GlyR α3: An Essential Target for Spinal PGE 2 -Mediated Inflammatory Pain Sensitization

Prostaglandin E 2 (PGE 2 ) is a crucial mediator of inflammatory pain sensitization. Here, we demonstrate that inhibition of a specific glycine receptor subtype (GlyR α3) by PGE 2 -induced receptor phosphorylation underlies central inflammatory pain sensitization. We show that GlyR α3 is distinctly...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Science (American Association for the Advancement of Science) 2004-05, Vol.304 (5672), p.884-887
Hauptverfasser: Harvey, Robert J., Depner, Ulrike B., Wässle, Heinz, Ahmadi, Seifollah, Heindl, Cornelia, Reinold, Heiko, Smart, Trevor G., Harvey, Kirsten, Schütz, Burkhard, Abo-Salem, Osama M., Zimmer, Andreas, Poisbeau, Pierrick, Welzl, Hans, Wolfer, David P., Betz, Heinrich, Zeilhofer, Hanns Ulrich, Müller, Ulrike
Format: Artikel
Sprache:eng
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:Prostaglandin E 2 (PGE 2 ) is a crucial mediator of inflammatory pain sensitization. Here, we demonstrate that inhibition of a specific glycine receptor subtype (GlyR α3) by PGE 2 -induced receptor phosphorylation underlies central inflammatory pain sensitization. We show that GlyR α3 is distinctly expressed in superficial layers of the spinal cord dorsal horn. Mice deficient in GlyR α3 not only lack the inhibition of glycinergic neurotransmission by PGE 2 seen in wild-type mice but also show a reduction in pain sensitization induced by spinal PGE 2 injection or peripheral inflammation. Thus, GlyR α3 may provide a previously unrecognized molecular target in pain therapy.
ISSN:0036-8075
1095-9203
DOI:10.1126/science.1094925