We have shown previously in dissociated cultures of foetal rat spinal cord that disinhibition-induced bursting is based on intrinsic spiking, network recruitment and a network refractory period following the bursts. A persistent sodium current (I_NaP) underlies intrinsic spiking, which, via recurrent excitation, generates the bursting activity. While full blockade of I_NaP with riluzole disrupts such bursting, the present study shows that partial blockade of I_NaP with low doses of riluzole (low riluzole) maintains bursting activity with unchanged burst rate and burst duration. Cultures were investigated with multi-electrode arrays. More importantly, low riluzole turned bursts composed of persistent activity into bursts composed of oscillatory activity at around 5 Hz. Looking for mechanisms underlying the generation of such intraburst oscillations, we found that activity-dependent synaptic depression was not changed with low riluzole. On the other hand, low riluzole strongly increased spike-frequency adaptation and led to early depolarization block when bursts were simulated by injecting long current pulses into single neurons in the absence of fast synaptic transmission. Phenytoin is another I_NaP blocker. When applied in doses that reduced intrinsic activity by 80-90 %, as did low riluzole, it had no effect in either spike-frequency adaptation or on depolarization block. Nor did phenytoin induce intraburst oscillations following disinhibition. A theoretical model incorporating a depolarization block mechanism could reproduce the generation of intraburst oscillations at the network level. From these findings we conclude that riluzole-induced intraburst oscillations are a network-driven phenomenon whose major accommodation mechanism is depolarization block due to strong sodium channel inactivation.