| pubmed-article:18678878 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18678878 | lifeskim:mentions | umls-concept:C0270611 | lld:lifeskim |
| pubmed-article:18678878 | lifeskim:mentions | umls-concept:C0064219 | lld:lifeskim |
| pubmed-article:18678878 | lifeskim:mentions | umls-concept:C0080093 | lld:lifeskim |
| pubmed-article:18678878 | lifeskim:mentions | umls-concept:C0282625 | lld:lifeskim |
| pubmed-article:18678878 | lifeskim:mentions | umls-concept:C0475224 | lld:lifeskim |
| pubmed-article:18678878 | lifeskim:mentions | umls-concept:C1519726 | lld:lifeskim |
| pubmed-article:18678878 | lifeskim:mentions | umls-concept:C1514758 | lld:lifeskim |
| pubmed-article:18678878 | lifeskim:mentions | umls-concept:C0598958 | lld:lifeskim |
| pubmed-article:18678878 | lifeskim:mentions | umls-concept:C0442797 | lld:lifeskim |
| pubmed-article:18678878 | lifeskim:mentions | umls-concept:C0127400 | lld:lifeskim |
| pubmed-article:18678878 | pubmed:issue | 43 | lld:pubmed |
| pubmed-article:18678878 | pubmed:dateCreated | 2008-10-20 | lld:pubmed |
| pubmed-article:18678878 | pubmed:abstractText | Previous studies indicate that cerebral ischemia breaks the dynamic balance between excitatory and inhibitory inputs. The neural excitotoxicity induced by ionotropic glutamate receptors gain the upper hand during ischemia-reperfusion. In this paper, we investigate whether GluR5 (glutamate receptor 5)-containing kainate receptor activation could lead to a neuroprotective effect against ischemic brain injury and the related mechanism. The results showed that (RS)-2-amino-3-(3-hydroxy-5-tert-butylisoxazol-4-yl) propanoic acid (ATPA), a selective GluR5 agonist, could suppress Src tyrosine phosphorylation and interactions among N-methyl-D-aspartate (NMDA) receptor subunit 2A (NR2A), postsynaptic density protein 95 (PSD-95), and Src and then decrease NMDA receptor activation through attenuating tyrosine phosphorylation of NR2A and NR2B. More importantly, ATPA had a neuroprotective effect against ischemia-reperfusion-induced neuronal cell death in vivo. However, four separate drugs were found to abolish the effects of ATPA. These were selective GluR5 antagonist NS3763; GluR5 antisense oligodeoxynucleotides; CdCl(2), a broad spectrum blocker of voltage-gated calcium channels; and bicuculline, an antagonist of gamma-aminobutyric acid A (GABA(A)) receptor. GABA(A) receptor agonist muscimol could attenuate Src activation and interactions among NR2A, PSD-95 and Src, resulting the suppression of NMDA receptor tyrosine phosphorylation. Moreover, patch clamp recording proved that the activated GABA(A) receptor could inhibit NMDA receptor-mediated whole-cell currents. Taken together, the results suggest that during ischemia-reperfusion, activated GluR5 may facilitate Ca(2+)-dependent GABA release from interneurons. The released GABA can activate postsynaptic GABA(A) receptors, which then attenuates NMDA receptor tyrosine phosphorylation through inhibiting Src activation and disassembling the signaling module NR2A-PSD-95-Src. The final result of this process is that the pyramidal neurons are rescued from hyperexcitability. | lld:pubmed |
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| pubmed-article:18678878 | pubmed:language | eng | lld:pubmed |
| pubmed-article:18678878 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18678878 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:18678878 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18678878 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:18678878 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:18678878 | pubmed:author | pubmed-author:LiuYongY | lld:pubmed |
| pubmed-article:18678878 | pubmed:author | pubmed-author:MEOLL | lld:pubmed |
| pubmed-article:18678878 | pubmed:author | pubmed-author:ZhangGuang-Yi... | lld:pubmed |
| pubmed-article:18678878 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:18678878 | pubmed:day | 24 | lld:pubmed |
| pubmed-article:18678878 | pubmed:volume | 283 | lld:pubmed |
| pubmed-article:18678878 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18678878 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18678878 | pubmed:pagination | 29355-66 | lld:pubmed |
| pubmed-article:18678878 | pubmed:dateRevised | 2010-9-21 | lld:pubmed |
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