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Sodium channels and pain.

Abstract
Human and mouse genetic studies have led to significant advances in our understanding of the role of voltage-gated sodium channels in pain pathways. In this chapter, we focus on Nav1.7, Nav1.8, Nav1.9 and Nav1.3 and describe the insights gained from the detailed analyses of global and conditional transgenic Nav knockout mice in terms of pain behaviour. The spectrum of human disorders caused by mutations in these channels is also outlined, concluding with a summary of recent progress in the development of selective Nav1.7 inhibitors for the treatment of pain.
AuthorsAbdella M Habib, John N Wood, James J Cox
JournalHandbook of experimental pharmacology (Handb Exp Pharmacol) Vol. 227 Pg. 39-56 ( 2015) ISSN: 0171-2004 [Print] Germany
PMID25846613 (Publication Type: Journal Article, Review)
Chemical References
  • Analgesics
  • NAV1.7 Voltage-Gated Sodium Channel
  • NAV1.9 Voltage-Gated Sodium Channel
  • SCN11A protein, human
  • Sodium Channel Blockers
  • Voltage-Gated Sodium Channels
Topics
  • Analgesics (pharmacology)
  • Animals
  • Erythromelalgia (physiopathology)
  • Humans
  • Mice
  • NAV1.7 Voltage-Gated Sodium Channel (physiology)
  • NAV1.9 Voltage-Gated Sodium Channel (physiology)
  • Pain (drug therapy, physiopathology)
  • Sodium Channel Blockers (therapeutic use)
  • Voltage-Gated Sodium Channels (physiology)

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