Unilateral labyrinthectomy (UL) causes ocular motor and postural disorders which disappear over time in a process of recovery known as vestibular compensation. Vestibular compensation is due to CNS plasticity which generates a partial recovery of resting activity in the vestibular nucleus ipsilateral to the UL, however the mechanism of this neural recovery is unknown. It has been suggested that other areas of the CNS may substitute non-vestibular sensory inputs for the missing labyrinthine input, thereby causing vestibular compensation. The present results show that resting activity can be recorded from medial vestibular nucleus (MVN) neurons in vitro, in brainstem slices from guinea pigs which have compensated for an ipsilateral UL. This result suggests that MVN neurons are capable of generating resting activity without inputs from many other CNS areas. Perfusion with high Mg2+ solution did not abolish resting activity in most cases, suggesting that part of the resting activity may be generated spontaneously by the neurons, possibly through changes in the electrical excitability of the cell membrane.