ArticleThe Journal of general physiology2013
Voltage-sensor movements describe slow inactivation of voltage-gated sodium channels II: a periodic paralysis mutation in Na(V)1.4 (L689I).
Article in The Journal of general physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed, 28 citations in OpenAlex.
- Sodium channel slow inactivation normalizes firing in axons with uneven conductance distributions.Current biology : CB · 2023Article
- Differential regulation of cardiac sodium channels by intracellular fibroblast growth factors.The Journal of general physiology · 2023Article
- Cannabidiol and Sodium Channel Pharmacology: General Overview, Mechanism, and Clinical Implications.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2022Review
- A Novel Spider Toxin Inhibits Fast Inactivation of the NaFrontiers in pharmacology · 2021Article
- Dynamic clamp constructed phase diagram for the Hodgkin and Huxley model of excitability.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Detection of NaBiophysical journal · 2019Article
- Mechanisms and models of cardiac sodium channel inactivation.Channels (Austin, Tex.) · 2017Review
- Mechanisms of noncovalent β subunit regulation of NaThe Journal of general physiology · 2017Article
- Regulation of NaThe Journal of general physiology · 2017Article
- Depolarization of the conductance-voltage relationship in the NaV1.5 mutant, E1784K, is due to altered fast inactivation.PloS one · 2017Article
- Effect of phenytoin on sodium conductances in rat hippocampal CA1 pyramidal neurons.Journal of neurophysiology · 2016Article
- Article
- Direct Measurement of Cardiac Na+ Channel Conformations Reveals Molecular Pathologies of Inherited Mutations.Circulation. Arrhythmia and electrophysiology · 2015Article
- Differential thermosensitivity in mixed syndrome cardiac sodium channel mutants.The Journal of physiology · 2015Article
- Fast-onset long-term open-state block of sodium channels by A-type FHFs mediates classical spike accommodation in hippocampal pyramidal neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- The Xenopus oocyte cut-open vaseline gap voltage-clamp technique with fluorometry.Journal of visualized experiments : JoVE · 2014Article
- Voltage-sensor movements describe slow inactivation of voltage-gated sodium channels I: wild-type skeletal muscle Na(V)1.4.The Journal of general physiology · 2013Article
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2 authors at 1 institution in 1 country.
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Abstract
In skeletal muscle, slow inactivation (SI) of Na(V)1.4 voltage-gated sodium channels prevents spontaneous depolarization and fatigue. Inherited mutations in Na(V)1.4 that impair SI disrupt activity-induced regulation of channel availability and predispose patients to hyperkalemic periodic paralysis. In our companion paper in this issue (Silva and Goldstein. 2013. J. Gen. Physiol. http://dx.doi.org/10.1085/jgp.201210909), the four voltage sensors in Na(V)1.4 responsible for activation of channels over microseconds are shown to slowly immobilize over 1-160 s as SI develops and to regain mobility on recovery from SI. Individual sensor movements assessed via attached fluorescent probes are nonidentical in their voltage dependence, time course, and magnitude: DI and DII track SI onset, and DIII appears to reflect SI recovery. A causal link was inferred by tetrodotoxin (TTX) suppression of both SI onset and immobilization of DI and DII sensors. Here, the association of slow sensor immobilization and SI is verified by study of Na(V)1.4 channels with a hyperkalemic periodic paralysis mutation; L689I produces complex changes in SI, and these are found to manifest directly in altered sensor movements. L689I removes a component of SI with an intermediate time constant (~10 s); the mutation also impedes immobilization of the DI and DII sensors over the same time domain in support of direct mechanistic linkage. A model that recapitulates SI attributes responsibility for intermediate SI to DI and DII (10 s) and a slow component to DIII (100 s), which accounts for residual SI, not impeded by L689I or TTX.
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