pubmed-article:8713451 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:8713451 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
pubmed-article:8713451 | lifeskim:mentions | umls-concept:C0025914 | lld:lifeskim |
pubmed-article:8713451 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
pubmed-article:8713451 | lifeskim:mentions | umls-concept:C0007776 | lld:lifeskim |
pubmed-article:8713451 | lifeskim:mentions | umls-concept:C0235032 | lld:lifeskim |
pubmed-article:8713451 | lifeskim:mentions | umls-concept:C0022655 | lld:lifeskim |
pubmed-article:8713451 | lifeskim:mentions | umls-concept:C0001613 | lld:lifeskim |
pubmed-article:8713451 | lifeskim:mentions | umls-concept:C0521390 | lld:lifeskim |
pubmed-article:8713451 | lifeskim:mentions | umls-concept:C0079883 | lld:lifeskim |
pubmed-article:8713451 | lifeskim:mentions | umls-concept:C0243046 | lld:lifeskim |
pubmed-article:8713451 | lifeskim:mentions | umls-concept:C1880022 | lld:lifeskim |
pubmed-article:8713451 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:8713451 | pubmed:dateCreated | 1997-2-18 | lld:pubmed |
pubmed-article:8713451 | pubmed:abstractText | Roles and mechanisms of N-methyl-D-aspartate (NMDA) receptors in glutamate neurotoxicity were investigated in cultures of NMDA receptor-deficient cortical neuronal cells. Mutant mice lacking a functional NMDA receptor were generated by gene targeting of the NR1 NMDA receptor subunit. Cortical neuronal cells prepared from wild-type NR1+/+, heterozygous NR1+/- and homozygous mutant NR1-/- mice at 15-17 days of gestation grew indistinguishably from each other. Brief exposures (5 min) of both NR1+/+ and NR1+/- neuronal cells to glutamate or NMDA, but not kainate or alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA), resulted in widespread neuronal degeneration by the following day. In contrast, neither glutamate nor NMDA treatment caused neuronal degeneration in NR1-/- cells, indicating that NMDA receptors are responsible for rapidly triggered glutamate neurotoxicity. The above four compounds were all effective in inducing the death of NR1+/+ and NR1+/- neuronal cells after prolonged exposure (20-24 h). However, NMDA had no neurotoxic effects on NR1-/- cells, although the other three compounds wer neurotoxic with potencies comparable to those for NR1+/+ and NR1+/- cells. The AMPA and kainate receptors are thus sufficient for inducing slowly triggered glutamate neurotoxicity. Brief exposure of a mixed population of NR1+/+ and NR1-/- neuronal cells to NMDA selectively killed the NMDA receptor-expressing cells without any appreciable effects on neighbouring NMDA receptor-deficient cells. This finding further supports a direct and indispensable role for NMDA receptors in NMDA-evoked neuronal cell death. | lld:pubmed |
pubmed-article:8713451 | pubmed:language | eng | lld:pubmed |
pubmed-article:8713451 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8713451 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:8713451 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8713451 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8713451 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8713451 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8713451 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8713451 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8713451 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:8713451 | pubmed:month | Jan | lld:pubmed |
pubmed-article:8713451 | pubmed:issn | 0953-816X | lld:pubmed |
pubmed-article:8713451 | pubmed:author | pubmed-author:NakanishiSS | lld:pubmed |
pubmed-article:8713451 | pubmed:author | pubmed-author:NakaiMM | lld:pubmed |
pubmed-article:8713451 | pubmed:author | pubmed-author:NakamuraKK | lld:pubmed |
pubmed-article:8713451 | pubmed:author | pubmed-author:KatsukiMM | lld:pubmed |
pubmed-article:8713451 | pubmed:author | pubmed-author:NEFFB JBJ | lld:pubmed |
pubmed-article:8713451 | pubmed:author | pubmed-author:TokitaYY | lld:pubmed |
pubmed-article:8713451 | pubmed:author | pubmed-author:BesshoYY | lld:pubmed |
pubmed-article:8713451 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:8713451 | pubmed:volume | 8 | lld:pubmed |
pubmed-article:8713451 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:8713451 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:8713451 | pubmed:pagination | 69-78 | lld:pubmed |
pubmed-article:8713451 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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pubmed-article:8713451 | pubmed:year | 1996 | lld:pubmed |
pubmed-article:8713451 | pubmed:articleTitle | Characterization of excitatory amino acid neurotoxicity in N-methyl-D-aspartate receptor-deficient mouse cortical neuronal cells. | lld:pubmed |
pubmed-article:8713451 | pubmed:affiliation | Institute for Immunology, Kyoto University Faculty of Medicine, Japan. | lld:pubmed |
pubmed-article:8713451 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:8713451 | pubmed:publicationType | Comparative Study | lld:pubmed |
pubmed-article:8713451 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
entrez-gene:14810 | entrezgene:pubmed | pubmed-article:8713451 | lld:entrezgene |