Acute requirement for the hippocampus in putatively conscious vision revealed by a mouse model of blindsight.

The phenomenon of blindsight provides a unique opportunity to uncover brain areas important for conscious vision. Patients with blindsight lose the conscious experience of seeing while still being able to detect and locate visual stimuli. Blindsight occurs after damage to the primary visual cortex (V1). Rodents are likewise able to detect and locate visual stimuli after damage to V1, though whether they lose conscious vision as humans do is unclear. Here, we report the first mouse model of blindsight that provides evidence that removal of V1 causes mice to lose their putatively conscious vision. This loss occurs only if dLGN, a brain area in the thalamus that connects to V1, is damaged in addition to V1. We use this model to discover that suppressing the hippocampus acutely causes blindsight-like behavior. This suggests that the hippocampus functions in the intact brain to support conscious, but not unconscious, vision. Furthermore, while single, selective ablations of V1 or the hippocampus have only a minor effect on vision, simultaneous ablation causes blindsight-like behavior. These results suggest that V1 and the hippocampus can compensate for the permanent loss of the other for conscious vision, revealing a novel form of plasticity that supports conscious vision. Although never causally implicated in conscious visual perception, the hippocampus emerges as a candidate brain area critical for conscious experience. More broadly, this mouse model of blindsight will enable the interrogation and identification of the neural circuits that underlie conscious and unconscious vision.