ArticleCellular and molecular neurobiology2000
The delay in recovery from fast inactivation in skeletal muscle sodium channels is deactivation.
Article in Cellular and molecular neurobiology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- A Historical Outline of Fluorescence Spectroscopy in Ion Channel Research.Advances in experimental medicine and biology · 2026Review
- Charge immobilization of skeletal muscle Na+ channels: role of residues in the inactivation linker.Biophysical journal · 2007Article
- Central charged residues in DIIIS4 regulate deactivation gating in skeletal muscle sodium channels.Cellular and molecular neurobiology · 2007Article
- K-aggravated myotonia mutations at residue G1306 differentially alter deactivation gating of human skeletal muscle sodium channels.Cellular and molecular neurobiology · 2005Article
- Functional characterization and cold sensitivity of T1313A, a new mutation of the skeletal muscle sodium channel causing paramyotonia congenita in humans.The Journal of physiology · 2004Article
- Negative charges in the DIII-DIV linker of human skeletal muscle Na+ channels regulate deactivation gating.The Journal of physiology · 2003Article
- Outer and central charged residues in DIVS4 of skeletal muscle sodium channels have differing roles in deactivation.Biophysical journal · 2002Article
- A single residue differentiates between human cardiac and skeletal muscle Na+ channel slow inactivation.Biophysical journal · 2001Article
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Authors and funding
3 authors.
Funding
Abstract
1. Using macropatch techniques, we tested the assumption that deactivation underlies the observed delay in the onset to recovery from fast inactivation by comparing open-state deactivation to recovery delay for rat skeletal muscle mutations R1441C and R1441P. 2. Deactivation kinetics from the open state were determined from the exponential decay of tail currents. R1441C and R1441P prolonged open-state deactivation, with the greatest effect produced by R1441P. 3. Delays in the onset to recovery from fast inactivation for R1441P and for R1441C were abbreviated compared to those for rSkM1. Recovery delay was longer in R1441P than R1441C at voltages more negative than -110 mV. Recovery from inactivation exhibited a voltage dependence which, unlike delay, saturated at depolarized voltages. Recovery rate constants were increased to a similar extent for R1441C and R1441P at -150 to -120 mV compared to rSkM1. 4. These results indicate that the delay in the onset to recovery from fast inactivation in skeletal muscle sodium channels is due to deactivation. Lessening of charge immobilization for R1441C and R1441P may contribute to observed biophysical defects underlying the hyperexcitability of muscle fibers containing paramyotonia congenita mutations. The second stage of recovery from fast inactivation may be affected differentially by these mutations.
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