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      Nav1.7 mutations associated with paroxysmal extreme pain disorder, but not erythromelalgia, enhance Navbeta4 peptide-mediated resurgent sodium currents.

      1 , , ,
      The Journal of physiology
      Wiley

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          Abstract

          Abnormal pain sensitivity associated with inherited and acquired pain disorders occurs through increased excitability of peripheral sensory neurons in part due to changes in the properties of voltage-gated sodium channels (Navs). Resurgent sodium currents (I(NaR)) are atypical currents believed to be associated with increased excitability of neurons and may have implications in pain. Mutations in Nav1.7 (peripheral Nav isoform) associated with two genetic pain disorders, inherited erythromelalgia (IEM) and paroxysmal extreme pain disorder (PEPD), enhance Nav1.7 function via distinct mechanisms. We show that changes in Nav1.7 function due to mutations associated with PEPD, but not IEM, are important in I(NaR) generation, suggesting that I(NaR) may play a role in pain associated with PEPD. This knowledge provides us with a better understanding of the mechanism of I(NaR) generation and may lead to the development of specialized treatment for pain disorders associated with I(NaR).

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          Author and article information

          Journal
          J Physiol
          The Journal of physiology
          Wiley
          1469-7793
          0022-3751
          Feb 01 2011
          : 589
          : Pt 3
          Affiliations
          [1 ] Department of Pharmacology and Toxicology, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
          Article
          jphysiol.2010.200915
          10.1113/jphysiol.2010.200915
          3055545
          21115638
          4a148b5a-ab6f-42bb-992a-9cccdd2ee82d
          History

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