Journal article
Ionic mechanisms underlying bistability in spinal motoneurons: insights from a computational model
Frontiers in cellular neuroscience, v 19, 1710893
11 Nov 2025
PMID: 41306652
Abstract
Spinal motoneurons are the final output of spinal circuits that engage skeletal muscles to generate motor behaviors. Many motoneurons exhibit bistable behavior, alternating between a quiescent resting state and a self-sustained firing mode, classically attributed to plateau potentials driven by persistent inward currents. This intrinsic property is important for normal movement control, but can become dysregulated, causing motor function deficits, like spasticity. Here we use a conductance-based single-compartment model, together with mouse spinal slice recordings, to investigate the ionic interactions underlying motoneuron bistability. We show that synergistic interactions among high-voltage-activated L-type Ca 2+ current ( I CaL ), calcium-induced calcium release (CICR) and the Ca 2+ -activated non-specific cation current ( I CAN ) constitute a minimal mechanistic core that produces plateau potentials and bistable firing. Within this framework, the persistent sodium current ( I NaP ) promotes plateau generation, in contrast to the Ca 2+ -dependent K + current ( I KCa ) which opposes it. These results delineate ionic dependencies at the level of interactions rather than spatial localization and provide a tractable basis for interpreting altered motoneuron excitability in disease.
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Details
- Title
- Ionic mechanisms underlying bistability in spinal motoneurons: insights from a computational model
- Creators
- Yaroslav I. Molkov - Georgia State UniversityFlorent Krust - Georgia State UniversityRussell Jeter - Georgia State UniversityTommy Stell - Institut de Neurosciences de la TimoneMohammed A. Y. Mohammed - Drexel UniversityFrédéric BrocardIlya A. Rybak
- Publication Details
- Frontiers in cellular neuroscience, v 19, 1710893
- Publisher
- Frontiers
- Number of pages
- 18
- Grant note
- ANR MotoBis grant: ANR-24-CE16-1548-01 NIH/NINDS: R01 NS130799
The author(s) declare that financial support was received for the research and/or publication of this article. This work was supported by the ANR MotoBis grant (ANR-24-CE16-1548-01) to FB and the NIH/NINDS grant (R01 NS130799) to IR.
- Resource Type
- Journal article
- Language
- English
- Academic Unit
- Neurobiology and Anatomy
- Web of Science ID
- WOS:001621858700001
- Scopus ID
- 2-s2.0-105023572201
- Other Identifier
- 991022132897804721
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- Collaboration types
- Domestic collaboration
- International collaboration
- Web of Science research areas
- Neurosciences