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Cell Rep. 2018 Mar 20;22(12):3315-3327. doi: 10.1016/j.celrep.2018.02.093.

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

Author information

1
Institut de Neurosciences de la Timone (UMR7289), Aix-Marseille Université and Centre National de la Recherche Scientifique (CNRS), Marseille, France.
2
Department of Neurobiology and Behavior, Cornell University, Ithaca, NY, USA.
3
Bogomoletz Institute of Physiology, National Academy of Sciences of Ukraine, Kiev, Ukraine.
4
Centre de Neurophysique, Physiologie et Pathologie, UMR 8119, CNRS/Université Paris Descartes, 45 rue des Saints-Pères, 75270 Paris Cedex 06, France.
5
Institut de Neurosciences de la Timone (UMR7289), Aix-Marseille Université and Centre National de la Recherche Scientifique (CNRS), Marseille, France. Electronic address: frederic.brocard@univ-amu.fr.

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 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.

KEYWORDS:

Kv1.2; bistability; locomotion; motoneuron; potassium channels; spinal cord

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