Persistent pain: the contribution of NaV1.9


  • E.S.J. Smith
  • A. Momin


  • Journal of Physiology


  • J Physiol 586 (9): 2249-2250


  • 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.