ArticleThe Journal of general physiology1998
Slow inactivation does not affect movement of the fast inactivation gate in voltage-gated Na+ channels.
Article in The Journal of general physiology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 73 citations in OpenAlex.
- Differential effects of modified batrachotoxins on voltage-gated sodium channel fast and slow inactivation.Cell chemical biology · 2022Article
- Inhibition of Nav1.7 channels by methyl eugenol as a mechanism underlying its antinociceptive and anesthetic actions.Acta pharmacologica Sinica · 2015Article
- Discovery of lacosamide affinity bait agents that exhibit potent voltage-gated sodium channel blocking properties.ACS chemical neuroscience · 2013Article
- Identification of sodium channel isoforms that mediate action potential firing in lamina I/II spinal cord neurons.Molecular pain · 2011Article
- Inhibition of neuronal voltage-gated sodium channels by brilliant blue G.Molecular pharmacology · 2011Article
- Sodium channelopathies of skeletal muscle result from gain or loss of function.Pflugers Archiv : European journal of physiology · 2010Review
- Sodium channels: ionic model of slow inactivation and state-dependent drug binding.Biophysical journal · 2007Article
- Outward stabilization of the S4 segments in domains III and IV enhances lidocaine block of sodium channels.The Journal of physiology · 2007Article
- Voltage-gated sodium channel modulation by scorpion alpha-toxins.Toxicon : official journal of the International Society on Toxinology · 2007Review
- Impaired inactivation gate stabilization predicts increased persistent current for an epilepsy-associated SCN1A mutation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006Article
- Slow sodium channel inactivation and use-dependent block modulated by the same domain IV S6 residue.The Journal of membrane biology · 2005Article
- Rapid protein kinase C-dependent reduction of rat skeletal muscle voltage-gated sodium channels by ciliary neurotrophic factor.The Journal of physiology · 2005Article
- Charge immobilization of the voltage sensor in domain IV is independent of sodium current inactivation.The Journal of physiology · 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
- Role of tetrodotoxin-resistant Na+ current slow inactivation in adaptation of action potential firing in small-diameter dorsal root ganglion neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003Article
- Molecular action of lidocaine on the voltage sensors of sodium channels.The Journal of general physiology · 2003Article
- Slow inactivation does not block the aqueous accessibility to the outer pore of voltage-gated Na channels.The Journal of general physiology · 2002Article
- Movement and crevices around a sodium channel S3 segment.The Journal of general physiology · 2002Article
- Cocaine binds to a common site on open and inactivated human heart (Na(v)1.5) sodium channels.The Journal of physiology · 2002Article
- Role of the C-terminal domain in inactivation of brain and cardiac sodium channels.Proceedings of the National Academy of Sciences of the United States of America · 2001Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Voltage-gated Na+ channels exhibit two forms of inactivation, one form (fast inactivation) takes effect on the order of milliseconds and the other (slow inactivation) on the order of seconds to minutes. While previous studies have suggested that fast and slow inactivation are structurally independent gating processes, little is known about the relationship between the two. In this study, we probed this relationship by examining the effects of slow inactivation on a conformational marker for fast inactivation, the accessibility of a site on the Na+ channel III-IV linker that is believed to form a part of the fast inactivation particle. When cysteine was substituted for phenylalanine at position 1304 in the rat skeletal muscle sodium channel (microl), application of [2-(trimethylammonium)ethyl]methanethiosulfonate (MTS-ET) to the cytoplasmic face of inside-out patches from Xenopus oocytes injected with F1304C RNA dramatically disrupted fast inactivation and displayed voltage-dependent reaction kinetics that closely paralleled the steady state availability (hinfinity) curve. Based on this observation, the accessibility of cys1304 was used as a conformational marker to probe the position of the fast inactivation gate during the development of and the recovery from slow inactivation. We found that burial of cys1304 is not altered by the onset of slow inactivation, and that recovery of accessibility of cys1304 is not slowed after long (2-10 s) depolarizations. These results suggest that (a) fast and slow inactivation are structurally distinct processes that are not tightly coupled, (b) fast and slow inactivation are not mutually exclusive processes (i.e., sodium channels may be fast- and slow-inactivated simultaneously), and (c) after long depolarizations, recovery from fast inactivation precedes recovery from slow inactivation.
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