ArticleBiophysical journal1993
Theoretical reconstruction of myotonia and paralysis caused by incomplete inactivation of sodium channels.
Article in Biophysical journal, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed, 179 citations in OpenAlex.
- Interplay between store-operated calcium entry and mitochondrial phosphate handling modulates force and fatigue during exercise.The Journal of physiology · 2026Article
- Article
- Potassium-sensitive loss of muscle force in the setting of reduced inward rectifier KProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Multi-scale modeling and simulation of skeletal muscles with different fatigue degrees based on microphysiology.Scientific reports · 2025Article
- Clinical, electromyographic, and biophysical characterization of the rare Nav1.4 channel mutationFrontiers in physiology · 2025Article
- Reduced KThe Journal of physiology · 2024Article
- BK channels promote action potential repolarization in skeletal muscle but contribute little to myotonia.Pflugers Archiv : European journal of physiology · 2024Article
- Cannabidiol and Sodium Channel Pharmacology: General Overview, Mechanism, and Clinical Implications.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2022Review
- Inhibition of sodium conductance by cannabigerol contributes to a reduction of dorsal root ganglion neuron excitability.British journal of pharmacology · 2022Article
- Ion Channel Gene Mutations Causing Skeletal Muscle Disorders: Pathomechanisms and Opportunities for Therapy.Cells · 2021Review
- Cannabidiol inhibits the skeletal muscle Nav1.4 by blocking its pore and by altering membrane elasticity.The Journal of general physiology · 2021Article
- Detection of biological signals from a live mammalian muscle using an early stage diamond quantum sensor.Scientific reports · 2021Article
- Preclinical pharmacological in vitro investigations on low chloride conductance myotonia: effects of potassium regulation.Pflugers Archiv : European journal of physiology · 2020Article
- Myotonic Myopathy With Secondary Joint and Skeletal Anomalies From the c.2386C>G, p.L769V Mutation inFrontiers in neurology · 2020Article
- Paxilline Prevents the Onset of Myotonic Stiffness in Pharmacologically Induced Myotonia: A Preclinical Investigation.Frontiers in physiology · 2020Article
- Modeling and simulation of excitation- contraction coupling of fast-twitch skeletal muscle fibers.Technology and health care : official journal of the European Society for Engineering and Medicine · 2020Article
- NaScientific reports · 2018Article
- A Mixed Periodic Paralysis & Myotonia Mutant, P1158S, Imparts pH-Sensitivity in Skeletal Muscle Voltage-gated Sodium Channels.Scientific reports · 2018Article
- Article
- Sodium Channelopathies of Skeletal Muscle.Handbook of experimental pharmacology · 2018Review
4 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Muscle fibers from individuals with hyperkalemic periodic paralysis generate repetitive trains of action potentials (myotonia) or large depolarizations and block of spike production (paralysis) when the extracellular K+ is elevated. These pathologic features are thought to arise from mutations of the sodium channel alpha subunit which cause a partial loss of inactivation (steady-state Popen approximately 0.02, compared to < 0.001 in normal channels). We present a model that provides a possible mechanism for how this small persistent sodium current leads to repetitive firing, why the integrity of the T-tubule system is required to produce myotonia, and why paralysis will occur when a slightly larger proportion of channels fails to inactivate. The model consists of a two-compartment system to simulate the surface and T-tubule membranes. When the steady-state sodium channel open probability exceeds 0.0075, trains of repetitive discharges occur in response to constant current injection. At the end of the current injection, the membrane potential may either return to the normal resting value, continue to discharge repetitive spikes, or settle to a new depolarized equilibrium potential. This after-response depends on both the proportion of noninactivating sodium channels and the magnitude of the activity-driven K+ accumulation in the T-tubular space. A reduced form of model is presented in which a two-dimensional phase-plane analysis shows graphically how this diversity of after-responses arises as extracellular [K+] and the proportion of noninactivating sodium channels are varied.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.