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

Citation
Rr. Ji et al., Nociceptive-specific activation of ERK in spinal neurons contributes to pain hypersensitivity, NAT NEUROSC, 2(12), 1999, pp. 1114-1119
Citations number
50
Categorie Soggetti
Neurosciences & Behavoir
Journal title
NATURE NEUROSCIENCE
ISSN journal
10976256 → ACNP
Volume
2
Issue
12
Year of publication
1999
Pages
1114 - 1119
Database
ISI
SICI code
1097-6256(199912)2:12<1114:NAOEIS>2.0.ZU;2-W
Abstract
We investigated the involvement of extracellular signal-regulated protein k inases (ERK) within spinal neurons in producing pain hypersensitivity. With in a minute of an intense noxious peripheral or C-fiber electrical stimulus , many phosphoERK-positive neurons were observed, most predominantly in lam ina I and IIo of the ipsilateral dorsal horn. This staining was intensity a nd NMDA receptor dependent. Low-intensity stimuli or A-fiber input had no e ffect. Inhibition of ERK phosphorylation by a MEK inhibitor reduced the sec ond phase of formalin-induced pain behavior, a measure of spinal neuron sen sitization. ERK signaling within the spinal cord is therefore involved in g enerating pain hypersensitivity. Because of its rapid activation, this effe ct probably involves regulation of neuronal excitability without changes in transcription.