glycine receptor alpha3 subunit

05/07/2004 - "GlyR alpha3: an essential target for spinal PGE2-mediated inflammatory pain sensitization."
05/07/2004 - "Thus, GlyR alpha3 may provide a previously unrecognized molecular target in pain therapy."
12/01/2009 - "Using mice older than postnatal day 21, we also characterized the plastic changes in glycinergic transmission resulting from the inactivation of the GlyR alpha3 subunit gene, a key player in inflammatory pain pathways. "
05/07/2004 - "Here, we demonstrate that inhibition of a specific glycine receptor subtype (GlyR alpha3) by PGE2-induced receptor phosphorylation underlies central inflammatory pain sensitization. "
05/07/2004 - "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. "

05/07/2004 - "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. "
01/01/2009 - "These data suggest that apart from its clear role in CFA- and zymosan-induced pain sensitisation, hypersensitivity associated with other models of inflammation, neuropathy and visceral disturbances involves mechanisms other than the EP2 receptor - GlyR alpha3 pathway."
01/01/2009 - "GlyR alpha3 has previously been found to play a critical role in pain hypersensitivity following spinal PGE(2) injection, complete Freund's adjuvant (CFA) and zymosan induced peripheral inflammation. "

12/15/2006 - "We found that EP2-/- mice and GlyR alpha3-/- mice develop thermal and mechanical hyperalgesia in the CCI model indistinguishable from that seen in wild-type mice. "
09/15/2008 - "These results suggest that the glutamate-NO-cGMP-PKG pathway in the spinal cord may be involved in the mechanism of PAF-induced tactile allodynia, and GlyR alpha3 could be a target molecule through which PKG induces allodynia."
09/15/2008 - "pCPT-cGMP, PAF, glutamate and SIN-1 all failed to induce allodynia after the knockdown of GlyR alpha3. "
09/15/2008 - "To identify signalling molecules through which PKG induces allodynia, glycine receptor alpha3 (GlyR alpha3) was knocked down by spinal transfection of siRNA for GlyR alpha3. "
09/15/2008 - "Functional targeting of GlyR alpha3 was suggested by the loss of PGE(2)-induced thermal hyperalgesia and the enhancement of allodynia induced by bicuculline, a GABA(A) receptor antagonist in mice after GlyR alpha3 siRNA treatment. "

12/15/2006 - "Spinal prostaglandin E receptors of the EP2 subtype and the glycine receptor alpha3 subunit, which mediate central inflammatory hyperalgesia, do not contribute to pain after peripheral nerve injury or formalin injection."

12/15/2006 - "To address this question, we have analyzed mice deficient in the EP2 receptor (EP2-/- mice) or in the GlyR alpha3 subunit (GlyR alpha3-/- mice) using the chronic constriction injury (CCI) model of neuropathic pain and the formalin test. "