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Titolo:
Electroconvulsive shock exposure prevents neuronal apoptosis after kainic acid-evoked status epilepticus
Autore:
Kondratyev, A; Sahibzada, N; Gale, K;
Indirizzi:
Georgetown Univ, Med Ctr, Dept Pharmacol, Washington, DC 20007 USA Georgetown Univ Washington DC USA 20007 armacol, Washington, DC 20007 USA
Titolo Testata:
MOLECULAR BRAIN RESEARCH
fascicolo: 1-2, volume: 91, anno: 2001,
pagine: 1 - 13
SICI:
0169-328X(20010713)91:1-2<1:ESEPNA>2.0.ZU;2-Q
Fonte:
ISI
Lingua:
ENG
Soggetto:
FIBROBLAST GROWTH-FACTOR; TRAUMATIC BRAIN INJURY; PROGRAMMED CELL-DEATH; KAINATE-INDUCED APOPTOSIS; DEEP PREPIRIFORM CORTEX; INDUCED SEIZURES; MESSENGER-RNA; BCL-X; DNA FRAGMENTATION; UP-REGULATION;
Keywords:
epilepsy; seizure; electroconvulsive shock; neuroprotection; apoptosis; gene induction;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
45
Recensione:
Indirizzi per estratti:
Indirizzo: Kondratyev, A Georgetown Univ, Med Ctr, Dept Pharmacol, Res Bldg,Room W217,3970 Reservoir Rd NW, Washington, DC 20007 USA Georgetown Univ Res Bldg,Room W217,3970 Reservoir Rd NW Washington DC USA 20007
Citazione:
A. Kondratyev et al., "Electroconvulsive shock exposure prevents neuronal apoptosis after kainic acid-evoked status epilepticus", MOL BRAIN R, 91(1-2), 2001, pp. 1-13

Abstract

In the aftermath of prolonged continuous seizure activity (status epilepticus. SE), neuronal cell death occurs in the brain regions through which theseizure 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 inthe 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-X-s 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 theincidence of apoptosis-like neuronal morphology and DNA fragmentation, anda prevention of the increase in Bcl-X-s 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-X-s, and that increases in bcl-X-s gene expression may serve as a sensitive indicator of neurodegeneration following SE. (C) 2001 Elsevier Science B.V. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 03/04/20 alle ore 04:01:20