The trafficking of Na(V)1.8

Neurosci Lett. 2010 Dec 10;486(2):78-83. doi: 10.1016/j.neulet.2010.08.074. Epub 2010 Sep 15.

Abstract

The α-subunit of tetrodotoxin-resistant voltage-gated sodium channel Na(V)1.8 is selectively expressed in sensory neurons. It has been reported that Na(V)1.8 is involved in the transmission of nociceptive information from sensory neurons to the central nervous system in nociceptive [1] and neuropathic [24] pain conditions. Thus Na(V)1.8 has been a promising target to treat chronic pain. Here we discuss the recent advances in the study of trafficking mechanism of Na(V)1.8. These pieces of information are particularly important as such trafficking machinery could be new targets for painkillers.

Publication types

  • Review

MeSH terms

  • Adaptor Proteins, Vesicular Transport / physiology
  • Animals
  • Annexin A2 / physiology
  • Cell Adhesion Molecules
  • Cell Membrane / metabolism
  • Contactins / physiology
  • Dinoprostone / physiology
  • Endoplasmic Reticulum / metabolism
  • Humans
  • Mice
  • NAV1.8 Voltage-Gated Sodium Channel
  • Nerve Tissue Proteins / physiology
  • Protein Subunits / metabolism
  • Protein Transport
  • S100 Proteins / physiology
  • Sodium Channels / metabolism*

Substances

  • Adaptor Proteins, Vesicular Transport
  • Annexin A2
  • Cell Adhesion Molecules
  • Contactins
  • NAV1.8 Voltage-Gated Sodium Channel
  • Nerve Tissue Proteins
  • Pdzd2 protein, mouse
  • Protein Subunits
  • S100 Proteins
  • S100 calcium binding protein A10
  • SCN10A protein, human
  • Scn10a protein, mouse
  • Sodium Channels
  • Dinoprostone