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• W2110107835 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." @default.
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• W2110107835 date "2004-05-07" @default.
• W2110107835 modified "2023-10-09" @default.
• W2110107835 title "GlyR α3: An Essential Target for Spinal PGE ₂ -Mediated Inflammatory Pain Sensitization" @default.
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• W2110107835 doi "https://doi.org/10.1126/science.1094925" @default.
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