ArticleBritish journal of pharmacology2011
Lidocaine reduces the transition to slow inactivation in Na(v)1.7 voltage-gated sodium channels.
Article in British journal of pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 45 citations in OpenAlex.
- Peptide-Based Approaches for Pain Relief and Healing in Wounds.International journal of molecular sciences · 2026Review
- Changes in the skeletal muscle transcriptome due to the intramuscular administration of lidocaine in wether lambs.Journal of animal science · 2025Article
- Molecular determinants of resurgent sodium currents mediated by Navβ4 peptide and A-type FHFs.Frontiers in molecular neuroscience · 2024Article
- Cold and warmth intensify pain-linked sodium channel gating effects and persistent currents.The Journal of general physiology · 2023Article
- Naphthylisoquinoline alkaloids, a new structural template inhibitor of Nav1.7 sodium channel.Acta pharmacologica Sinica · 2023Article
- Iontophoresis on Porcine and Human Gingiva.Pharmaceutical research · 2023Article
- Assessment of potassium ion channel during electric signalling in biofilm formation ofHeliyon · 2023Article
- A novel definition and treatment of hyperinflammation in COVID-19 based on purinergic signalling.Purinergic signalling · 2022Review
- Topical Treatments and Their Molecular/Cellular Mechanisms in Patients with Peripheral Neuropathic Pain-Narrative Review.Pharmaceutics · 2021Review
- Touch inhibits touch: sanshool-induced paradoxical tingling reveals perceptual interaction between somatosensory submodalities.Proceedings. Biological sciences · 2021Article
- Lacosamide Inhibition of NaFrontiers in pharmacology · 2021Article
- Lidocaine Binding Enhances Inhibition of Nav1.7 Channels by the Sulfonamide PF-05089771.Molecular pharmacology · 2020Article
- A Potential Mechanism of Sodium Channel Mediating the General Anesthesia Induced by Propofol.Frontiers in cellular neuroscience · 2020Article
- Comparison of permeation mechanisms in sodium-selective ion channels.Neuroscience letters · 2019Review
- Article
- The gravity dependence of pharmacodynamics: the integration of lidocaine into membranes in microgravity.NPJ microgravity · 2019Article
- Enhancing inactivation rather than reducing activation of Nav1.7 channels by a clinically effective analgesic CNV1014802.Acta pharmacologica Sinica · 2018Article
- Discovery and hit-to-lead evaluation of piperazine amides as selective, state-dependent NaMedChemComm · 2017Article
- Lacosamide Inhibition of Nav1.7 Voltage-Gated Sodium Channels: Slow Binding to Fast-Inactivated States.Molecular pharmacology · 2017Article
- Sodium channel slow inactivation interferes with open channel block.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
background and purposeThe primary use of local anaesthetics is to prevent or relieve pain by reversibly preventing action potential propagation through the inhibition of voltage-gated sodium channels. The tetrodotoxin-sensitive voltage-gated sodium channel subtype Na(v)1.7, abundantly expressed in pain-sensing neurons, plays a crucial role in perception and transmission of painful stimuli and in inherited chronic pain syndromes. Understanding the interaction of lidocaine with Na(v)1.7 channels could provide valuable insight into the drug's action in alleviating pain in distinct patient populations. The aim of this study was to determine how lidocaine interacts with multiple inactivated conformations of Na(v)1.7 channels. EXPERIMENTAL APPROACH: We investigated the interactions of lidocaine with wild-type Na(v)1.7 channels and a paroxysmal extreme pain disorder mutation (I1461T) that destabilizes fast inactivation. Whole cell patch clamp recordings were used to examine the activity of channels expressed in human embryonic kidney 293 cells. KEY
resultsDepolarizing pulses that increased slow inactivation of Na(v)1.7 channels also reduced lidocaine inhibition. Lidocaine enhanced recovery of Na(v)1.7 channels from prolonged depolarizing pulses by decreasing slow inactivation. A paroxysmal extreme pain disorder mutation that destabilizes fast inactivation of Na(v)1.7 channels decreased lidocaine inhibition. CONCLUSIONS AND IMPLICATIONS: Lidocaine decreased the transition of Na(v)1.7 channels to the slow inactivated state. The fast inactivation gate (domain III-IV linker) is important for potentiating the interaction of lidocaine with the Na(v)1.7 channel.
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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.