Click here to close
Hello! We notice that you are using Internet Explorer, which is not supported by Xenbase and may cause the site to display incorrectly.
We suggest using a current version of Chrome,
FireFox, or Safari.
Channels (Austin)
2011 Jan 01;51:65-78. doi: 10.4161/chan.5.1.14031.
Show Gene links
Show Anatomy links
Open- and closed-state fast inactivation in sodium channels: differential effects of a site-3 anemone toxin.
Groome J
,
Lehmann-Horn F
,
Holzherr B
.
???displayArticle.abstract???
The role of sodium channel closed-state fast inactivation in membrane excitability is not well understood. We compared open- and closed-state fast inactivation, and the gating charge immobilized during these transitions, in skeletal muscle channel hNa(V)1.4. A significant fraction of total charge movement and its immobilization occurred in the absence of channel opening. Simulated action potentials in skeletal muscle fibers were attenuated when pre-conditioned by sub-threshold depolarization. Anthopleurin A, a site-3 toxin that inhibits gating charge associated with the movement of DIVS4, was used to assess the role of this voltage sensor in closed-state fast inactivation. Anthopleurin elicited opposing effects on the gating mode, kinetics and charge immobilized during open- versus closed-state fast inactivation. This same toxin produced identical effects on recovery of channel availability and remobilization of gating charge, irrespective of route of entry into fast inactivation. Our findings suggest that depolarization promoting entry into fast inactivation from open versus closed states provides access to the IFMT receptor via different rate-limiting conformational translocations of DIVS4.
Aldrich,
A reinterpretation of mammalian sodium channel gating based on single channel recording.
, Pubmed
Aldrich,
A reinterpretation of mammalian sodium channel gating based on single channel recording.
,
Pubmed
Armstrong,
Inactivation of the sodium channel. II. Gating current experiments.
1977,
Pubmed
Armstrong,
Voltage-gated ion channels and electrical excitability.
1998,
Pubmed
Armstrong,
Na channel inactivation from open and closed states.
2006,
Pubmed
Bean,
Sodium channel inactivation in the crayfish giant axon. Must channels open before inactivating?
1981,
Pubmed
Bendahhou,
Characterization of a new sodium channel mutation at arginine 1448 associated with moderate Paramyotonia congenita in humans.
1999,
Pubmed
Campos,
Voltage-dependent displacement of the scorpion toxin Ts3 from sodium channels and its implication on the control of inactivation.
2004,
Pubmed
Campos,
beta-Scorpion toxin modifies gating transitions in all four voltage sensors of the sodium channel.
2007,
Pubmed
,
Xenbase
Campos,
Alpha-scorpion toxin impairs a conformational change that leads to fast inactivation of muscle sodium channels.
2008,
Pubmed
,
Xenbase
Cannon,
Theoretical reconstruction of myotonia and paralysis caused by incomplete inactivation of sodium channels.
1993,
Pubmed
Cannon,
Pathomechanisms in channelopathies of skeletal muscle and brain.
2006,
Pubmed
Catterall,
Voltage-gated ion channels and gating modifier toxins.
2007,
Pubmed
Catterall,
From ionic currents to molecular mechanisms: the structure and function of voltage-gated sodium channels.
2000,
Pubmed
Cestèle,
Voltage sensor-trapping: enhanced activation of sodium channels by beta-scorpion toxin bound to the S3-S4 loop in domain II.
1998,
Pubmed
Cha,
Voltage sensors in domains III and IV, but not I and II, are immobilized by Na+ channel fast inactivation.
1999,
Pubmed
,
Xenbase
Chahine,
Sodium channel mutations in paramyotonia congenita uncouple inactivation from activation.
1994,
Pubmed
Chanda,
Tracking voltage-dependent conformational changes in skeletal muscle sodium channel during activation.
2002,
Pubmed
,
Xenbase
Chen,
Enhancement of closed-state inactivation in long QT syndrome sodium channel mutation DeltaKPQ.
2002,
Pubmed
Chen,
A unique role for the S4 segment of domain 4 in the inactivation of sodium channels.
1996,
Pubmed
,
Xenbase
Chen,
Reduced voltage dependence of inactivation in the SCN5A sodium channel mutation delF1617.
2005,
Pubmed
Cummins,
Nav1.3 sodium channels: rapid repriming and slow closed-state inactivation display quantitative differences after expression in a mammalian cell line and in spinal sensory neurons.
2001,
Pubmed
,
Xenbase
Cummins,
Electrophysiological properties of mutant Nav1.7 sodium channels in a painful inherited neuropathy.
2004,
Pubmed
Filatov,
Resting potential-dependent regulation of the voltage sensitivity of sodium channel gating in rat skeletal muscle in vivo.
2005,
Pubmed
George,
Inherited disorders of voltage-gated sodium channels.
2005,
Pubmed
Groome,
Outer and central charged residues in DIVS4 of skeletal muscle sodium channels have differing roles in deactivation.
2002,
Pubmed
,
Xenbase
Groome,
Central charged residues in DIIIS4 regulate deactivation gating in skeletal muscle sodium channels.
2007,
Pubmed
,
Xenbase
Groome,
Charge immobilization of skeletal muscle Na+ channels: role of residues in the inactivation linker.
2007,
Pubmed
,
Xenbase
Groome,
Differential effects of paramyotonia congenita mutations F1473S and F1705I on sodium channel gating.
2008,
Pubmed
,
Xenbase
HODGKIN,
A quantitative description of membrane current and its application to conduction and excitation in nerve.
1952,
Pubmed
Hanck,
Modification of inactivation in cardiac sodium channels: ionic current studies with Anthopleurin-A toxin.
1995,
Pubmed
Hanck,
Site-3 toxins and cardiac sodium channels.
2007,
Pubmed
Herzog,
Distinct repriming and closed-state inactivation kinetics of Nav1.6 and Nav1.7 sodium channels in mouse spinal sensory neurons.
2003,
Pubmed
Horn,
Immobilizing the moving parts of voltage-gated ion channels.
2000,
Pubmed
Jurkat-Rott,
Muscle channelopathies and critical points in functional and genetic studies.
2005,
Pubmed
Kambouris,
A revised view of cardiac sodium channel "blockade" in the long-QT syndrome.
2000,
Pubmed
,
Xenbase
Khera,
Multiple cationic residues of anthopleurin B that determine high affinity and channel isoform discrimination.
1995,
Pubmed
Kontis,
Sodium channel inactivation is altered by substitution of voltage sensor positive charges.
1997,
Pubmed
,
Xenbase
Kuo,
Na+ channels must deactivate to recover from inactivation.
1994,
Pubmed
Kühn,
Movement of voltage sensor S4 in domain 4 is tightly coupled to sodium channel fast inactivation and gating charge immobilization.
1999,
Pubmed
,
Xenbase
Mohammadi,
Preferred mexiletine block of human sodium channels with IVS4 mutations and its pH-dependence.
2005,
Pubmed
Noda,
Primary structure of Electrophorus electricus sodium channel deduced from cDNA sequence.
,
Pubmed
Nuss,
Isoform-specific lidocaine block of sodium channels explained by differences in gating.
2000,
Pubmed
,
Xenbase
Richard Benzinger,
Augmentation of recovery from inactivation by site-3 Na channel toxins. A single-channel and whole-cell study of persistent currents.
1999,
Pubmed
Rogers,
Molecular determinants of high affinity binding of alpha-scorpion toxin and sea anemone toxin in the S3-S4 extracellular loop in domain IV of the Na+ channel alpha subunit.
1996,
Pubmed
Santarelli,
A cation-pi interaction discriminates among sodium channels that are either sensitive or resistant to tetrodotoxin block.
2007,
Pubmed
,
Xenbase
Sheets,
The role of the putative inactivation lid in sodium channel gating current immobilization.
2000,
Pubmed
Sheets,
Voltage-dependent open-state inactivation of cardiac sodium channels: gating current studies with Anthopleurin-A toxin.
1995,
Pubmed
Sheets,
Optimization of a mammalian expression system for the measurement of sodium channel gating currents.
1996,
Pubmed
Sheets,
Gating of skeletal and cardiac muscle sodium channels in mammalian cells.
1999,
Pubmed
Stühmer,
Structural parts involved in activation and inactivation of the sodium channel.
1989,
Pubmed
,
Xenbase
Vassilev,
Identification of an intracellular peptide segment involved in sodium channel inactivation.
1988,
Pubmed
West,
A cluster of hydrophobic amino acid residues required for fast Na(+)-channel inactivation.
1992,
Pubmed
,
Xenbase
Wu,
A C-terminal skeletal muscle sodium channel mutation associated with myotonia disrupts fast inactivation.
2005,
Pubmed
el-Sherif,
Dose-dependent modulation of the cardiac sodium channel by sea anemone toxin ATXII.
1992,
Pubmed
