Persistent Nav1.1 and Nav1.6 currents drive spinal locomotor functions through nonlinear dynamics.

Persistent sodium current (I) in the spinal locomotor network promotes two distinct nonlinear firing patterns: a self-sustained spiking triggered by a brief excitation in bistable motoneurons and bursting oscillations in interneurons of the central pattern generator (CPG). Here, we identify the NaV channels responsible for I and their role in motor behaviors. We report the axonal Nav1.6 as the main molecular player for I in lumbar motoneurons. The inhibition of Nav1.6, but not of Nav1.1, in motoneurons impairs I, bistability, postural tone, and locomotor performance. In interneurons of the rhythmogenic CPG region, both Nav1.6 and Nav1.1 equally mediate I. Inhibition of both channels is required to abolish oscillatory bursting activities and the locomotor rhythm. Overall, Nav1.6 plays a significant role both in posture and locomotion by governing I-dependent bistability in motoneurons and working in tandem with Nav1.1 to provide I-dependent rhythmogenic properties of the CPG.