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Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-874

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.

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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.

Item Type:Journal Article, refereed
Communities & Collections:04 Faculty of Medicine > Institute of Pharmacology and Toxicology
DDC:570 Life sciences; biology
610 Medicine & health
Language:English
Date:7 May 2004
Deposited On:11 Feb 2008 12:19
Last Modified:27 Nov 2013 19:11
Publisher:American Association for the Advancement of Science (AAAS)
ISSN:0036-8075
Additional Information:Authors have permission by AAAS to show PDF
Publisher DOI:10.1126/science.1094925
PubMed ID:15131310
Citations:Web of Science®. Times Cited: 254
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Scopus®. Citation Count: 286

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