Kv1.2 Channels Promote Nonlinear Spiking Motoneurons for Powering Up Locomotion

Abstract

Summary: Spinal motoneurons are endowed with nonlinear spiking behaviors manifested by a spike acceleration whose functional significance remains uncertain. Here, we show in rodent lumbar motoneurons that these nonlinear spiking properties do not rely only on activation of dendritic nifedipine-sensitive L-type Ca2+ channels, as assumed for decades, but also on the slow inactivation of a nifedipine-sensitive K+ current mediated by Kv1.2 channels that are highly expressed in axon initial segments. Specifically, the pharmacological and computational inhibition of Kv1.2 channels occluded the spike acceleration of rhythmically active motoneurons and the correlated slow buildup of rhythmic motor output recorded at the onset of locomotor-like activity. This study demonstrates that slow inactivation of Kv1.2 channels provides a potent gain control mechanism in mammalian spinal motoneurons and has a behavioral role in enhancing locomotor drive during the transition from immobility to steady-state locomotion. : Bos et al. demonstrate that slow inactivation of Kv1.2 channels is critical in shaping nonlinear firing properties in mammalian spinal cord. It provides a potent gain control mechanism in spinal motoneurons and has a behavioral role in enhancing locomotor drive during the transition from immobility to steady-state locomotion. Keywords: locomotion, spinal cord, motoneuron, bistability, potassium channels, Kv1.2