Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
The neuroprotective effects of non-NMDA antagonists in the cerebellum of the spastic Han Wistar mutant
Autore:
Nisim, AA; Hernandez, CM; Cohen, RW;
Indirizzi:
Calif State Univ Northridge, Dept Biol, Northridge, CA 91330 USA Calif State Univ Northridge Northridge CA USA 91330 thridge, CA 91330 USA
Titolo Testata:
DEVELOPMENTAL NEUROSCIENCE
fascicolo: 1, volume: 21, anno: 1999,
pagine: 76 - 86
SICI:
0378-5866(199901/02)21:1<76:TNEONA>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
GLUTAMATE-RECEPTOR CHANNELS; EXCITATORY AMINO-ACIDS; D-ASPARTATE ANTAGONIST; GYKI 52466; HIPPOCAMPAL-NEURONS; CEREBRAL-ISCHEMIA; ION FLOW; RAT; NEUROTOXICITY; CALCIUM;
Keywords:
cerebellum; Purkinje cells; GYKI 52466; CNQX; osmotic pumps;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
47
Recensione:
Indirizzi per estratti:
Indirizzo: Cohen, RW Calif1330te Univ Northridge, Dept Biol, 18111 Nordhoff St, Northridge, CA 9 Calif State Univ Northridge 18111 Nordhoff St Northridge CA USA91330
Citazione:
A.A. Nisim et al., "The neuroprotective effects of non-NMDA antagonists in the cerebellum of the spastic Han Wistar mutant", DEV NEUROSC, 21(1), 1999, pp. 76-86

Abstract

Excitotoxicity resulting from the dysfunction of glutamate receptors has been attributed to neurodegeneration seen in many brain disorders. In our laboratory, the spastic Han Wistar mutant is currently utilized as a potential model of excitotoxicity. The mutant is characterized by progressive neuronal degeneration, hindlimb paresis and ataxia which culminates in the animal's death at approximately 65 days of age. In this study, neuroprotection derived from acute administration of the non-NMDA antagonist GYKI 52466, andchronic administration of the non-NMDA antagonist CNQX was examined in order to determine the potential roles of non-NMDA receptors in the observed neurodegeneration. Mutants injected with GYKI 52466 (15 mg/kg), twice a weekfor 3 weeks, exhibited increased life spans (14%) and extended motor activity than their vehicle-treated mutant siblings. in a separate group of mutants, CNQX (either 50 or 500 mu M) was infused directly into the third ventricle of the mutant's brain utilizing osmotic pumps. A statistically significant increase in motor activity (22%) was detected for mutants treated witha dose of 50 mu M CNQX compared to their vehicle-treated siblings. Finally, cerebellar histological evaluations of mutants treated with both 50 and 500 mu M CNQX showed dose-dependent higher cerebellar Purkinje cell counts. These findings suggest that non-NMDA receptors play a significant role in neurodegeneration in this animal.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 01/04/20 alle ore 23:58:38