OBJECTIVE: The cerebral cortex can modulate vestibular functions through direct control of neuronal activities in the vestibular nuclei. The purpose of this study was to investigate the effect of unilateral cortical lesion or cortical stimulation on static vestibular symptoms and vestibular nuclear activities at the acute stage of vestibular compensation following unilateral labyrinthectomy (UL) in rats. METHODS: The photothrombic ischemic injury using rose bengal was induced in the primary motor cortex or primary sensory cortex, and electrical stimulation was applied to the primary motor cortex, primary sensory cortex, or sencondary sensory cortex, respectively, in unilateral labyrinthectomized rats. Static vestibular symptoms including ocular movement and postural deficits, and expression of c-Fos protein in the medial vestibular nucleus (MVN) were measured. RESULTS: Lesion of the motor cortex produced a marked postural deficit with paralytic weakness in the hindlimb contralateral to UL. Number of spontaneous nystagmus in animals receiving cortical lesion was significantly increased 2, 6, and 12 hours after UL compared with animals being UL only. Lesion of the primary motor cortex or stimulation of the S2 sensory cortex decreased expression of c-Fos protein in MVN following UL compared with UL only group. Electrical stimulation of S2 sensory areas caused significant reduction of static vestibular symptoms and decreased expression of c-Fos protein in MVN 24 hours following UL. CONCLUSION: The present results suggest that cerebral cortex involves in recovery of static vestibular symptoms during vestibular compensation following UL.