GlyR α3: an essential target for spinal PG[E.sub.2]-mediated inflammatory pain sensitization

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

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Bibliographic Details
Published in:Science (American Association for the Advancement of Science) 2004-05, Vol.304 (5672), p.884
Main Authors: Harvey, Robert J, Depner, Ulrike B, Wassle, Heinz, Ahmadi, Seifollah, Heindl, Cornelia, Reinold, Heiko, Smart, Trevor G, Harvey, Kirsten, Schutz, Burkhard, Abo-Salem, Osama M, Zimmer, Andreas, Poisbeau, Pierrick, Welzl, Hans, Wolfer, David P, Betz, Heinrich, Zeilhofer, Hanns Ulrich, Muller, Ulrike
Format: Article
Language:English
Subjects:
Nervous system
Pain
Physiological aspects
Online Access:Get full text
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Summary:Prostaglandin [E.sub.2](PG[E.sub.2]) is a crucial mediator of inflammatory pain sensitization. Here, we demonstrate that inhibition of a specific glycine receptor subtype (GlyR α3) by PG[E.sub.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 PG[E.sub.2] seen in wild-type mice but also show a reduction in pain sensitization induced by spinal PG[E.sub.2] injection or peripheral inflammation. Thus, GlyR α3 may provide a previously unrecognized molecular target in pain therapy.
ISSN:0036-8075
1095-9203