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Titolo:
A quantitative analysis of L-glutamate-regulated Na+ dynamics in mouse cortical astrocytes: implications for cellular bioenergetics
Autore:
Chatton, JY; Marquet, P; Magistretti, PJ;
Indirizzi:
Univ Lausanne, Sch Med, Inst Physiol, CH-1005 Lausanne, Switzerland Univ Lausanne Lausanne Switzerland CH-1005 CH-1005 Lausanne, Switzerland Univ Lausanne, Sch Med, Dept Neurol, Lab Neurol Res, CH-1005 Lausanne, Switzerland Univ Lausanne Lausanne Switzerland CH-1005 CH-1005 Lausanne, Switzerland
Titolo Testata:
EUROPEAN JOURNAL OF NEUROSCIENCE
fascicolo: 11, volume: 12, anno: 2000,
pagine: 3843 - 3853
SICI:
0953-816X(200011)12:11<3843:AQAOLN>2.0.ZU;2-9
Fonte:
ISI
Lingua:
ENG
Soggetto:
RAT HIPPOCAMPAL ASTROCYTES; GLIAL-CELLS; GLUCOSE-METABOLISM; NEURONAL-ACTIVITY; BRAIN; TRANSPORTERS; ENERGY; SODIUM; ASPARTATE; CHANNELS;
Keywords:
Na+ homeostasis; brain energy metabolism; glutamate transport; non-NMDA receptors; Na+/K+ ATPase;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
41
Recensione:
Indirizzi per estratti:
Indirizzo: Chatton, JY Univ Lausanne, Sch Med, Inst Physiol, Rue Bugnon 7, CH-1005 Lausanne, Switzerland Univ Lausanne Rue Bugnon 7 Lausanne Switzerland CH-1005 rland
Citazione:
J.Y. Chatton et al., "A quantitative analysis of L-glutamate-regulated Na+ dynamics in mouse cortical astrocytes: implications for cellular bioenergetics", EUR J NEURO, 12(11), 2000, pp. 3843-3853

Abstract

The mode of Na+ entry and the dynamics of intracellular Na+ concentration ([Na+](i)) changes consecutive to the application of the neurotransmitter glutamate were investigated in mouse cortical astrocytes in primary culture by video fluorescence microscopy. An elevation of [Na+](i) was evoked by glutamate, whose amplitude and initial rate were concentration dependent. Theglutamate-evoked Na+ increase was primarily due to Na+-glutamate cotransport, as inhibition of non-NMDA ionotropic receptors by 6-cyano-7-nitroquinoxiline-2,3-dione (CNQX) only weakly diminished the response and d-aspartate,a substrate of the glutamate transporter, produced [Na+](i) elevations similar to those evoked by glutamate. Non-NMDA receptor activation could nevertheless be demonstrated by preventing receptor desensitization using cyclothiazide. Thus, in normal conditions non-NMDA receptors do not contribute significantly to the glutamate-evoked Na+ response. The rate of Na+ influx decreased during glutamate application, with kinetics that correlate well with the increase in [Na+](i) and which depend on the extracellular concentration of glutamate. A tight coupling between Na+ entry and Na+/K+ ATPase activity was revealed by the massive [Na+](i) increase evoked by glutamate whenpump activity was inhibited by ouabain. During prolonged glutamate application, [Na+](i) remains elevated at a new steady-state where Na+ influx through the transporter matches Na+ extrusion through the Na+/K+ ATPase. A mathematical model of the dynamics of [Na+](i) homeostasis is presented which precisely defines the critical role of Na+ influx kinetics in the establishment of the elevated steady state and its consequences on the cellular bioenergetics. Indeed, extracellular glutamate concentrations of 10 mum already markedly increase the energetic demands of the astrocytes.

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Documento generato il 26/01/20 alle ore 01:11:31