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| pubmed-article:9763481 | lifeskim:mentions | umls-concept:C0175677 | lld:lifeskim |
| pubmed-article:9763481 | lifeskim:mentions | umls-concept:C0521390 | lld:lifeskim |
| pubmed-article:9763481 | lifeskim:mentions | umls-concept:C0449438 | lld:lifeskim |
| pubmed-article:9763481 | lifeskim:mentions | umls-concept:C1527148 | lld:lifeskim |
| pubmed-article:9763481 | lifeskim:mentions | umls-concept:C0449774 | lld:lifeskim |
| pubmed-article:9763481 | lifeskim:mentions | umls-concept:C0443252 | lld:lifeskim |
| pubmed-article:9763481 | lifeskim:mentions | umls-concept:C0686907 | lld:lifeskim |
| pubmed-article:9763481 | pubmed:issue | 20 | lld:pubmed |
| pubmed-article:9763481 | pubmed:dateCreated | 1998-10-23 | lld:pubmed |
| pubmed-article:9763481 | pubmed:abstractText | The lithium-pilocarpine model of status epilepticus (SE) was used to study the type and distribution of seizure-induced neuronal injury in the rat and its consequences during development. Cell death was evaluated in hematoxylin- and eosin-stained sections and by electron microscopy. Damage to the CA1 neurons was maximal in the 2- and 3-week-old pups and decreased as a function of age. On the other hand, damage to the hilar and CA3 neurons was minimal in the 2-week-old rat pups but reached an adult-like pattern in the 3-week-old animals, and damage to amygdalar neurons increased progressively with age. The 3-week-old animals also demonstrated vulnerability of the dentate granule cells. To evaluate neuronal apoptosis, we used terminal deoxynucleotidyl transferase-mediated biotinylated UTP nick end labeling (TUNEL) stain, confocal fluorescence microscopy of ethidium bromide-stained sections, electron microscopy, and DNA electrophoresis. Neurons displaying all of those features of apoptotic death in response to SE were seen in the CA1 region of the 2-week-old pups and in the hilar border of the dentate granule cells of the 3-week-old animals. Some (3/11) of the animals that underwent SE at 2 weeks of age and most of the animals that underwent SE at 3 or 4 weeks of age (8/11 and 6/8, respectively) developed spontaneous seizures later in life; the latter showed SE-induced synaptic reorganization as demonstrated by Timm methodology. These results provide strong evidence for the vulnerability of the immature brain to seizure-induced damage, which bears features of both necrotic and apoptotic death and contributes to synaptic reorganization and the development of chronic epilepsy. | lld:pubmed |
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| pubmed-article:9763481 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:9763481 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:9763481 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9763481 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:9763481 | pubmed:issn | 0270-6474 | lld:pubmed |
| pubmed-article:9763481 | pubmed:author | pubmed-author:ShinD HDH | lld:pubmed |
| pubmed-article:9763481 | pubmed:author | pubmed-author:LiuHH | lld:pubmed |
| pubmed-article:9763481 | pubmed:author | pubmed-author:WasterlainC... | lld:pubmed |
| pubmed-article:9763481 | pubmed:author | pubmed-author:SankarRR | lld:pubmed |
| pubmed-article:9763481 | pubmed:author | pubmed-author:Pereira de... | lld:pubmed |
| pubmed-article:9763481 | pubmed:author | pubmed-author:MazaratiAA | lld:pubmed |
| pubmed-article:9763481 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9763481 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:9763481 | pubmed:volume | 18 | lld:pubmed |
| pubmed-article:9763481 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9763481 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9763481 | pubmed:pagination | 8382-93 | lld:pubmed |
| pubmed-article:9763481 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:9763481 | pubmed:year | 1998 | lld:pubmed |
| pubmed-article:9763481 | pubmed:articleTitle | Patterns of status epilepticus-induced neuronal injury during development and long-term consequences. | lld:pubmed |
| pubmed-article:9763481 | pubmed:affiliation | Department of Neurology, University of California Los Angeles School of Medicine, Los Angeles, California 90095-1752, USA. | lld:pubmed |
| pubmed-article:9763481 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9763481 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:9763481 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
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