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SCN11A variant as possible pain generator in sensory axonal neuropathy

  • Federica GinanneschiEmail author
  • Anna Rubegni
  • Francesca Moro
  • Nila Volpi
  • Filippo Maria Santorelli
  • Alessandro Rossi
Letter to the Editor
  • 82 Downloads

Dear Editor,

Voltage-gated sodium channel (NaV) Nav1.9 is expressed in dorsal root ganglion and their axons and has been shown to play an important role both in regulating sensory neuron excitability and in pain signaling [1]. Heterozygous missense mutations in the SCN11A gene encoding NaV1.9 have been recently described in individuals with painful peripheral neuropathy [2]. It is thought that enhanced NaV channel activity may directly contribute to the pain because some of the missense variants identified depolarize resting membrane potential of dorsal root ganglion neurons through a gain-of-function mechanism, enhance spontaneous firing, and increase evoked firing of these neurons [2]. A recent report on SCN11A variants influencing postoperative pain sensitivity suggests that Nav1.9 can be considered among the main effectors of peripheral inflammatory and neuropathic pain hypersensitivity [1, 3] and should be regarded as an attractive target while searching more effective treatments...

Notes

Compliance with ethical standards

Conflict of interest

The authors declare that they have no conflicts of interest.

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Copyright information

© Fondazione Società Italiana di Neurologia 2019

Authors and Affiliations

  1. 1.Department of Medical, Surgical and Neurological Sciences, Neurology-Neurophysiology UnitUniversity of SienaSienaItaly
  2. 2.Molecular Medicine & NeurogeneticsIRCCS Stella MarisPisaItaly

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