Nociceptive-specific activation of ERK in spinal neurons contributes to pain hypersensitivity.

Journal Article (Journal Article)

We investigated the involvement of extracellular signal-regulated protein kinases (ERK) within spinal neurons in producing pain hypersensitivity. Within a minute of an intense noxious peripheral or C-fiber electrical stimulus, many phosphoERK-positive neurons were observed, most predominantly in lamina I and IIo of the ipsilateral dorsal horn. This staining was intensity and NMDA receptor dependent. Low-intensity stimuli or A-fiber input had no effect. Inhibition of ERK phosphorylation by a MEK inhibitor reduced the second phase of formalin-induced pain behavior, a measure of spinal neuron sensitization. ERK signaling within the spinal cord is therefore involved in generating pain hypersensitivity. Because of its rapid activation, this effect probably involves regulation of neuronal excitability without changes in transcription.

Full Text

Duke Authors

Cited Authors

  • Ji, RR; Baba, H; Brenner, GJ; Woolf, CJ

Published Date

  • December 1999

Published In

Volume / Issue

  • 2 / 12

Start / End Page

  • 1114 - 1119

PubMed ID

  • 10570489

International Standard Serial Number (ISSN)

  • 1097-6256

Digital Object Identifier (DOI)

  • 10.1038/16040


  • eng

Conference Location

  • United States