Na+ channel Nav1.9: in search of a gating mechanism

Trends Neurosci. 2003 Feb;26(2):55-7. doi: 10.1016/s0166-2236(02)00030-9.

Abstract

Voltage-gated Na(+) channels play key roles in generating and propagating action potentials. Their gating is believed to rely exclusively on changes in membrane potential. However, recent data from Blum, Kafitz and Konnerth provide direct evidence that the opening of Na(v)1.9, a member of the voltage-gated Na(+) channel family, is mediated by ligand binding rather than by voltage. This is arguably one of the most influential ideas brought to us in the history of the Na(+) channel field.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Brain-Derived Neurotrophic Factor / pharmacology
  • Cell Line
  • Cells, Cultured
  • Cloning, Molecular
  • Electric Conductivity
  • Hippocampus / cytology
  • Hippocampus / drug effects
  • Hippocampus / metabolism
  • Humans
  • Ion Channel Gating / drug effects*
  • Molecular Sequence Data
  • NAV1.9 Voltage-Gated Sodium Channel
  • Nerve Growth Factors / pharmacology*
  • Neuroblastoma
  • Neurons / drug effects
  • Neurons / metabolism
  • Neuropeptides / genetics
  • Neuropeptides / metabolism*
  • RNA, Antisense / genetics
  • RNA, Antisense / metabolism
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Rats
  • Rats, Wistar
  • Receptor, trkB / genetics
  • Receptor, trkB / metabolism
  • Saxitoxin / pharmacology
  • Sodium / metabolism
  • Sodium Channels / genetics
  • Sodium Channels / metabolism*

Substances

  • Brain-Derived Neurotrophic Factor
  • NAV1.9 Voltage-Gated Sodium Channel
  • Nerve Growth Factors
  • Neuropeptides
  • RNA, Antisense
  • RNA, Messenger
  • SCN11A protein, human
  • Scn11a protein, rat
  • Sodium Channels
  • neurotrophin 5
  • Saxitoxin
  • Sodium
  • Receptor, trkB
  • neurotrophin 4