Neurons from the mammalian CNS have a noninactivating component of the tetrodotoxin-sensitive sodium current (INaP). Although its magnitude is < 1% of the transient sodium current, INaP has functional significance because it is activated about 10 mV negative to the transient sodium current, where few voltage-gated channels are activated and neuron input resistance is high. INaP adds to synaptic current, and evidence indicates that it is present in dendrites where relatively small depolarizations will activate INaP, thereby increasing effectiveness of distal depolarizing synaptic activity. The mechanism for INaP is not known. Research in striated muscle and neurons suggests a modal change in gating of conventional sodium channels, but it is also possible that INaP flows through a distinct subtype of noninactivating sodium channels. Modulation of INaP could have a significant effect on the transduction of synaptic currents by neurons.