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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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

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.[1]


  1. NGF rapidly increases membrane expression of TRPV1 heat-gated ion channels. Zhang, X., Huang, J., McNaughton, P.A. EMBO J. (2005) [Pubmed]
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