ArticleThe Journal of general physiology2002
Slow inactivation does not block the aqueous accessibility to the outer pore of voltage-gated Na channels.
Article in The Journal of general physiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 36 citations in OpenAlex.
- SCN4A pore mutation pathogenetically contributes to autosomal dominant essential tremor and may increase susceptibility to epilepsy.Human molecular genetics · 2015Article
- Gating transitions in the selectivity filter region of a sodium channel are coupled to the domain IV voltage sensor.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Inhibition of neuronal voltage-gated sodium channels by brilliant blue G.Molecular pharmacology · 2011Article
- Possible roles of exceptionally conserved residues around the selectivity filters of sodium and calcium channels.The Journal of biological chemistry · 2011Article
- A molecular switch between the outer and the inner vestibules of the voltage-gated Na+ channel.The Journal of biological chemistry · 2010Article
- The outer vestibule of the Na+ channel-toxin receptor and modulator of permeation as well as gating.Marine drugs · 2010Review
- Cold-induced disruption of Na+ channel slow inactivation underlies paralysis in highly thermosensitive paramyotonia.The Journal of physiology · 2009Article
- Slow inactivation of the NaV1.4 sodium channel in mammalian cells is impeded by co-expression of the beta1 subunit.Pflugers Archiv : European journal of physiology · 2009Article
- Sodium channels: ionic model of slow inactivation and state-dependent drug binding.Biophysical journal · 2007Article
- Subunit dependence of Na channel slow inactivation and open channel block in cerebellar neurons.Biophysical journal · 2007Article
- A conserved ring of charge in mammalian Na+ channels: a molecular regulator of the outer pore conformation during slow inactivation.The Journal of physiology · 2006Article
- Tryptophan substitution of a putative D4S6 gating hinge alters slow inactivation in cardiac sodium channels.Biophysical journal · 2005Article
- Compound-specific Na+ channel pore conformational changes induced by local anaesthetics.The Journal of physiology · 2005Article
- Accessibility of mid-segment domain IV S6 residues of the voltage-gated Na+ channel to methanethiosulfonate reagents.The Journal of physiology · 2004Article
- Molecular motions of the outer ring of charge of the sodium channel: do they couple to slow inactivation?The Journal of general physiology · 2003Article
- Tryptophan scanning of D1S6 and D4S6 C-termini in voltage-gated sodium channels.Biophysical journal · 2003Article
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Slow inactivation of voltage-gated Na channels is kinetically and structurally distinct from fast inactivation. Whereas structures that participate in fast inactivation are well described and include the cytoplasmic III-IV linker, the nature and location of the slow inactivation gating mechanism remains poorly understood. Several lines of evidence suggest that the pore regions (P-regions) are important contributors to slow inactivation gating. This has led to the proposal that a collapse of the pore impedes Na current during slow inactivation. We sought to determine whether such a slow inactivation-coupled conformational change could be detected in the outer pore. To accomplish this, we used a rapid perfusion technique to measure reaction rates between cysteine-substituted side chains lining the aqueous pore and the charged sulfhydryl-modifying reagent MTS-ET. A pattern of incrementally slower reaction rates was observed at substituted sites at increasing depth in the pore. We found no state-dependent change in modification rates of P-region residues located in all four domains, and thus no change in aqueous accessibility, between slow- and nonslow-inactivated states. In domains I and IV, it was possible to measure modification rates at residues adjacent to the narrow DEKA selectivity filter (Y401C and G1530C), and yet no change was observed in accessibility in either slow- or nonslow-inactivated states. We interpret these results as evidence that the outer mouth of the Na pore remains open while the channel is slow inactivated.
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