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Recent advances in voltage-gated sodium channels, their pharmacology, and related diseases

Authors
Journal
Frontiers in Pharmacology
1663-9812
Publisher
Frontiers Media SA
Publication Date
Volume
4
Identifiers
DOI: 10.3389/fphar.2013.00052
Keywords
  • Pharmacology
  • Editorial Article
Disciplines
  • Biology
  • Chemistry
  • Medicine
  • Pharmacology

Abstract

Recent advances in voltage-gated sodium channels, their pharmacology, and related diseases EDITORIAL published: 18 April 2013 doi: 10.3389/fphar.2013.00052 Recent advances in voltage-gated sodium channels, their pharmacology, and related diseases Jean-François Desaphy1*and Mohamed Chahine2 1 Section of Pharmacology, Department of Pharmacy and Drug Sciences, University of Bari – Aldo Moro, Bari, Italy 2 Department of Medicine, Centre de Recherche de l’IUSMQ, Laval University, Québec, QC, Canada *Correspondence: [email protected] Edited by: Philippe Lory, CNRS and University of Montpellier, France Because of their fundamental role in generating electrical impulses in many excitable tissues, sodium channels were among the first voltage-gated ion channels to be extensively investigated. Neurons bathed in a physiological solution containing 150mM sodium ions respond to a threshold electrical stimulus by gener- ating an action potential, whereas such a response is abolished in a Na+-free medium. Since the classic 1952 studies of squid axon sodium conductance, the Hodgkin and Huxley model of sodium channel gating has served as a framework for under- standing the time and voltage-dependent properties of these channels (Hodgkin and Huxley, 1952). The advent of sophisti- cated biochemical and molecular approaches eventually lead to sodium channel purification (Hartshorne and Catterall, 1981) and cloning (Noda et al., 1984). To date nine genes encod- ing voltage-gated sodium channels are found in the human genome. Dysfunction of these channels causes diseases known as sodium channelopathies. In the 1990’s, the term “channelopathy” was first coined to describe skeletal muscle hereditary diseases, including periodic paralysis and myotonia, due to mutations in the SCN4A gene encoding the muscle isoform of voltage-gated sodium channels (Wang et al., 1993). Many of these aspects are reviewed in this special issue dedicated to voltage-gated sodium channels (Simkin and Bendahhou, 201

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