Description:
<jats:title>Abstract</jats:title><jats:p>We have shown previously that rhythm generation in disinhibited spinal networks is based on intrinsic spiking, network recruitment and a network refractory period following the bursts. This refractory period is based mainly on electrogenic Na/K pump activity. In the present work, we have investigated the role of the persistent sodium current (I<jats:sub>NaP</jats:sub>) in the generation of bursting using patch‐clamp and multielectrode array recordings. We detected I<jats:sub>NaP</jats:sub> exclusively in the intrinsic spiking cells. The blockade of I<jats:sub>NaP</jats:sub> by riluzole suppressed the bursting by silencing the intrinsic spiking cells and suppressing network recruitment. The blockade of the persistent sodium current produced a hyperpolarization of the membrane potential of the intrinsic spiking cells, but had no effect on non‐spiking cells. We also investigated the involvement of the hyperpolarization‐activated cationic current (I<jats:sub>h</jats:sub>) in the rhythmic activity. The bath application of ZD7288, a specific I<jats:sub>h</jats:sub> antagonist, slowed down the rate of the bursts by increasing the interburst intervals. I<jats:sub>h</jats:sub> was present in ∼ 70% of the cells, both in the intrinsic spiking cells as well as in the non‐spiking cells. We also found both kinds of cells in which I<jats:sub>h</jats:sub> was not detected. In summary, in disinhibited spinal cord cultures, a persistent sodium current underlies intrinsic spiking, which, via recurrent excitation, generates the bursting activity. The hyperpolarization‐activated cationic current contributes to intrinsic spiking and modulates the burst frequency.</jats:p>