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GlyR alpha3: an essential target for spinal PGE2-mediated inflammatory pain sensitization |
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| Authors: | 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 |
| Institution: | Department of Pharmacology, The School of Pharmacy, London WC1N 1AX, UK. |
| Abstract: | 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. |
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