The pre-Bötzinger complex (preBötC) in the ventrolateral medulla contains interneurons important for respiratory rhythm generation. Voltage-dependent sodium channels mediate transient current (I NaT ), underlying action potentials, and persistent current (I NaP ), contributing to repetitive firing, pacemaker properties, and the amplification of synaptic inputs. Voltage-clamp studies of the biophysical properties of these sodium currents were conducted on acutely dissociated preBötC region neurons. Reverse transcription-PCR demonstrated the presence of mRNA for Nav1.1, Nav1.2, and Nav1.6 ␣-subunits in individual neurons. A TTX-sensitive I NaP was evoked in all tested neurons by ramp depolarization from Ϫ80 to 0 mV. Including a constant in the Boltzmann equation for inactivation by estimating the steady-state fraction of Na ϩ channels available for inactivation allowed prediction of a window current that did not decay to 0 at voltages positive to Ϫ20 mV and closely matched the measured I NaP . Riluzole (3 M), a putative I NaP antagonist, reduced both I NaP and I NaT and produced a hyperpolarizing shift in the voltage dependence of steady-state inactivation. The latter decreased the predicted window current by an amount equivalent to the decrease in I NaP . Riluzole also decreased the inactivation time constant at potentials in which the peak window/persistent currents are generated. Together, these findings imply that I NaP and I NaT arise from the same channels and that a simple modification of the Hodgkin-Huxley model can satisfactorily account for both currents. In the rostral ventral respiratory group (immediately caudal to preBötC), I NaP was also detected, but peak conductance, current density, and input resistance were smaller than in preBötC region cells.

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