Article Dans Une Revue Science Année : 2004

GlyR alpha3: an essential target for spinal PGE2-mediated inflammatory pain sensitization

Trevor G Smart
  • Fonction : Auteur
  • PersonId : 965916
Andreas Zimmer
  • Fonction : Auteur
  • PersonId : 916803
Heinrich Betz
  • Fonction : Auteur
  • PersonId : 897519

Résumé

Prostaglandin E2 (PGE2) is a crucial mediator of inflammatory pain sensitization. Here, we demonstrate that inhibition of a specific glycine receptor subtype (GlyR alpha3) by PGE2-induced receptor phosphorylation underlies central inflammatory pain sensitization. We show that GlyR alpha3 is distinctly expressed in superficial layers of the spinal cord dorsal horn. Mice deficient in GlyR alpha3 not only lack the inhibition of glycinergic neurotransmission by PGE2 seen in wild-type mice but also show a reduction in pain sensitization induced by spinal PGE2 injection or peripheral inflammation. Thus, GlyR alpha3 may provide a previously unrecognized molecular target in pain therapy.

Dates et versions

hal-00142904 , version 1 (23-04-2007)

Identifiants

Citer

Robert J. Harvey, Ulrike B. Depner, Heinz Wässle, Seifollah Ahmadi, Cornelia Heindle, et al.. GlyR alpha3: an essential target for spinal PGE2-mediated inflammatory pain sensitization. Science, 2004, 304 (5672), pp.884-887. ⟨10.1126/science.1094925⟩. ⟨hal-00142904⟩
74 Consultations
0 Téléchargements

Altmetric

Partager

  • More