Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
COMPLEX-I DEFICIENCY WHAT THE MPTP MODEL TEACHES US
Autore:
NICKLAS WJ;
Indirizzi:
UNIV MED & DENT NEW JERSEY,ROBERT WOOD JOHNSON MED SCH,DEPT NEUROL,675 HOES LANE PISCATAWAY NJ 08854
Titolo Testata:
Clinical neuroscience
fascicolo: 2, volume: 2, anno: 1994,
pagine: 151 - 157
SICI:
1065-6766(1994)2:2<151:CDWTMM>2.0.ZU;2-1
Fonte:
ISI
Lingua:
ENG
Soggetto:
1-METHYL-4-PHENYL-1,2,3,6-TETRAHYDROPYRIDINE (MPTP)-INDUCED NEUROTOXICITY; RAT DOPAMINERGIC-NEURONS; D-ASPARTATE ANTAGONISTS; PARKINSONS-DISEASE; 1-METHYL-4-PHENYLPYRIDINIUM ION; EXCITOTOXIC LESIONS; ELECTRON-TRANSPORT; SUBSTANTIA-NIGRA; MITOCHONDRIAL RESPIRATION; MANGANESE NEUROTOXICITY;
Keywords:
MITOCHONDRIAL COMPLEX I ACTIVITY; GENE LESION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
79
Recensione:
Indirizzi per estratti:
Citazione:
W.J. Nicklas, "COMPLEX-I DEFICIENCY WHAT THE MPTP MODEL TEACHES US", Clinical neuroscience, 2(2), 1994, pp. 151-157

Abstract

A major feature in the etiology of Leber's hereditary optic neuropathy (LHON) is inhibition of mitochondrial complex I activity. However, little is known about why this genetic lesion is so tissue-specific. Studies in this laboratory on the cellular mechanisms of neurodegeneration have focused on the propensity of some endogenous and environmentalchemicals to cause neurotoxicity that appears to be associated with disturbances in neuronal energy metabolism and may be mediated by glutamate receptors. Recognition of these processes has not only allowed elaboration of the mechanism of action of these chemicals and suggested a role for them in human disease, but also has furnished useful animalmodels of human neurodegenerative disorders. This report deals with the use of 1-methyl-4-phenyl-1-1,2 3, 6,-tetrahydropyridine (MPTP) and its analogs to produce an important animal model of Parkinson's disease. The mechanism whereby these substances cause cell death may provideinsights into the pathophysiology of Parkinson's disease. The metabolite of MPTP, 1-methyl-4-phenylpyridine, is the true toxin; it apparently acts by blocking mitochondrial complex I activity in the basal ganglia after selective uptake into the dopaminergic neurons. This model may be important not only as a paradigm for drug testing, but may also help define the etiology of other disorders, including LHON, that involve mitochondrial dysfunction.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/07/20 alle ore 21:23:56