Journal
NEUROCHEMICAL RESEARCH
Volume 38, Issue 3, Pages 472-485Publisher
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s11064-012-0938-3
Keywords
Astrocyte; Cell signaling; Glycogen; Na+; K+-ATPase; Ouabain; Potassium homeostasis
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Funding
- National Natural Science Foundation of China [31171036]
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The importance of astrocytic K+ uptake for extracellular K+ ([K+](e)) clearance during neuronal stimulation or pathophysiological conditions is increasingly acknowledged. It occurs by preferential stimulation of the astrocytic Na+,K+-ATPase, which has higher K-m and V-max values than its neuronal counterpart, at more highly increased [K+](e) with additional support of the cotransporter NKCC1. Triggered by a recent DiNuzzo et al. paper, we used administration of the glycogenolysis inhibitor DAB to primary cultures of mouse astrocytes to determine whether K+ uptake required K+-stimulated glycogenolysis. KCl was increased by either 5 mM (stimulating only the Na+,K+-ATPase) or 10 mM (stimulating both transporters) in glucose-containing saline media prepared to become iso-osmotic after the addition. DAB completely inhibited both uptakes, the Na+,K+-ATPase-mediated by preventing Na+ uptake for stimulation of its intracellular Na+-activated site, and the NKCC1-mediated uptake by inhibition of depolarization- and L-channel-mediated Ca2+ uptake. Drugs inhibiting the signaling pathways involved in either of these processes also abolished K+ uptake. Assuming similar in vivo characteristics, partly supported by literature data, K+-stimulated astrocytic K+ uptake must discontinue after normalization of extracellular K+. This will allow Kir1.4-mediated release and reuptake by the less powerful neuronal Na+,K+-ATPase.
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