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Related Experiment Video

Updated: Jul 17, 2025

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

Benoît Drouillas1, Cécile Brocard1, Sébastien Zanella1

  • 1Institut de Neurosciences de la Timone, UMR 7289, Aix-Marseille Université and Centre National de la Recherche Scientifique (CNRS), Marseille, France.

Cell Reports
|September 4, 2023
PubMed
Summary

Nav1.6 channels are key for motor control, driving persistent sodium current (INaP) in spinal motoneurons for posture and locomotion. They also work with Nav1.1 channels in central pattern generators for rhythmic movement.

Keywords:
CP: NeuroscienceCPGNav1.1Nav1.6bistabilityinterneuronlocomotionmotoneuronpacemakersposturespinal cord

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Motor Control

Background:

  • Persistent sodium current (INaP) is crucial for spinal network function, enabling distinct firing patterns in motoneurons and central pattern generators (CPGs).
  • Understanding the specific sodium channel (NaV) subtypes responsible for INaP is essential for elucidating their roles in motor behaviors.

Purpose of the Study:

  • To identify the specific NaV channel subtypes responsible for INaP in spinal motoneurons and CPG interneurons.
  • To determine the distinct roles of these NaV channels in motor behaviors, including posture and locomotion.

Main Methods:

  • Utilized electrophysiological recordings in spinal cord preparations.
  • Employed targeted inhibition of specific NaV channel subtypes (Nav1.1, Nav1.6) in motoneurons and CPG interneurons.
  • Assessed the impact of channel inhibition on INaP, neuronal firing patterns, and locomotor activity.

Main Results:

  • Axonal Nav1.6 was identified as the primary contributor to INaP in lumbar motoneurons, mediating bistability and essential for postural tone and locomotion.
  • Inhibition of Nav1.6 in motoneurons impaired INaP, bistability, and locomotor performance, while Nav1.1 inhibition had no significant effect.
  • Both Nav1.6 and Nav1.1 equally mediated INaP in CPG interneurons, with dual inhibition required to abolish rhythmic bursting and locomotor activity.

Conclusions:

  • Nav1.6 channels play a dual role in motor control: governing INaP-dependent bistability in motoneurons for posture and locomotion, and collaborating with Nav1.1 in the CPG for rhythm generation.
  • Targeting Nav1.6 offers a potential therapeutic strategy for motor disorders associated with altered INaP and neuronal excitability.