Linked Life Data

11457487

Source:http://linkedlifedata.com/resource/pubmed/id/11457487

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2001-7-17
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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0169-328X
pubmed:author
pubmed:issnType
Print
pubmed:day
13
pubmed:volume
91
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1-13
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:11457487-Animals, pubmed-meshheading:11457487-Apoptosis, pubmed-meshheading:11457487-Biological Markers, pubmed-meshheading:11457487-DNA Fragmentation, pubmed-meshheading:11457487-Electroconvulsive Therapy, pubmed-meshheading:11457487-Entorhinal Cortex, pubmed-meshheading:11457487-Excitatory Amino Acid Agonists, pubmed-meshheading:11457487-Gene Expression, pubmed-meshheading:11457487-Hippocampus, pubmed-meshheading:11457487-Kainic Acid, pubmed-meshheading:11457487-Male, pubmed-meshheading:11457487-Nerve Degeneration, pubmed-meshheading:11457487-Neurons, pubmed-meshheading:11457487-Proto-Oncogene Proteins c-bcl-2, pubmed-meshheading:11457487-RNA, Messenger, pubmed-meshheading:11457487-Rats, pubmed-meshheading:11457487-Rats, Sprague-Dawley, pubmed-meshheading:11457487-Status Epilepticus, pubmed-meshheading:11457487-bcl-X Protein
pubmed:year
2001
pubmed:articleTitle
Electroconvulsive shock exposure prevents neuronal apoptosis after kainic acid-evoked status epilepticus.
pubmed:affiliation
Department of Pharmacology, Georgetown University Medical Center, Washington, DC 20007, USA. kondrata@georgetown.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.