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

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-sensi...

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Main Authors: Rémi Bos, Ronald M. Harris-Warrick, Cécile Brocard, Liliia E. Demianenko, Marin Manuel, Daniel Zytnicki, Sergiy M. Korogod, Frédéric Brocard
Format: Article
Language:English
Published: Elsevier 2018-03-01
Series:Cell Reports
Online Access:http://www.sciencedirect.com/science/article/pii/S2211124718303036
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author Rémi Bos
Ronald M. Harris-Warrick
Cécile Brocard
Liliia E. Demianenko
Marin Manuel
Daniel Zytnicki
Sergiy M. Korogod
Frédéric Brocard
author_facet Rémi Bos
Ronald M. Harris-Warrick
Cécile Brocard
Liliia E. Demianenko
Marin Manuel
Daniel Zytnicki
Sergiy M. Korogod
Frédéric Brocard
author_sort Rémi Bos
collection DOAJ
description 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
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spelling doaj.art-2dc2b16fa3d9495f9e6e7fd187299eef2022-12-22T03:03:37ZengElsevierCell Reports2211-12472018-03-01221233153327Kv1.2 Channels Promote Nonlinear Spiking Motoneurons for Powering Up LocomotionRémi Bos0Ronald M. Harris-Warrick1Cécile Brocard2Liliia E. Demianenko3Marin Manuel4Daniel Zytnicki5Sergiy M. Korogod6Frédéric Brocard7Institut de Neurosciences de la Timone (UMR7289), Aix-Marseille Université and Centre National de la Recherche Scientifique (CNRS), Marseille, FranceDepartment of Neurobiology and Behavior, Cornell University, Ithaca, NY, USAInstitut de Neurosciences de la Timone (UMR7289), Aix-Marseille Université and Centre National de la Recherche Scientifique (CNRS), Marseille, FranceBogomoletz Institute of Physiology, National Academy of Sciences of Ukraine, Kiev, UkraineCentre de Neurophysique, Physiologie et Pathologie, UMR 8119, CNRS/Université Paris Descartes, 45 rue des Saints-Pères, 75270 Paris Cedex 06, FranceCentre de Neurophysique, Physiologie et Pathologie, UMR 8119, CNRS/Université Paris Descartes, 45 rue des Saints-Pères, 75270 Paris Cedex 06, FranceBogomoletz Institute of Physiology, National Academy of Sciences of Ukraine, Kiev, UkraineInstitut de Neurosciences de la Timone (UMR7289), Aix-Marseille Université and Centre National de la Recherche Scientifique (CNRS), Marseille, France; Corresponding authorSummary: 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, Kv1.2http://www.sciencedirect.com/science/article/pii/S2211124718303036
spellingShingle Rémi Bos
Ronald M. Harris-Warrick
Cécile Brocard
Liliia E. Demianenko
Marin Manuel
Daniel Zytnicki
Sergiy M. Korogod
Frédéric Brocard
Kv1.2 Channels Promote Nonlinear Spiking Motoneurons for Powering Up Locomotion
Cell Reports
title Kv1.2 Channels Promote Nonlinear Spiking Motoneurons for Powering Up Locomotion
title_full Kv1.2 Channels Promote Nonlinear Spiking Motoneurons for Powering Up Locomotion
title_fullStr Kv1.2 Channels Promote Nonlinear Spiking Motoneurons for Powering Up Locomotion
title_full_unstemmed Kv1.2 Channels Promote Nonlinear Spiking Motoneurons for Powering Up Locomotion
title_short Kv1.2 Channels Promote Nonlinear Spiking Motoneurons for Powering Up Locomotion
title_sort kv1 2 channels promote nonlinear spiking motoneurons for powering up locomotion
url http://www.sciencedirect.com/science/article/pii/S2211124718303036
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