Separate neuronal and glial Na+,K+-ATPase isoforms regulate glucose utilization in response to membrane depolarization and elevated extracellular potassium.

Details

Serval ID
serval:BIB_0FD24C351407
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Separate neuronal and glial Na+,K+-ATPase isoforms regulate glucose utilization in response to membrane depolarization and elevated extracellular potassium.
Journal
Journal of Cerebral Blood Flow and Metabolism
Author(s)
Honegger P., Pardo B.
ISSN
0271-678X (Print)
ISSN-L
0271-678X
Publication state
Published
Issued date
1999
Volume
19
Number
9
Pages
1051-1059
Language
english
Abstract
The role of cell type-specific Na+,K+-ATPase isozymes in function-related glucose metabolism was studied using differentiated rat brain cell aggregate cultures. In mixed neuron-glia cultures, glucose utilization, determined by measuring the rate of radiolabeled 2-deoxyglucose accumulation, was markedly stimulated by the voltage-dependent sodium channel agonist veratridine (0.75 micromol/L), as well as by glutamate (100 micromol/L) and the ionotropic glutamate receptor agonist N-methyl-D-aspartate (NMDA) (10 micromol/L). Significant stimulation also was elicited by elevated extracellular potassium (12 mmol/L KCl), which was even more pronounced at 30 mmol/L KCl. In neuron-enriched cultures, a similar stimulation of glucose utilization was obtained with veratridine, specific ionotropic glutamate receptor agonists, and 30 mmol/L but not 12 mmol/L KCl. The effects of veratridine, glutamate, and NMDA were blocked by specific antagonists (tetrodotoxin, CNQX, or MK801, respectively). Low concentrations of ouabain (10(-6) mol/L) prevented stimulation by the depolarizing agents but reduced only partially the response to 12 mmol/L KCl. Together with previous data showing cell type-specific expression of Na+,K+-ATPase subunit isoforms in these cultures, the current results support the view that distinct isoforms of Na+,K+-ATPase regulate glucose utilization in neurons in response to membrane depolarization, and in glial cells in response to elevated extracellular potassium.
Keywords
Animals, Biological Transport/physiology, Cells, Cultured, Glucose/metabolism, Isoenzymes/physiology, Membrane Potentials, Neuroglia/physiology, Neurons/physiology, Rats, Rats, Sprague-Dawley, Sodium-Potassium-Exchanging ATPase/physiology
Pubmed
Web of science
Open Access
Yes
Create date
24/01/2008 13:11
Last modification date
20/08/2019 12:36
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