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

ABSTRACT: 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 sl

SUBMITTER: Bos R 

PROVIDER: S-EPMC5907934 | biostudies-literature | 2018 Mar

REPOSITORIES: biostudies-literature