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GlyR alpha3: an essential target for spinal PGE2-mediated inflammatory pain sensitization

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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Journal articles
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https://hal.archives-ouvertes.fr/hal-00142904
Contributor : Jean-Luc Rodeau <>
Submitted on : Monday, April 23, 2007 - 3:34:38 PM
Last modification on : Thursday, April 23, 2020 - 2:26:33 PM

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  • HAL Id : hal-00142904, version 1

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R.J. Harvey, U.B. Depner, H. Wässle, S. Ahmadi, C. Heindle, et al.. GlyR alpha3: an essential target for spinal PGE2-mediated inflammatory pain sensitization. Science, American Association for the Advancement of Science, 2004, 304 (5672), pp.884-887. ⟨hal-00142904⟩

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