GlyR alpha3: an essential target for spinal PGE2-mediated inflammatory pain sensitization
| Autor: | Harvey, R J, Depner, U B, Wässle, H, Ahmadi, Seifollah, 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, Hanns Ulrich, Müller, U |
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| Přispěvatelé: | University of Zurich, Betz, H, Rodeau, Jean-Luc, Institut des Neurosciences Cellulaires et Intégratives (INCI), Université Louis Pasteur - Strasbourg I-Centre National de la Recherche Scientifique (CNRS) |
| Rok vydání: | 2004 |
| Předmět: |
1000 Multidisciplinary
570 Life sciences biology 10050 Institute of Pharmacology and Toxicology [SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC] lipids (amino acids peptides and proteins) 610 Medicine & health macromolecular substances [SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC] environment and public health |
| Zdroj: | Science Science, American Association for the Advancement of Science, 2004, 304 (5672), pp.884-887 |
| ISSN: | 0036-8075 1095-9203 |
| DOI: | 10.5167/uzh-874 |
| Popis: | International audience; 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. |
| Databáze: | OpenAIRE |
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