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Updated: Jan 10, 2026
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Spinal Cord Electrophysiology
Published on: January 18, 2010
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Ionic mechanisms underlying bistability in spinal motoneurons: insights from a computational model
Yaroslav I Molkov1,2, Florent Krust3, Russell Jeter1,2
1Department of Mathematics and Statistics, Georgia State University, Atlanta, GA, United States.
Frontiers in Cellular Neuroscience
|November 27, 2025
Summary
Spinal motoneuron bistability, crucial for movement, arises from interactions between L-type calcium currents, calcium-induced calcium release, and cation currents. This finding offers insights into motor control and neurological disorders like spasticity.
Area of Science:
- Neuroscience
- Computational Neuroscience
- Motor Control
Background:
- Spinal motoneurons control skeletal muscles and exhibit bistable firing, characterized by plateau potentials.
- Dysregulation of this intrinsic property is linked to motor deficits such as spasticity.
Purpose of the Study:
- To investigate the ionic interactions underlying spinal motoneuron bistability.
- To identify the minimal set of ionic currents required for plateau potential generation and bistable firing.
Main Methods:
- Utilized a conductance-based single-compartment model of a motoneuron.
- Validated model findings with experimental recordings from mouse spinal slices.
Main Results:
- Identified synergistic interactions between L-type Ca2+ current (ICaL), calcium-induced calcium release (CICR), and Ca2+-activated non-specific cation current (ICAN) as a core mechanism for bistability.
- Demonstrated that persistent sodium current (INaP) promotes plateau generation, while Ca2+-activated K+ current (IKCa) opposes it.
Conclusions:
- Delineated the ionic dependencies underlying motoneuron bistability at the interaction level, not just spatial localization.
- Provided a mechanistic framework for understanding altered motoneuron excitability in disease states.
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