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Titolo:
EFFECTS OF GLUCOSE DEPRIVATION, CHEMICAL HYPOXIA, AND SIMULATED ISCHEMIA ON NA-CORD ASTROCYTES( HOMEOSTASIS IN RAT SPINAL)
Autore:
ROSE CR; WAXMAN SG; RANSOM BR;
Indirizzi:
UNIV SAARLAND,INST PHYSIOL 1 D-66421 HOMBURG GERMANY VET ADM MED CTR,NEUROSCI RES CTR W HAVEN CT 06516 YALE UNIV,SCH MED,DEPT NEUROL NEW HAVEN CT 06520 UNIV WASHINGTON,SCH MED,DEPT NEUROL SEATTLE WA 98195
Titolo Testata:
The Journal of neuroscience
fascicolo: 10, volume: 18, anno: 1998,
pagine: 3554 - 3562
SICI:
0270-6474(1998)18:10<3554:EOGDCH>2.0.ZU;2-Q
Fonte:
ISI
Lingua:
ENG
Soggetto:
NERVE MYELINATED AXONS; SODIUM-CALCIUM EXCHANGE; CNS WHITE MATTER; IN-VITRO ANOXIA; CULTURED ASTROCYTES; HIPPOCAMPAL ASTROCYTES; INTRACELLULAR CALCIUM; CORTICAL ASTROCYTES; NA+-CA2+ EXCHANGER; SECONDARY INJURY;
Keywords:
GLIA; HYPOGLYCEMIA; ANOXIA; SODIUM-BINDING BENZOFURAN ISOPHTHALATE; NA+/K+-ATPASE; KAINATE; EXCITOTOXICITY;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
64
Recensione:
Indirizzi per estratti:
Citazione:
C.R. Rose et al., "EFFECTS OF GLUCOSE DEPRIVATION, CHEMICAL HYPOXIA, AND SIMULATED ISCHEMIA ON NA-CORD ASTROCYTES( HOMEOSTASIS IN RAT SPINAL)", The Journal of neuroscience, 18(10), 1998, pp. 3554-3562

Abstract

A steep inwardly directed Na+ gradient is essential for glial functions such as glutamate reuptake and regulation of intracellular ion concentrations, We investigated the effects of glucose deprivation, chemical hypoxia, and simulated ischemia on intracellular Na+ concentration ([Na+](i)) in cultured spinal cord astrocytes using fluorescence ratioimaging with sodium binding benzofuran isophthalate (SBFI) AM. Glucose removal or chemical hypoxia (induced by 10 mM NaN3) for 60 min increased [Na+](i) from a baseline of 8.3 to 11 mM. Combined glycolytic andrespiratory blockage by NaN3 and 0 glucose saline caused [Na+](i) to increase by 20 mM, similar to the [Na+](i) increases elicited by blocking the Na+/K+-ATPase with ouabain. Recovery from large [Na+](i) increases (>15 mM) induced by the glutamatergic agonist kainate was attenuated during glucose deprivation or NaN3 application and was blocked in NaN3 and 0 glucose. To mimic in vivo ischemia, we exposed astrocytes to NaN3 and 0 glucose saline containing L-lactate and glutamate with increased [K+] and decreased [Na+], [Ca2+], and pH. This induced an [Na+](i) decrease followed by an [Na+](i) rise and a further [Na+](i) increase after reperfusion with standard saline, Similar multiphasic [Na+](i) changes were observed after NaN3 and 0 glucose saline with only reduced [Na+](e). Our results suggest that the ability to maintain a low[Na+](i) enables spinal cord astrocytes to continue uptake of K+ and/or glutamate at the onset of energy failure. With prolonged energy failure, however, astrocytic [Na+](i) rises with loss of their steep transmembrane Na+ gradient, astrocytes may aggravate metabolic insults by carrier reversal and release of acid, K+, and/or glutamate into the extracellular space.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 13/07/20 alle ore 13:41:50