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


Harvey, R J; Depner, U B; Wässle, H; Ahmadi, S; Heindl, C; Reinold, H; Smart, T G; Harvey, K; Schütz, B; Abo-Salem, O M; Zimmer, A; Poisbeau, P; Welzl, H; Wolfer, D P; Betz, H; Zeilhofer, H U; Müller, U (2004). GlyR alpha3: an essential target for spinal PGE2-mediated inflammatory pain sensitization. Science, 304(5672):884-887.

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.

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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Additional indexing

Item Type:Journal Article, refereed
Communities & Collections:04 Faculty of Medicine > Institute of Pharmacology and Toxicology
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Language:English
Date:7 May 2004
Deposited On:11 Feb 2008 12:19
Last Modified:05 Apr 2016 12:16
Publisher:American Association for the Advancement of Science (AAAS)
ISSN:0036-8075
Additional Information:Authors have permission by AAAS to show PDF
Publisher DOI:https://doi.org/10.1126/science.1094925
PubMed ID:15131310

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