ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2000
Facilitation of recovery from inactivation by external Na+ and location of the activation gate in neuronal Na+ channels.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- Structural and functional mechanisms underlying activation gate dynamics and IFM motif accessibility in human NaNature communications · 2026Article
- Article
- Fluorine-19 NMR and computational quantification of isoflurane binding to the voltage-gated sodium channel NaChBac.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- The Biophysical Basis Underlying Gating Changes in the p.V1316A Mutant Nav1.7 Channel and the Molecular Pathogenesis of Inherited Erythromelalgia.PLoS biology · 2016Article
- Exploring volatile general anesthetic binding to a closed membrane-bound bacterial voltage-gated sodium channel via computation.PLoS computational biology · 2013Article
- Hinge-bending motions in the pore domain of a bacterial voltage-gated sodium channel.Biochimica et biophysica acta · 2012Article
- Extracellular sodium modulates the excitability of cultured hippocampal pyramidal cells.Brain research · 2011Article
- Gating behaviour of sodium currents in adult mouse muscle recorded with an improved two-electrode voltage clamp.The Journal of physiology · 2011Article
- Capillary endothelial Na(+), K(+), ATPase transporter homeostasis and a new theory for migraine pathophysiology.Headache · 2010Review
- Cerebrospinal fluid sodium rhythms.Cerebrospinal fluid research · 2010Article
- The activation gate and gating mechanism of the NMDA receptor.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
- Subunit dependence of Na channel slow inactivation and open channel block in cerebellar neurons.Biophysical journal · 2007Article
- Dopamine receptor activation can reduce voltage-gated Na+ current by modulating both entry into and recovery from inactivation.Journal of neurophysiology · 2004Article
- Block of tetrodotoxin-resistant Na+ channel pore by multivalent cations: gating modification and Na+ flow dependence.The Journal of general physiology · 2004Article
- Sodium along with low-threshold potassium currents enhance coincidence detection of subthreshold noisy signals in MSO neurons.Journal of neurophysiology · 2004Article
- Inactivation of BK channels by the NH2 terminus of the beta2 auxiliary subunit: an essential role of a terminal peptide segment of three hydrophobic residues.The Journal of general physiology · 2003Article
- Outer and central charged residues in DIVS4 of skeletal muscle sodium channels have differing roles in deactivation.Biophysical journal · 2002Article
- Recovery from inactivation of t-type ca2+ channels in rat thalamic neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2001Article
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fast inactivation of the Na(+) channel presumably is produced by binding of the inactivating peptide (the "hinged lid") to the internal pore mouth of the activated channel. It has been shown that recovery from inactivation in Na(+) channels begins with a delay, which corresponds to deactivation of the channel, and is then followed by an exponential phase, which corresponds to unbinding of the inactivating peptide. We found that the exponential phase is approximately 1.6-fold faster in 150 mm than in 0 mm external Na(+), but the initial delays are the same. External Na(+) also increases the late steady-state Na(+) current during a step depolarization and shifts the inactivation curve accordingly but has no effect on the activation and deactivation kinetics of the current. Quantitative analysis of the data reveals that external Na(+) has the same facilitation effect on the unbinding of the bound inactivating peptide whether the channel is activated or deactivated but has no effect on the other gating processes of the channel. These findings suggest that permeating Na(+) ions directly knock off the bound inactivating peptide and that channel activation or deactivation does not affect the accessibility of the bound inactivation peptide to external Na(+). The activation gate (the key gating change transforming a Na(+)-nonconducting pore into a Na(+)-conducting one) therefore should not be located external to the inactivation gate, which presumably is already located close to the internal end of the pore.
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10908601PMC6772556What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.