Persistent sodium current in mammalian central neurons

Neurons from the mammalian CNS have a noninactivating component of the tetrodotoxin-sensitive sodium current (I-NaP). Although its magnitude is <1% of the transient sodium current, I-NaP 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. I-NaP adds to synaptic current, and evidence indicates that it is present in dendrites where relatively small depolarizations will activate I-NaP, thereby increasing effectiveness of distal depolarizing synaptic activity. The mechanism for I-NaP 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 I-NaP flows through a distinct subtype of noninactivating sodium channels. Modulation of I-NaP could have a significant effect on the transduction of synaptic currents by neurons.