neurons remain unclear. To address this question, we investigated Pavlovian conditioning in macaque monkeys with unilateral primary visual cortex (V1) lesions (an animal model of 'blindsight').