We tested the hypothesis that pacemaker neurons generate breathing rhythm in mammals. We monitored respiratory-related motor nerve rhythm in neonatal rodent slice preparations. Blockade of the persistent sodium current (INaP), which was postulated to underlie voltage-dependent bursting in respiratory pacemaker neurons, with riluzole (≤200 μM) did not alter the frequency of respiratory-related motor output. Yet, in every pacemaker neuron recorded (50/50), bursting was abolished at much lower concentrations of riluzole (≤20 μM). Thus, eliminating the pacemaker population (our statistics confirm that this population is reduced at least 94%, p < 0.05) does not affect respiratory rhythm. These results suggest that voltage-dependent bursting in pacemaker neurons is not essential for respiratory rhythmogenesis, which may instead be an emergent network property.