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Titolo:
Kainic acid-induced seizures produce necrotic, not apoptotic, neurons withinternucleosomal DNA cleavage: Implications for programmed cell death mechanisms
Autore:
Fujikawa, DG; Shinmei, SS; Cai, B;
Indirizzi:
VA Greater Los Angeles Healthcare Syst, Expt Neurol Lab, Sepulveda Ambulatory Care Ctr, Sepulveda, CA 91343 USA VA Greater Los Angeles Healthcare Syst Sepulveda CA USA 91343 A 91343 USA VA Greater Los Angeles Healthcare Syst, Expt Neurol Lab, Nursing Home CareUnit, Sepulveda, CA 91343 USA VA Greater Los Angeles Healthcare Syst Sepulveda CA USA 91343 A 91343 USA Univ Calif Los Angeles, Sch Med, Dept Neurol, Los Angeles, CA 90095 USA Univ Calif Los Angeles Los Angeles CA USA 90095 Los Angeles, CA 90095 USA Univ Calif Los Angeles, Sch Med, Brain Res Inst, Los Angeles, CA 90095 USAUniv Calif Los Angeles Los Angeles CA USA 90095 Los Angeles, CA 90095 USA
Titolo Testata:
NEUROSCIENCE
fascicolo: 1, volume: 98, anno: 2000,
pagine: 41 - 53
SICI:
0306-4522(2000)98:1<41:KASPNN>2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
INDUCED STATUS EPILEPTICUS; NMDA RECEPTOR ANTAGONIST; CENTRAL-NERVOUS-SYSTEM; DEVELOPING RAT-BRAIN; ELECTRICAL-STIMULATION; HIPPOCAMPAL-NEURONS; PROTEIN-SYNTHESIS; CAUTIONARY NOTE; PERFORANT PATH; CYCLIN D1;
Keywords:
apoptosis; DNA laddering; necrosis; programmed cell death; status epilepticus; TUNEL;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
69
Recensione:
Indirizzi per estratti:
Indirizzo: Fujikawa, DG VA Greater Los Angeles Healthcare Syst, Expt Neurol Lab, Sepulveda Ambulatory Care Ctr, Sepulveda, CA 91343 USA VA Greater Los Angeles Healthcare Syst Sepulveda CA USA 91343
Citazione:
D.G. Fujikawa et al., "Kainic acid-induced seizures produce necrotic, not apoptotic, neurons withinternucleosomal DNA cleavage: Implications for programmed cell death mechanisms", NEUROSCIENC, 98(1), 2000, pp. 41-53

Abstract

Prolonged seizures (status epilepticus) induced by kainic acid activate programmed cell death mechanisms, and it is believed that kainic acid-inducedstatus epilepticus induces neuronal apoptosis. In order to test this hypothesis, adult rats were subjected to 3-h kainic acid-induced seizures, with 24- or 72-h recovery periods. Neuronal death was assessed by light microscopy with the Hematoxylin and Eosin stain and with in situ terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL stain), by electron microscopy, and by agarose gel electrophoresis of DNA extracted from five vulnerable brain regions. Spontaneous and MK-801-induced apoptotic neurons from retrosplenial cortex of neonatal rats, evaluated by light and electron microscopy, were used as positive controls for apoptosis. Surprisingly, the large chromatin clumps of apoptotic neurons were TUNEL negative, whereas the cytoplasm showed light-to-moderate TUNEL staining, consistent with a lack of identifiable nuclear membranes ultrastructurally, and with intermingling ofnuclear and cytoplasmic contents. Ultrastructurally, the acidophilic neurons produced by kainic acid-induced status epilepticus, identified with Hematoxylin and Eosin stain, were dark, shrunken and necrotic, with pyknotic nuclei containing small, dispersed chromatin clumps, and with cytoplasmic vacuoles, some of which were swollen, disrupted mitochondria. No apoptotic cells were seen. Acidophilic neurons were found in up to 20 of 23 brain regions examined and comprised 10-25% of the total number of neurons examined. A subset of these neurons (<10% of the total number of neurons in five of 23 regions) had TUNEL-positive nuclei 72 h but not 23 h after status epilepticus. Internucleosomal DNA cleavage (DNA "laddering") occurred in the four most damaged brain regions examined by electron microscopy 24 h after SE and the three most damaged regions 72 h after status epilepticus. Our results demonstrate that kainic acid-induced status epilepticus produces neuronal necrosis and not apoptosis in adult rats. The necrotic neurons show nuclear pyknosis, chromatin condensation and DNA laddering. Programmedcell death mechanisms activated by kainic acid-induced status epilepticus occur in neurons which become necrotic and could contribute to necrotic, aswell as apoptotic, neuronal death. Published by Elsevier Science Ltd.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/02/20 alle ore 14:32:39