GlyR$\alpha3$: An Essential Target for Spinal$PGE_2-Mediated$Inflammatory Pain Sensitization
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$PGE_2-induced$receptor phosphorylation underlies central inflammatory pain sensitization. We show that GlyR$\alpha3$is dist...
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| Veröffentlicht in: | Science (American Association for the Advancement of Science) 2004-05, Vol.304 (5672), p.884-887 |
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| container_title | Science (American Association for the Advancement of Science) |
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| creator | Harvey, Robert J. Depner, Ulrike B. Wässle, Heinz Ahmadi, Seifollah Heindl, Cornelia Reinold, Heiko Smart, Trevor G. Harvey, Kirsten Schütz, Burkhard Abo-Salem, Osama M. Zimmer, Andreas Poisbeau, Pierrick Welzl, Hans Wolfer, David P. Betz, Heinrich Zeilhofer, Hanns Ulrich Müller, Ulrike |
| description | 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$PGE_2-induced$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 PGE2seen in wildtype mice but also show a reduction in pain sensitization induced by spinal PGE2injection or peripheral inflammation. Thus, GlyR$\alpha3$may provide a previously unrecognized molecular target in pain therapy. |
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Here, we demonstrate that inhibition of a specific glycine receptor subtype ($GlyR \alpha3$) by$PGE_2-induced$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 PGE2seen in wildtype mice but also show a reduction in pain sensitization induced by spinal PGE2injection or peripheral inflammation. 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Here, we demonstrate that inhibition of a specific glycine receptor subtype ($GlyR \alpha3$) by$PGE_2-induced$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 PGE2seen in wildtype mice but also show a reduction in pain sensitization induced by spinal PGE2injection or peripheral inflammation. Thus, GlyR$\alpha3$may provide a previously unrecognized molecular target in pain therapy.</description><subject>Circles</subject><subject>Complementary DNA</subject><subject>Inflammation</subject><subject>Mice</subject><subject>Neurons</subject><subject>Neuroscience</subject><subject>Pain</subject><subject>Receptors</subject><subject>Sensitization</subject><subject>Spinal cord</subject><issn>0036-8075</issn><issn>1095-9203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid/><recordid>eNqFy00LgjAcgPERBdnLN-iww67CdGiuW4RZh0DSoyB_cNZkTtl2sU-fh-6dnsOPZ4G8gPLI5yFlS-RRymI_ocdojTbWdpTOxpmHqkxNT1KBGt_AyAmfNU6tFdpJULgE8xIOt4PBxSg1KJJnaR36D9FIcKIhd90q6Htwg5lwDlLjQmgrnfyAk4PeoVULyor9r1t0uKbl5eZ3dj7q0cgezFSzhMWcBewPfwEziz6S</recordid><startdate>20040507</startdate><enddate>20040507</enddate><creator>Harvey, Robert J.</creator><creator>Depner, Ulrike B.</creator><creator>Wässle, Heinz</creator><creator>Ahmadi, Seifollah</creator><creator>Heindl, Cornelia</creator><creator>Reinold, Heiko</creator><creator>Smart, Trevor G.</creator><creator>Harvey, Kirsten</creator><creator>Schütz, Burkhard</creator><creator>Abo-Salem, Osama M.</creator><creator>Zimmer, Andreas</creator><creator>Poisbeau, Pierrick</creator><creator>Welzl, Hans</creator><creator>Wolfer, David P.</creator><creator>Betz, Heinrich</creator><creator>Zeilhofer, Hanns Ulrich</creator><creator>Müller, Ulrike</creator><general>American Association for the Advancement of Science</general><scope/></search><sort><creationdate>20040507</creationdate><title>GlyR$\alpha3$: An Essential Target for Spinal$PGE_2-Mediated$Inflammatory Pain Sensitization</title><author>Harvey, Robert J. ; Depner, Ulrike B. ; Wässle, Heinz ; Ahmadi, Seifollah ; Heindl, Cornelia ; Reinold, Heiko ; Smart, Trevor G. ; Harvey, Kirsten ; Schütz, Burkhard ; Abo-Salem, Osama M. ; Zimmer, Andreas ; Poisbeau, Pierrick ; Welzl, Hans ; Wolfer, David P. ; Betz, Heinrich ; Zeilhofer, Hanns Ulrich ; Müller, Ulrike</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-jstor_primary_38369313</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Circles</topic><topic>Complementary DNA</topic><topic>Inflammation</topic><topic>Mice</topic><topic>Neurons</topic><topic>Neuroscience</topic><topic>Pain</topic><topic>Receptors</topic><topic>Sensitization</topic><topic>Spinal cord</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Harvey, Robert J.</creatorcontrib><creatorcontrib>Depner, Ulrike B.</creatorcontrib><creatorcontrib>Wässle, Heinz</creatorcontrib><creatorcontrib>Ahmadi, Seifollah</creatorcontrib><creatorcontrib>Heindl, Cornelia</creatorcontrib><creatorcontrib>Reinold, Heiko</creatorcontrib><creatorcontrib>Smart, Trevor G.</creatorcontrib><creatorcontrib>Harvey, Kirsten</creatorcontrib><creatorcontrib>Schütz, Burkhard</creatorcontrib><creatorcontrib>Abo-Salem, Osama M.</creatorcontrib><creatorcontrib>Zimmer, Andreas</creatorcontrib><creatorcontrib>Poisbeau, Pierrick</creatorcontrib><creatorcontrib>Welzl, Hans</creatorcontrib><creatorcontrib>Wolfer, David P.</creatorcontrib><creatorcontrib>Betz, Heinrich</creatorcontrib><creatorcontrib>Zeilhofer, Hanns Ulrich</creatorcontrib><creatorcontrib>Müller, Ulrike</creatorcontrib><jtitle>Science (American Association for the Advancement of Science)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Harvey, Robert J.</au><au>Depner, Ulrike B.</au><au>Wässle, Heinz</au><au>Ahmadi, Seifollah</au><au>Heindl, Cornelia</au><au>Reinold, Heiko</au><au>Smart, Trevor G.</au><au>Harvey, Kirsten</au><au>Schütz, Burkhard</au><au>Abo-Salem, Osama M.</au><au>Zimmer, Andreas</au><au>Poisbeau, Pierrick</au><au>Welzl, Hans</au><au>Wolfer, David P.</au><au>Betz, Heinrich</au><au>Zeilhofer, Hanns Ulrich</au><au>Müller, Ulrike</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>GlyR$\alpha3$: An Essential Target for Spinal$PGE_2-Mediated$Inflammatory Pain Sensitization</atitle><jtitle>Science (American Association for the Advancement of Science)</jtitle><date>2004-05-07</date><risdate>2004</risdate><volume>304</volume><issue>5672</issue><spage>884</spage><epage>887</epage><pages>884-887</pages><issn>0036-8075</issn><eissn>1095-9203</eissn><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$PGE_2-induced$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 PGE2seen in wildtype mice but also show a reduction in pain sensitization induced by spinal PGE2injection or peripheral inflammation. Thus, GlyR$\alpha3$may provide a previously unrecognized molecular target in pain therapy.</abstract><pub>American Association for the Advancement of Science</pub></addata></record> |
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| source | JSTOR Archive Collection A-Z Listing; American Association for the Advancement of Science |
| subjects | Circles Complementary DNA Inflammation Mice Neurons Neuroscience Pain Receptors Sensitization Spinal cord |
| title | GlyR$\alpha3$: An Essential Target for Spinal$PGE_2-Mediated$Inflammatory Pain Sensitization |
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