Unilateral peripheral vestibular dysfunction disrupts motion-evoked neuronal responses in primary visual cortex.

Acute unilateral peripheral vestibular destruction (AUPVD) causes dizziness, characterized by both visual and motion-related disturbances. Although it is well established that the vestibular nuclei receive auditory and visual sensory inputs and play a critical role in maintaining balance and gaze, the extent to which vestibular activity influences the primary visual cortex (V1) remains unclear. In this study, we observed that V1 neurons failed to generate appropriate responses to motion stimuli using chronic two-photon microscopy in awake AUPVD mice, despite responding normally to static visual inputs. Pharmacological and chemogenetic manipulation of GABAergic signaling in the vestibular nuclei of healthy mice further confirmed that aberrant activity in vestibular inhibitory neurons disrupts V1 neuronal processing. Our findings reveal that the compensatory firing of vestibular inhibitory neurons disrupts normal neuronal responses to motion-related visual stimuli in V1, contributing to dizziness symptoms following peripheral vestibular damage.