Scn8a encodes the NaV1.6 voltage-gated sodium channel α subunit. In cerebellar Purkinje neurons, expression of NaV1.6 produces channels that carry TTX-sensitive transient and resurgent current. Scn8a null mice, which lack NaV1.6, have severe motor deficits and die prematurely. The extent to which the pathophysiology results specifically from the change in Na currents in Purkinje neurons, however, is unknown. Recently, mice with Scn8a deleted exclusively in Purkinje neurons were generated. These animals are viable, but show impaired performance on specific motor tasks (S.I. Levin et al., SFN abstract 2004). Here, we have studied Na currents and spiking in Purkinje neurons of adult mutant mice lacking expression of NaV1.6 only in these cells. Transient and resurgent Na currents were elicited in Purkinje neurons acutely dissociated from 7-8 week old mutant animals and wild-type siblings. Relative to wild-type cells (N=5), transient current in mutant cells (N=16) was reduced by 44% (p<0.05). The resurgent curr...