Two synergistic plastic mechanisms have recently been identified in rat medial vestibular nucleus (MVN) neurons during 'vestibular compensation', the behavioral recovery that follows damage to the vestibular receptors or nerve of one inner ear. Ipsi-lesional MVN neurons develop a significant increase in their intrinsic excitability, and a marked decrease in the functional efficacy of GABA(A) and GABA(B) receptors, within 4 h of unilateral vestibular deafferentation. These mechanisms presumably counteract the disfacilitation and excessive commissural inhibition of the ipsi-lesional cells after deafferentation, and thus promote the recovery of resting activity. In this study, we investigated the intrinsic membrane properties and spike firing characteristics of rostral ipsi-lesional MVN neurons in slices from animals that underwent vestibular compensation for either 24-72 h or 7-10 days. Significant changes were observed in the spontaneous in vitro discharge rate, resting membrane potentials and voltage-activated membrane conductances of type B cells, but not type A cells. There was a significant increase in the number of type B(LTS) cells compared to normal. These findings indicate that during vestibular compensation marked changes occur in ion channel expression and function selectively in type B MVN neurons. These changes are appropriate to increase the responsiveness of type B cells both to their own intrinsic pacemaker-like membrane conductances and excitatory synaptic inputs. Together with the downregulation of inhibitory receptor efficacy, this increased intrinsic excitability may be sufficient to restore the resting discharge of the deafferented neurons in vivo. These results therefore provide further evidence for synaptic and neuronal plasticity in ipsi-lesional MVN neurons during vestibular compensation.