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Titolo:
PATHOPHYSIOLOGY OF OLIGODENDROGLIAL EXCITOTOXICITY
Autore:
YOSHIOKA A; BACSKAI B; PLEASURE D;
Indirizzi:
CHILDRENS HOSP PHILADELPHIA,DIV NEUROL PHILADELPHIA PA 19104 CHILDRENS HOSP PHILADELPHIA,DIV NEUROL PHILADELPHIA PA 19104 UNIV PENN,DEPT NEUROL & PEDIAT PHILADELPHIA PA 19104
Titolo Testata:
Journal of neuroscience research
fascicolo: 4, volume: 46, anno: 1996,
pagine: 427 - 437
SICI:
0360-4012(1996)46:4<427:POOE>2.0.ZU;2-Z
Fonte:
ISI
Lingua:
ENG
Soggetto:
GLUTAMATE RECEPTOR CHANNELS; CORTICAL NEURONAL INJURY; AMINO-ACID RECEPTORS; CELL-DEATH; MULTIPLE-SCLEROSIS; KAINATE RECEPTORS; AMPA RECEPTORS; GROWTH-FACTOR; WHITE MATTER; GLIAL-CELLS;
Keywords:
APOPTOSIS; GLUTAMATE RECEPTOR; OLIGODENDROGLIA; KAINATE; EXCITOTOXICITY; CYCLOTHIAZIDE; RECEPTOR DESENSITIZATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
59
Recensione:
Indirizzi per estratti:
Citazione:
A. Yoshioka et al., "PATHOPHYSIOLOGY OF OLIGODENDROGLIAL EXCITOTOXICITY", Journal of neuroscience research, 46(4), 1996, pp. 427-437

Abstract

Oligodendrocyte-like cells (OLD) derived from the rat oligodendroglial precursor line, CG-4, express Ca2+-permeable non-methyl-D-aspartate glutamate receptor channels (GluR). Exposure, to kainate, an L-glutamate analogue, markedly elevates OLC Ca2+ influx and cytosolic [Ca2+], and results in damage to both OLC plasma membrane and OLC nuclear DNA. Two observations indicate that kainate-induced OLC internucleosomal DNA nicking is not simply a delayed consequence of cell necrosis: 1) there is no temporal lag between onset of plasma membrane injury and of DNA nicking; and 2) aurintricarboxylic acid, an endonuclease inhibitor,blocks kainate-induced damage to the plasma membrane, N-acetyl-L-cysteine also inhibits OLC kainate injury, suggesting that reactive oxygenspecies participate in OLC excitotoxicity. Kainate-induced OLC Ca2+ influx and excitotoxicity are blocked by alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA), indicating that these kainate effects are mediated by AMPA-GluR, AMPA and L-glutamate fail to elicit OLC damage unless cyclothiazide, an AMPA-GluR desensitization blocker, is present, OLC express both the ''flip'' and ''flop'' forms of GluR2, GluR3, and GluR4 mRNAs, but neither flip nor flop GluR1 mRNA, These data, together with the restriction of the desensitization-blocking activity of cyclothiazide to GluR containing flip-encoded GluR subunits, and the sharply diminished Ca2+ permeability of GluR containing edited GluR2, suggest OLC excitotoxicity is mediated by AMPA-GluR that contain flip GluR3 and/or flip GluR4 protein subunits, but neither flip nor flop GluR2 protein subunits, Rapid desensitization of these GluR is likely to be important in protecting cells of the oligodendroglial lineage from excitotoxicity, (C) 1996 Wiley-Liss, Inc.

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Documento generato il 15/07/20 alle ore 04:06:13