ArticleThe Journal of general physiology2013
Voltage-sensor movements describe slow inactivation of voltage-gated sodium channels I: wild-type skeletal muscle Na(V)1.4.
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 20 papers.
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Who cites it
20 citing papers in PubMed, 37 citations in OpenAlex.
- A biophysical perspective on the resilience of neuronal excitability across timescales.Nature reviews. Neuroscience · 2023Review
- 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
- Chemical and Biological Tools for the Study of Voltage-Gated Sodium Channels in Electrogenesis and Nociception.Chembiochem : a European journal of chemical biology · 2022Review
- Cannabidiol Inhibition of Murine Primary Nociceptors: Tight Binding to Slow Inactivated States of NaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Epilepsy-Related Voltage-Gated Sodium Channelopathies: A Review.Frontiers in pharmacology · 2020Review
- The voltage-gated sodium channel pore exhibits conformational flexibility during slow inactivation.The Journal of general physiology · 2018Article
- Using voltage-sensor toxins and their molecular targets to investigate NaThe Journal of physiology · 2018Review
- 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
- Pharmacology of the NaProceedings of the National Academy of Sciences of the United States of America · 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
- Cardiac Na Channels: Structure to Function.Current topics in membranes · 2016Article
- Direct Measurement of Cardiac Na+ Channel Conformations Reveals Molecular Pathologies of Inherited Mutations.Circulation. Arrhythmia and electrophysiology · 2015Article
- Synergetic action of domain II and IV underlies persistent current generation in Nav1.3 as revealed by a tarantula toxin.Scientific reports · 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
- Inhibitory effects of capsaicin on voltage-gated potassium channels by TRPV1-independent pathway.Cellular and molecular neurobiology · 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 II: a periodic paralysis mutation in Na(V)1.4 (L689I).The Journal of general physiology · 2013Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The number of voltage-gated sodium (Na(V)) channels available to generate action potentials in muscles and nerves is adjusted over seconds to minutes by prior electrical activity, a process called slow inactivation (SI). The basis for SI is uncertain. Na(V) channels have four domains (DI-DIV), each with a voltage sensor that moves in response to depolarizing stimulation over milliseconds to activate the channels. Here, SI of the skeletal muscle channel Na(V)1.4 is induced by repetitive stimulation and is studied by recording of sodium currents, gating currents, and changes in the fluorescence of probes on each voltage sensor to assess their movements. The magnitude, voltage dependence, and time course of the onset and recovery of SI are observed to correlate with voltage-sensor movements 10,000-fold slower than those associated with activation. The behavior of each voltage sensor is unique. Development of SI over 1-160 s correlates best with slow immobilization of the sensors in DI and DII; DIII tracks the onset of SI with less fidelity. Showing linkage to the sodium conduction pathway, pore block by tetrodotoxin affects both SI and immobilization of all the sensors, with DI and DII significantly suppressed. Recovery from SI correlates best with slow restoration of mobility of the sensor in DIII. The findings suggest that voltage-sensor movements determine SI and thereby mediate Na(V) channel availability.
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