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Titolo:
Intracerebral injection of caspase-3 inhibitor prevents neuronal apoptosisafter kainic acid-evoked status epilepticus
Autore:
Kondratyev, A; 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: 2, volume: 75, anno: 2000,
pagine: 216 - 224
SICI:
0169-328X(20000222)75:2<216:IIOCIP>2.0.ZU;2-E
Fonte:
ISI
Lingua:
ENG
Soggetto:
CEREBELLAR GRANULE NEURONS; DEPENDENT PROTEIN-KINASE; PROGRAMMED CELL-DEATH; ICE-LIKE PROTEASE; CYSTEINE PROTEASES; FAMILY PROTEASES; INTERLEUKIN-1-BETA-CONVERTING ENZYME; POLY(ADP-RIBOSE) POLYMERASE; ICE/CED-3 FAMILY; INDUCED SEIZURES;
Keywords:
epilepsy; limbic system; rhinal cortex; caspase-3; neuronal apoptosis; DNA fragmentation;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
46
Recensione:
Indirizzi per estratti:
Indirizzo: Kondratyev, A Georgetown Univ, Med Ctr, Dept Pharmacol, Washington, DC 20007 USA Georgetown Univ Washington DC USA 20007 ngton, DC 20007 USA
Citazione:
A. Kondratyev e K. Gale, "Intracerebral injection of caspase-3 inhibitor prevents neuronal apoptosisafter kainic acid-evoked status epilepticus", MOL BRAIN R, 75(2), 2000, pp. 216-224

Abstract

In the after math of prolonged continuous seizure activity (status epilepticus, SE), neuronal cell death occurs in the brain regions through which the seizure propagates. Recent studies have implicated apoptotic processes inthis seizure-related injury. Because activation of caspase-3-like cysteineproteases plays a crucial role in mammalian neuronal apoptosis, we explored the possibility that activation of caspase-3 is involved in the neuronal apoptotic cell death that occurs in rat brain following SE induced by systemic kainic acid. Caspase-3 activity was determined immunocytochemically using CMI antibodies specific for catalytically active subunit (p17) or the enzyme. We found an induction of caspase-3 activity in rhinal cortex and amygdala at 24 h after SE. To determine whether activation of caspase-3-like proteases is a necessary component of the injury process, we delivered a caspase-3 inhibitor, z-DEVD-fmk, into the lateral ventricle prior to, and following SE. z-DEVD-fmk treatment substantially attenuated apoptotic cell deathafter SE, both in hippocampus and rhinal cortex, as evaluated by analysis of internucleosomal DNA fragmentation and neuronal nuclear morphology. Our findings implicate caspase-3 cysteine protease in the neurodegenerative response to SE and suggest that this degeneration can be attenuated by inhibition of caspase-3-like enzyme activity. (C) 2000 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 19/09/20 alle ore 21:16:15