Unilateral labyrinthine lesion causes the vestibular symptoms such as nausea, vomiting, dizziness, and spontaneous nystagmus. This experiment was performed to study the action mechanism of flunarizine, a Ca²⁺ antagonist, on the compensation of vestibular function following labyrinthine lesion. Flunarizine was injected into the 4th ventricle in intact and unilateral labyrinthectomized rats. Spontaneous nystagmus in terms of static vestibular signs and eye movement induced by sinusoidal rotation of the whole body in terms of dynamic symptom were recorded, and electrophysiological activity of the vestibular nucleus was also recorded. Eye movements induced by sinusoidal rotation were decreased by flunarizine in the intact rats. Spontaneous nystagmus disappeared and eye movements induced by sinusoidal rotation recovered to normal vestibuloocular reflex by flunarizine in the unilateral labyrinthectomized rats. After flunarizine injection activity of resting potential in the vestibular nucleus was decreased. Latencies of field potentials were not changed but amplitudes of P wave, N1 wave and N2 wave were decreased to 74%, 42% and 0% respectively. These results may suggest that flunarizine, a Ca²⁺ antagonist, facilitates the vestibular compensation by inhibition of intact sided vestibular nucleus as well as lesion sided vestibular nucleus following unilateral labyrinthectomy.