ArticleThe Journal of physiology2000
Lidocaine induces a slow inactivated state in rat skeletal muscle sodium channels.
Article in The Journal of physiology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 67 citations in OpenAlex.
- Sodium Channels and Local Anesthetics-Old Friends With New Perspectives.Frontiers in pharmacology · 2022Review
- Comparison of permeation mechanisms in sodium-selective ion channels.Neuroscience letters · 2019Review
- Structural basis for antiarrhythmic drug interactions with the human cardiac sodium channel.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Isoflurane modulates activation and inactivation gating of the prokaryotic NaThe Journal of general physiology · 2017Article
- The hitchhiker's guide to the voltage-gated sodium channel galaxy.The Journal of general physiology · 2016Review
- Understanding Sodium Channel Function and Modulation Using Atomistic Simulations of Bacterial Channel Structures.Current topics in membranes · 2016Article
- Comparison of Gating Properties and Use-Dependent Block of Nav1.5 and Nav1.7 Channels by Anti-Arrhythmics Mexiletine and Lidocaine.PloS one · 2015Article
- Local anesthetic and antiepileptic drug access and binding to a bacterial voltage-gated sodium channel.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Ion conduction and conformational flexibility of a bacterial voltage-gated sodium channel.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Article
- Lidocaine reduces the transition to slow inactivation in Na(v)1.7 voltage-gated sodium channels.British journal of pharmacology · 2011Article
- Molecular basis for class Ib anti-arrhythmic inhibition of cardiac sodium channels.Nature communications · 2011Article
- A molecular switch between the outer and the inner vestibules of the voltage-gated Na+ channel.The Journal of biological chemistry · 2010Article
- Fast- or slow-inactivated state preference of Na+ channel inhibitors: a simulation and experimental study.PLoS computational biology · 2010Article
- Structural model for dihydropyridine binding to L-type calcium channels.The Journal of biological chemistry · 2009Article
- Modulation of sodium channel inactivation gating by a novel lactam: implications for seizure suppression in chronic limbic epilepsy.The Journal of pharmacology and experimental therapeutics · 2009Article
- Mechanisms of action of ligands of potential-dependent sodium channels.Neuroscience and behavioral physiology · 2008Article
- Speeding the recovery from ultraslow inactivation of voltage-gated Na+ channels by metal ion binding to the selectivity filter: a foot-on-the-door?Biophysical journal · 2007Article
- 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
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
1. Local anaesthetics such as lidocaine (lignocaine) interact with sodium channels in a manner that is exquisitely sensitive to the voltage-dependent conformational state of the ion channel. When depolarized in the presence of lidocaine, sodium channels assume a long-lived quiescent state. Although studies over the last decade have localized the lidocaine receptor to the inner aspect of the aqueous pore, the mechanistic basis of depolarization-induced 'use-dependent' lidocaine block remains uncertain. 2. Recent studies have shown that lowering the extracellular Na+ concentration ([Na+]o) and mutations in the sodium channel outer P-loop modulate occupancy of a quiescent 'slow' inactivated state with intermediate kinetics (termed IM) that involves structural rearrangements in the outer pore. 3. Site-directed mutagenesis and ion-replacement experiments were performed using voltage-clamped Xenopus oocytes and cultured (HEK-293) cells expressing wild-type and mutant rat skeletal muscle (mu1) sodium channels. 4. Our results show that lowering [Na+]o potentiates use-dependent lidocaine block. The effect of [Na+]o is maintained despite a III-IV linker mutation that partially disrupts fast inactivation (F1304Q). In contrast, the effect of lowering [Na+]o on lidocaine block is reduced by a P-loop mutation (W402A) that limits occupancy of IM. 5. Our findings are consistent with a simple allosteric model where lidocaine binding induces channels to occupy a native slow inactivated state that is inhibited by [Na+]o.
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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.