NGF rapidly increases membrane expression of TRPV1 heat-gated ion channels

Xuming Zhang, Jiehong Huang, Peter A. McNaughton*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review


Nociceptors, or pain-sensitive receptors, are unique among sensory receptors in that their sensitivity is increased by noxious stimulation. This process, called sensitization or hyperalgesia, is mediated by a variety of proinflammatory factors, including bradykinin, ATP and NGF, which cause sensitization to noxious heat stimuli by enhancing the membrane current carried by the heat- and capsaicin-gated ion channel, TRPV1. Several different mechanisms for sensitization of TRPV1 have been proposed. Here we show that NGF, acting on the TrkA receptor, activates a signalling pathway in which PI3 kinase plays a crucial early role, with Src kinase as the downstream element which binds to and phosphorylates TRPV1. Phosphorylation of TRPV1 at a single tyrosine residue, Y200, followed by insertion of TRPV1 channels into the surface membrane, explains most of the rapid sensitizing actions of NGF.

Original languageEnglish
Pages (from-to)4211-4223
Number of pages13
JournalEMBO Journal
Issue number24
Publication statusPublished - 21 Dec 2005


  • Membrane trafficking
  • Neurotrophic factor
  • Pain
  • Sensory transduction
  • Tyrosine kinase


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