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Persistent pain: the contribution of NaV1.9

Authors

  • E.S.J. Smith
  • A. Momin

Journal

  • Journal of Physiology

Citation

  • J Physiol 586 (9): 2249-2250

Abstract

  • Sodium channels are crucial to the ability of sensory neurones to fire action potentials. Modulation of these ion channels can cause neurones to become sensitised leading to a state called hyperalgesia. A recent article by Ostman et al. demonstrates that the decreased inflammatory hyperalgesia observed in NaV1.9 knockout mice is due to the lack of upregulation of a persistent sodium current in sensory neurones by GTP-gamma-S. In neurones from wild type mice this upregulation causes a negative shift in sensory neurone threshold activation: sensitisation. This short article reviews the set of experiments that brought about this finding.


DOI

doi:10.1113/jphysiol.2008.152520