Involvement of Na+ channels in pain pathways.
Voltage-dependent Na+ channels in sensory nerves contribute to the control of membrane excitability and underlie action potential generation. Na+ channel subtypes exhibit a neurone-specific and developmentally regulated pattern of expression, and changes in both channel expression and function are caused by disease. Recent evidence implicates specific roles for Na+ channel subtypes Na(v)1.3 and Na(v)1.8 in pain states that are associated with nerve injury and inflammation, respectively. Insight into the role of Na(v)1.8 in pain pathways has been gained by the generation of a null mutant. Although drugs discriminate poorly between subtypes, the molecular diversity of channels and subtype-specific modulation might provide opportunities to target pain pathways selectively.
Baker
M D
MD
Dept. of Biology, Medawar Building, University College London, Gower St., WC1E 6BT, London, UK. mark.baker@ucl.ac.uk
Wood
J N
JN
D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D018685:Anesthetics, Inhalation / Q000494:pharmacology; D000779:Anesthetics, Local / Q000494:pharmacology; D000818:Animals; D006221:Halothane / Q000494:pharmacology; D006801:Humans; D009475:Neurons, Afferent / Q000502:physiology; D010146:Pain / Q000188:drug therapy / Q000503:physiopathology*; D026941:Sodium Channel Blockers; D015222:Sodium Channels / Q000502:physiology*
D018685:Anesthetics, Inhalation; D000779:Anesthetics, Local; D026941:Sodium Channel Blockers; D015222:Sodium Channels; D006221:Halothane