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Titolo:
ENDOTHELIN EVOKES EFFLUX OF GLUTAMATE IN CULTURES OF RAT ASTROCYTES
Autore:
SASAKI Y; TAKIMOTO M; ODA K; FRUH T; TAKAI M; OKADA T; HORI S;
Indirizzi:
CIBA GEIGY LTD,INT RES LABS TAKARAZUKA HYOGO 665 JAPAN CIBA GEIGY LTD,INT RES LABS TAKARAZUKA HYOGO 665 JAPAN
Titolo Testata:
Journal of neurochemistry
fascicolo: 5, volume: 68, anno: 1997,
pagine: 2194 - 2200
SICI:
0022-3042(1997)68:5<2194:EEEOGI>2.0.ZU;2-Y
Fonte:
ISI
Lingua:
ENG
Soggetto:
TRANSPORTER; RECEPTOR; EXPRESSION; CLONING; SUBTYPES; POTENT; NEUROTRANSMITTER; ANTAGONISTS; ASPARTATE; RELEASE;
Keywords:
BRAIN ISCHEMIA; NEURONAL CELL DEATH; GLUTAMATE TRANSPORTER; IRL 2500; IRL 1620;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
31
Recensione:
Indirizzi per estratti:
Citazione:
Y. Sasaki et al., "ENDOTHELIN EVOKES EFFLUX OF GLUTAMATE IN CULTURES OF RAT ASTROCYTES", Journal of neurochemistry, 68(5), 1997, pp. 2194-2200

Abstract

Excessive release of glutamate, from glial cells as well as neurons, is thought to be a major cause of neuronal death in ischemia. To investigate glutamate release from glial cells, we measured glutamate efflux from cultures of rat astrocytes preloaded with L-[H-3]-glutamate. Glutamate efflux was induced by either 60 mM KCl or Na+-free medium, suggesting that the efflux is due to the reversed operation of a Na+- andK+-coupled glutamate uptake machinery. While investigating various neuropeptides and neurotransmitters, we found that endothelin (ET) specifically induced efflux of glutamate. Northern blot analysis and binding study showed that the ET type B receptor (ETB-R) subtype was expressed two to three times more densely than the ET type A receptor (ETA-R)in astrocytes. The ETA-R antagonist IRL 2500 partially inhibited efflux of glutamate induced by 1 nM ET-1 in a concentration-dependent manner, causing a maximal inhibition of 60% at 1 mu M. However, the ETA-R antagonist BQ-123 did not cause significant inhibition even at 10 mu M. Combination of both antagonists completely inhibited the ET-1-induced efflux. These results indicate that both receptor subtypes are involved in efflux of glutamate with a major contribution from the ETA-R. Our findings suggest that ET, which is known to be released in ischemia, may exacerbate neurodegeneration by stimulating efflux of glutamate.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 10/07/20 alle ore 15:26:31