| pubmed-article:11457487 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11457487 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
| pubmed-article:11457487 | lifeskim:mentions | umls-concept:C0038220 | lld:lifeskim |
| pubmed-article:11457487 | lifeskim:mentions | umls-concept:C0521390 | lld:lifeskim |
| pubmed-article:11457487 | lifeskim:mentions | umls-concept:C0332157 | lld:lifeskim |
| pubmed-article:11457487 | lifeskim:mentions | umls-concept:C0013870 | lld:lifeskim |
| pubmed-article:11457487 | lifeskim:mentions | umls-concept:C1292733 | lld:lifeskim |
| pubmed-article:11457487 | pubmed:issue | 1-2 | lld:pubmed |
| pubmed-article:11457487 | pubmed:dateCreated | 2001-7-17 | lld:pubmed |
| pubmed-article:11457487 | pubmed:abstractText | In the aftermath of prolonged continuous seizure activity (status epilepticus, SE), neuronal cell death occurs in the brain regions through which the seizure propagates. The vulnerability to adrenalectomy-induced apoptotic neuronal death was recently reported to be reduced by prior exposure to repeated daily noninjurious electroconvulsive shock (ECS). The present studies identified apoptosis and apoptosis-associated gene products in the neurodegenerative response to experimentally controlled periods (1 or 2 h) of SE in the rat, and determined whether exposure to ECS can interrupt these apoptotic responses mechanisms. Internucleosomal DNA fragmentation and the presence of apoptotic-like neurons (as assessed by in situ double labeling technique) was detected in hippocampus and rhinal cortex at 24 h after SE. Under these conditions, levels of both mRNA and protein encoded by the 'death promoting' bcl-XS gene were increased in the same brain areas. Pretreatment of animals for 7 days with low intensity (minimal) ECS conferred resistance to SE-evoked neurodegeneration, as assessed histopathologically by silver staining. Associated with this neuroprotective action was a reduction in the incidence of apoptosis-like neuronal morphology and DNA fragmentation, and a prevention of the increase in Bcl-XS protein and mRNA in hippocampus and rhinal cortex. These data suggest that pre-exposure to controlled, brief noninjurious seizures decreases vulnerability to programmed neuronal cell death, that this neuroprotective action occurs upstream from Bcl-XS, and that increases in bcl-XS gene expression may serve as a sensitive indicator of neurodegeneration following SE. | lld:pubmed |
| pubmed-article:11457487 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11457487 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11457487 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11457487 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11457487 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11457487 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:11457487 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11457487 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11457487 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11457487 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11457487 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11457487 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11457487 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11457487 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11457487 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:11457487 | pubmed:issn | 0169-328X | lld:pubmed |
| pubmed-article:11457487 | pubmed:author | pubmed-author:BükyPP | lld:pubmed |
| pubmed-article:11457487 | pubmed:author | pubmed-author:KondratyevAA | lld:pubmed |
| pubmed-article:11457487 | pubmed:author | pubmed-author:SahibzadaNN | lld:pubmed |
| pubmed-article:11457487 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11457487 | pubmed:day | 13 | lld:pubmed |
| pubmed-article:11457487 | pubmed:volume | 91 | lld:pubmed |
| pubmed-article:11457487 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11457487 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11457487 | pubmed:pagination | 1-13 | lld:pubmed |
| pubmed-article:11457487 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:11457487 | pubmed:meshHeading | pubmed-meshheading:11457487... | lld:pubmed |
| pubmed-article:11457487 | pubmed:meshHeading | pubmed-meshheading:11457487... | lld:pubmed |
| pubmed-article:11457487 | pubmed:meshHeading | pubmed-meshheading:11457487... | lld:pubmed |
| pubmed-article:11457487 | pubmed:meshHeading | pubmed-meshheading:11457487... | lld:pubmed |
| pubmed-article:11457487 | pubmed:year | 2001 | lld:pubmed |
| pubmed-article:11457487 | pubmed:articleTitle | Electroconvulsive shock exposure prevents neuronal apoptosis after kainic acid-evoked status epilepticus. | lld:pubmed |
| pubmed-article:11457487 | pubmed:affiliation | Department of Pharmacology, Georgetown University Medical Center, Washington, DC 20007, USA. kondrata@georgetown.edu | lld:pubmed |
| pubmed-article:11457487 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11457487 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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