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

@article{citeulike:3404146, 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.}, author = {Harvey, R. J. and Depner, U. B. and W\"{a}ssle, H. and Ahmadi, S. and Heindl, C. and Reinold, H. and Smart, T. G. and Harvey, K. and Sch\"{u}tz, B. and Abo-Salem, O. M. and Zimmer, A. and Poisbeau, P. and Welzl, H. and Wolfer, D. P. and Betz, H. and Zeilhofer, H. U. and M\"{u}ller, U.}, citeulike-article-id = {3404146}, citeulike-linkout-0 = {http://dx.doi.org/10.1126/science.1094925}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/15131310}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=15131310}, day = {7}, doi = {10.1126/science.1094925}, issn = {1095-9203}, journal = {Science (New York, N.Y.)}, keywords = {glycin-receptor}, month = {May}, number = {5672}, pages = {884--887}, posted-at = {2008-10-14 12:50:37}, priority = {2}, title = {GlyR alpha3: an essential target for spinal PGE2-mediated inflammatory pain sensitization.}, url = {http://dx.doi.org/10.1126/science.1094925}, volume = {304}, year = {2004} }

TY - JOUR ID - citeulike:3404146 L3 - citeulike-article-id:3404146 N2 - 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. IS - 5672 JF - Science (New York, N.Y.) SN - 1095-9203 EP - 887 TI - GlyR alpha3: an essential target for spinal PGE2-mediated inflammatory pain sensitization. VL - 304 SP - 884 KW - glycin-receptor AU - Harvey, RJ AU - Depner, UB AU - Wässle, H AU - Ahmadi, S AU - Heindl, C AU - Reinold, H AU - Smart, TG AU - Harvey, K AU - Schütz, B AU - Abo-Salem, OM AU - Zimmer, A AU - Poisbeau, P AU - Welzl, H AU - Wolfer, DP AU - Betz, H AU - Zeilhofer, HU AU - Müller, U PY - 2004/05/07/ UR - http://dx.doi.org/10.1126/science.1094925 ER -