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Titolo:
Characterization of endogenous amino acid efflux from hippocampal slices during chemically-induced ischemia
Autore:
Djali, S; Dawson, LA;
Indirizzi:
Wyeth Ayerst Res, Neurosci Res, Princeton, NJ 08543 USA Wyeth Ayerst Res Princeton NJ USA 08543 osci Res, Princeton, NJ 08543 USA
Titolo Testata:
NEUROCHEMICAL RESEARCH
fascicolo: 2, volume: 26, anno: 2001,
pagine: 135 - 143
SICI:
0364-3190(200102)26:2<135:COEAAE>2.0.ZU;2-3
Fonte:
ISI
Lingua:
ENG
Soggetto:
RAT CEREBRAL-CORTEX; INDUCED GLUTAMATE RELEASE; CHANNEL BLOCKER; EXTRACELLULAR CONCENTRATIONS; TRANSIENT ISCHEMIA; CHLORIDE CHANNELS; ASPARTATE RELEASE; CALCIUM CHANNELS; NMDA ANTAGONISTS; NERVOUS-SYSTEM;
Keywords:
ischemia; glutamate; aspartate; GABA; hippocampal slice; neuronal; glial/astrocyte; endogenous efflux;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
60
Recensione:
Indirizzi per estratti:
Indirizzo: Dawson, LA Wyeth Ayerst Res, Neurosci Res, CN8000, Princeton, NJ 08543 USAWyeth Ayerst Res CN8000 Princeton NJ USA 08543 on, NJ 08543 USA
Citazione:
S. Djali e L.A. Dawson, "Characterization of endogenous amino acid efflux from hippocampal slices during chemically-induced ischemia", NEUROCHEM R, 26(2), 2001, pp. 135-143

Abstract

Using sodium (NaN3)-induced anoxia plus aglycaemia as a model of chemically-induced ischemia, we have characterized the endogenous release of excitatory and inhibitory amino acids from superfused hippocampal slices. Chemicalischemia produced an azide (1-30 mM) dose-dependent increase in the effluxof glutamate, aspartate and GABA. These increases were attenuated to varying degrees by removal of Ca2+, or the addition of the voltage dependent Na+-channel blocker tetrodotoxin (TTX), the selective Ca2+ channel blockers conotoxin MVIIA, MVIIC, and nifedipine, the NMDA antagonist MK801, the AMPA antagonist GYKI-52466. Similarly, addition of the GLT-1 glutamate transport inhibitor dihydrokainate (DHK) and the anti-estrogen/anion channel blocker tamoxifen also attenuated the efflux of glutamate and GABA. It would therefore appear that the increases in amino acid efflux induced by chemical ischemia originates from both the neuronal pool, via conventional exocytotic release, and glial sources via reversal of the GLT-1 transporter and anion channel regulated cell swelling.

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Documento generato il 18/01/20 alle ore 07:28:01