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Titolo:
AMPA/Kainate receptor activation mediates hypoxic oligodendrocyte death and axonal injury in cerebral white matter
Autore:
Tekkok, SB; Goldberg, MP;
Indirizzi:
Washington Univ, Ctr Study Nervous Syst Injury, Dept Neurol, St Louis, MO 63110 USA Washington Univ St Louis MO USA 63110 Dept Neurol, St Louis, MO 63110 USA
Titolo Testata:
JOURNAL OF NEUROSCIENCE
fascicolo: 12, volume: 21, anno: 2001,
pagine: 4237 - 4248
SICI:
0270-6474(20010615)21:12<4237:ARAMHO>2.0.ZU;2-Y
Fonte:
ISI
Lingua:
ENG
Soggetto:
RAT OPTIC-NERVE; ANOXIC INJURY; GLIAL-CELLS; GLUTAMATE RECEPTORS; MONOCLONAL-ANTIBODIES; EXTRACELLULAR CALCIUM; NA+-CA2+ EXCHANGER; CORPUS-CALLOSUM; AMPA RECEPTORS; ISCHEMIA;
Keywords:
oligodendrocyte; white matter injury; AMPA/kainate receptors; axonal injury; brain slices; compound action potential; ischemia; glutamate;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
62
Recensione:
Indirizzi per estratti:
Indirizzo: Goldberg, MP Washington Univ, Ctr Study Nervous Syst Injury, Dept Neurol, Campus Box 8111,660 S Euclid St, St Louis, MO 63110 USA Washington Univ Campus Box 8111,660 S Euclid St St Louis MO USA 63110
Citazione:
S.B. Tekkok e M.P. Goldberg, "AMPA/Kainate receptor activation mediates hypoxic oligodendrocyte death and axonal injury in cerebral white matter", J NEUROSC, 21(12), 2001, pp. 4237-4248

Abstract

We developed an in situ model to investigate the hypothesis that AMPA/kainate (AMPA/KA) receptor activation contributes to hypoxic-ischemic white matter injury in the adult brain. Acute coronal brain slices, including corpuscallosum, were prepared from adult mice. After exposure to transient oxygen and glucose deprivation (OGD), white matter injury was assessed by electrophysiology and immunofluorescence for oligodendrocytes and axonal neurofilaments. White matter cellular components and the stimulus-evoked compound action potential (CAP) remained stable for 12 hr after preparation. OGD for 30 min resulted in an irreversible loss of the CAP as well as structural disruption of axons and subsequent loss of neurofilament immunofluorescence. OGD also caused widespread oligodendrocyte death, demonstrated by the loss of APC labeling and the gain of pyknotic nuclear morphology and propidium iodide labeling. Blockade of AMPA/KA receptors with 30 muM NBQX or the AMPA-selective antagonist 30 mM GYKI 52466 prevented OGD-induced oligodendrocytedeath. Oligodendrocytes also were preserved by the removal of Ca2+, but not by a blockade of voltage-gated Na+ channels. The protective action of NBQX was still present in isolated corpus callosum slices. CAP areas and axonal structure were preserved by Ca2+ removal and partially protected by a blockade of voltage-gated Na+ channels. NBQX prevented OGD-induced CAP loss and preserved axonal structure. These observations highlight convergent pathways leading to hypoxic-ischemic damage of cerebral white matter. In accordance with previous suggestions, the activation of voltage-gated Na+ channelscontributes to axonal damage. Overactivation of glial AMPA/KA receptors leads to oligodendrocyte death and also plays an important role in structuraland functional disruption of axons.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/06/20 alle ore 01:06:47