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Article

Lidocaine reduces the transition to slow inactivation in Na(v)1.7 voltage-gated sodium channels.

British journal of pharmacology - 1 Sept 2011

Sheets Patrick L, Jarecki Brian W, Cummins Theodore R

Abstract excerpt

BACKGROUND AND PURPOSE: The 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...

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Identifiers

PMID: 21232038
DOI: 10.1111/j.1476-5381.2011.01209.x
PMCID: PMC3188891

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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Lidocaine reduces the transition to slow inactivation in Na(v)1.7 voltage-gated sodium channels.PMID 21232038Read ↗

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Depolarized inactivation overcomes impaired activation to produce DRG neuron hyperexcitability in a Nav1.7 mutation in a patient with distal limb pain.Semantic proximity Read ↗

Slow inactivation in voltage-gated sodium channels: molecular substrates and contributions to channelopathies.Semantic proximity Read ↗

Discovery of a Selective, State-Independent Inhibitor of Na <sub>V</sub> 1.7 by Modification of Guanidinium ToxinsSemantic proximity Read ↗

Pharmacology of the Nav1.1 domain IV voltage sensor reveals coupling between inactivation gating processes.Semantic proximity Read ↗

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A Nav1.7 channel mutation associated with hereditary erythromelalgia contributes to neuronal hyperexcitability and displays reduced lidocaine sensitivity.Semantic proximity Read ↗

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