Recently, we reported the tetrodotoxin (TTX)- and dihydropyridine (DHP)-resistant (TDR) inward currents in neonatal mouse spinal neurons. In this study, we further characterized these currents in the presence of 1–5 μM TTX and 20–30 μM DHP (nifedipine, nimodipine, or isradipine). TDR inward currents were recorded by voltage ramp (persistent inward current, TDR-PIC) and step (TDR- Ip) protocols. TDR-PIC and TDR- Ip were found in 80.2% of recorded neurons (101/126) crossing laminae I to X from T12 to L6. TDR-PIC activated at −28.6 ± 13 mV with an amplitude of 80.6 ± 75 pA and time constant of 470.6 ± 240 ms ( n = 75). TDR- Ip had an amplitude of 151.2 ± 151 pA and a voltage threshold of −17.0 ± 9 mV ( n = 54) with a wide range of kinetics parameters. The half-maximal activation was −21.5 ± 8 mV (−37 to −12 mV, n = 29) with a time constant of 5.2 ± 2 ms (1.2–11.2 ms, n = 19), whereas the half-maximal inactivation was −26.9 ± 9 mV (−39 to −18 mV, n = 14) with a time constant of 1.4 ± 0.4 s (0.5–2.2 s, n = 19). TDR-PIC and TDR- Ip could be reduced by 60% in zero calcium and completely removed in zero sodium solutions, suggesting that they were mediated by sodium ions. Furthermore, the reversal potential of TDR- Ip was estimated as 56.6 ± 3 mV ( n = 10). TDR-PIC and TDR- Ip persisted in 1–205 μM TTX, 20–100 μM DHP, 3–30 μM riluzole, 50–300 μM flufenamic acid, and 2–30 mM intracellular BAPTA. They also persisted with T-, N-, P/Q-, and R-type calcium channel blockers. In conclusion, we demonstrated novel TTX-, DHP-, and riluzole-resistant sodium channels in neonatal rodent spinal neurons. The unique pharmacological and electrophysiological properties would allow these channels to play a functional role in spinal motor system.