GlyR α3: An Essential Target for Spinal PGE 2 -Mediated Inflammatory Pain Sensitization
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- 7 May 2004
- journal article
- other
- Published by American Association for the Advancement of Science (AAAS) in Science
- Vol. 304 (5672) , 884-887
- https://doi.org/10.1126/science.1094925
Abstract
Prostaglandin E2 (PGE2) is a crucial mediator of inflammatory pain sensitization. Here, we demonstrate that inhibition of a specific glycine receptor subtype (GlyR α3) by PGE2-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 PGE2 seen in wild-type mice but also show a reduction in pain sensitization induced by spinal PGE2 injection or peripheral inflammation. Thus, GlyR α3 may provide a previously unrecognized molecular target in pain therapy.Keywords
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