Previous studies using pharmacological methods suggest that subthreshold sodium currents are critical for rhythmical burst generation in mesencephalic trigeminal neurons (Mes V). In the present study we characterized transient (I_NaT), persistent (I_NaP) and resurgent (I_res) sodium currents in Na_v1.6-null mice (med mouse, Na_v1.6^-/-) lacking expression of the sodium channel gene Scn8a. We found that peak transient, persistent and resurgent sodium currents from med (Na_v1.6^-/-) mice were reduced by 18%, 39% and 76% relative to their wild-type (Na_v1.6^+/+) littermates, respectively. Current clamp recordings indicated that in response to sinusoidal constant amplitude current (ZAP function) all neurons exhibited membrane resonance. However, Mes V neurons from med mice had reduced peak amplitudes in the impedance-frequency relationship (resonant Q-value), and attenuated subthreshold oscillations in spite of the similar passive membrane properties compared to wild-type littermates. The spike frequency current relationship exhibited reduced instantaneous discharge frequencies and spike block at low stimulus currents, and seldom showed maintained spike discharge throughout the stimulus in the majority of med neurons compared to wild-type neurons. Importantly, med neurons never exhibited maintained stimulus induced rhythmical burst discharge unlike those of wild type littermates. The data show that subthreshold sodium currents are critical determinants of Mes V electrogenesis and burst generation and suggest a role for resurgent sodium currents in control of spike discharge.