| pubmed-article:9826726 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9826726 | lifeskim:mentions | umls-concept:C0010453 | lld:lifeskim |
| pubmed-article:9826726 | lifeskim:mentions | umls-concept:C0027882 | lld:lifeskim |
| pubmed-article:9826726 | lifeskim:mentions | umls-concept:C0012621 | lld:lifeskim |
| pubmed-article:9826726 | lifeskim:mentions | umls-concept:C0019564 | lld:lifeskim |
| pubmed-article:9826726 | lifeskim:mentions | umls-concept:C0015127 | lld:lifeskim |
| pubmed-article:9826726 | lifeskim:mentions | umls-concept:C0079883 | lld:lifeskim |
| pubmed-article:9826726 | lifeskim:mentions | umls-concept:C1314792 | lld:lifeskim |
| pubmed-article:9826726 | lifeskim:mentions | umls-concept:C0034897 | lld:lifeskim |
| pubmed-article:9826726 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
| pubmed-article:9826726 | lifeskim:mentions | umls-concept:C1160185 | lld:lifeskim |
| pubmed-article:9826726 | lifeskim:mentions | umls-concept:C0205359 | lld:lifeskim |
| pubmed-article:9826726 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
| pubmed-article:9826726 | lifeskim:mentions | umls-concept:C0439590 | lld:lifeskim |
| pubmed-article:9826726 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:9826726 | pubmed:issue | 24 | lld:pubmed |
| pubmed-article:9826726 | pubmed:dateCreated | 1998-12-28 | lld:pubmed |
| pubmed-article:9826726 | pubmed:abstractText | The molecular basis for developing symptomatic epilepsy (epileptogenesis) remains ill defined. We show here in a well characterized hippocampal culture model of epilepsy that the induction of epileptogenesis is Ca2+-dependent. The concentration of intracellular free Ca2+ ([Ca2+]i) was monitored during the induction of epileptogenesis by prolonged electrographic seizure activity induced through low-Mg2+ treatment by confocal laser-scanning fluorescent microscopy to directly correlate changes in [Ca2+]i with alterations in membrane excitability measured by intracellular recording using whole-cell current-clamp techniques. The induction of long-lasting spontaneous recurrent epileptiform discharges, but not the Mg2+-induced spike discharges, was prevented in low-Ca2+ solutions and was dependent on activation of the N-methyl-D-aspartate (NMDA) receptor. The results provide direct evidence that prolonged activation of the NMDA-Ca2+ transduction pathway causes a long-lasting plasticity change in hippocampal neurons causing increased excitability leading to the occurrence of spontaneous, recurrent epileptiform discharges. | lld:pubmed |
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| pubmed-article:9826726 | pubmed:language | eng | lld:pubmed |
| pubmed-article:9826726 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9826726 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:9826726 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9826726 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:9826726 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:9826726 | pubmed:author | pubmed-author:DeLorenzoR... | lld:pubmed |
| pubmed-article:9826726 | pubmed:author | pubmed-author:PalSS | lld:pubmed |
| pubmed-article:9826726 | pubmed:author | pubmed-author:SombatiSS | lld:pubmed |
| pubmed-article:9826726 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9826726 | pubmed:day | 24 | lld:pubmed |
| pubmed-article:9826726 | pubmed:volume | 95 | lld:pubmed |
| pubmed-article:9826726 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9826726 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9826726 | pubmed:pagination | 14482-7 | lld:pubmed |
| pubmed-article:9826726 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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