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Titolo:
Chronic mitochondrial inhibition induces glutamate-mediated corticomotoneuron death in an organotypic culture model
Autore:
Van Westerlaak, MGH; Joosten, EAJ; Gribnau, AAM; Cools, AR; Bar, PR;
Indirizzi:
UMC Utrecht, RMI Neurosci, Dept Expt Neurol, NL-3508 GA Utrecht, Netherlands UMC Utrecht Utrecht Netherlands NL-3508 GA -3508 GA Utrecht, Netherlands Univ Nijmegen, Dept Anat & Embryol, Nijmegen, Netherlands Univ Nijmegen Nijmegen Netherlands nat & Embryol, Nijmegen, Netherlands Univ Nijmegen, Dept Psychoneuropharmacol, Nijmegen, Netherlands Univ Nijmegen Nijmegen Netherlands europharmacol, Nijmegen, Netherlands
Titolo Testata:
EXPERIMENTAL NEUROLOGY
fascicolo: 2, volume: 167, anno: 2001,
pagine: 393 - 400
SICI:
0014-4886(200102)167:2<393:CMIIGC>2.0.ZU;2-U
Fonte:
ISI
Lingua:
ENG
Soggetto:
AMYOTROPHIC-LATERAL-SCLEROSIS; RAT CORTICOSPINAL NEURONS; CALCIUM-BINDING PROTEINS; ELECTRON-TRANSPORT CHAIN; NEURODEGENERATIVE DISEASES; IN-VITRO; ALZHEIMERS-DISEASE; SUPEROXIDE-DISMUTASE; MONOCLONAL-ANTIBODY; NEOCORTEX EXPLANTS;
Keywords:
corticomotoneurons; organotypic; long-term culture; SMI-32; malonate; glutamate; neurodegeneration; ALS; rat;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
56
Recensione:
Indirizzi per estratti:
Indirizzo: Van Westerlaak, MGH Dept Neurol, Room G02320,POBN 85500, NL-3508 GA Utrecht, Netherlands Dept Neurol Room G02320,POBN 85500 Utrecht Netherlands NL-3508 GA
Citazione:
M.G.H. Van Westerlaak et al., "Chronic mitochondrial inhibition induces glutamate-mediated corticomotoneuron death in an organotypic culture model", EXP NEUROL, 167(2), 2001, pp. 393-400

Abstract

There is growing evidence that mitochondrial dysfunction is an important factor in a cascade of neurotoxic events as observed during pathogenesis of various neurodegenerative diseases. In the neurodegenerative disease amyotrophic lateral sclerosis (ALS) both spinal and cortical motoneurons degenerate, but in experimental studies most attention so far has been focussed on the spinal motoneurons, In order to study the role of mitochondrial dysfunction in the pathways leading to cortical (upper) motoneuron (CMN) death, a long-term culture system of rat cortical explants was used. CMNs were visualized by immunocytochemical labeling with antibodies directed against nonphosphorylated neurofilament, SMI-32, and for their identification we also used their location in layer V of the explant, their size, and their morphological appearance. In this model the effect of mitochondrial inhibition was studied through chronic malonate treatment. For 2 weeks, low doses of complex II inhibitor malonate were added to the cultures twice a week. The malonate-induced chronic mitochondrial inhibition resulted in a dose-dependent increase of CMN death in the slices. Neuroprotection was achieved with the NMDA antagonist MK-801 and the non-NMDA antagonist CNQX indicating the involvement of glutamate in the malonate-induced CMN death. Furthermore, our data indicate that chronic mitochondrial inhibition results in CMN death, which is mediated by glutamate excitotoxicity via both non-NMDA and NMDA receptors, In this respect the present in vitro approach may act as a model for understanding mechanisms underlying CMN death in ALS. (C) 2001 Academic Press.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 27/01/20 alle ore 02:29:06