Voltage-gated Na⁺ channels (VGSCs) consist of a large α subunit and one or more auxiliary β subunits. It is generally known that VGSC β subunits modulate Na⁺ current kinetics, regulate channel cell surface expression, and cell adhesion. VGSC β subunits (β1-β4), encoded by Scn1b-Scn4b, are expressed in nervous system. Although striatal neurons show the highest expression of β4 in the nervous system (Oyama et al, 2006), physiological roles of β4 in the striatum are not well understood. In this study, we focused on electrophysiological properties of β4 in the striatum and used Scn4b-null mice. Previous studies have reported that VGSC β4 is an endogenous open-channel blocker that causes resurgent Na⁺ current, a transient inward Na⁺ current. Resurgent Na⁺ current is produced during repolarization of the membrane after action potential generation, and reduction of resurgent Na⁺ current might disrupt repetitive firing of striatal neurons. We therefore tested whether knockout of Scn4b altered resurgent Na⁺ current using whole-cell patch clamp recordings in acutely-dissociated cells and slice preparations. Resurgent Na⁺ current recorded from a medium spiny neuron (MSN) was significantly reduced in Scn4b-null mice relative to their wild-type littermates. Knockout of Scn4b significantly decreased repetitive firing frequency in MSNs. We also examined whether knockout of Scn4b altered conduction velocity of action potentials in slice preparations, however there was no significant difference between genotypes. Thus, VGSC β4 might contribute to the repetitive firing of MSNs by which striatal signals are transferred to output nuclei of the basal ganglia. These studies would help explain the physiological roles of VGSC β4 in the striatum.