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Network activity in the brain is associated with a transient increase in extracellular K(+) concentration. The excess K(+) is removed from the extracellular space by mechanisms proposed to involve Kir4.1-mediated spatial buffering, the Na(+)/K(+)/2Cl(-) cotransporter 1 (NKCC1), and/or Na(+)/K(+)-ATPase activity. Their individual contribution to [K(+)]o(More)
Neuronal activity results in release of K(+) into the extracellular space of the central nervous system. If the excess K(+) is allowed to accumulate, neuronal firing will be compromised by the ensuing neuronal membrane depolarization. The surrounding glial cells are involved in clearing K(+) from the extracellular space by molecular mechanism(s), the(More)
During neuronal activity in the brain, extracellular K(+) rises and is subsequently removed to prevent a widespread depolarization. One of the key players in regulating extracellular K(+) is the Na(+)/K(+)-ATPase, although the relative involvement and physiological impact of the different subunit isoform compositions of the Na(+)/K(+)-ATPase remain(More)
Aquaporin 4 (AQP4) is the predominant water channel in the mammalian brain and is mainly expressed in the perivascular glial endfeet at the brain-blood interface. AQP4 serves as a water entry site during brain edema formation, and regulation of AQP4 may therefore be of therapeutic interest. Phosphorylation of aquaporins can regulate plasma membrane(More)
Aquaporin 4 (AQP4) is the predominant water channel in the mammalian brain and is mainly expressed in the perivascular glial endfeet at the brain–blood interface. Based on studies on AQP4−/− mice, AQP4 has been assigned physiological roles in stimulus-induced K+ clearance, paravascular fluid flow, and brain edema formation. Conflicting data have been(More)
Hepatocyte growth factor activator inhibitor-2 (HAI-2) is an inhibitor of many proteases in vitro, including the membrane-bound serine protease, matriptase. Studies of knock-out mice have shown that HAI-2 is essential for placental development only in mice expressing matriptase, suggesting that HAI-2 is important for regulation of matriptase. Previous(More)
KEY POINTS Management of glutamate and K(+) in brain extracellular space is of critical importance to neuronal function. The astrocytic α2β2 Na(+) /K(+) -ATPase isoform combination is activated by the K(+) transients occurring during neuronal activity. In the present study, we report that glutamate transporter-mediated astrocytic Na(+) transients stimulate(More)
During neuronal activity in the mammalian brain, the K+ released into the synaptic space is initially buffered by the astrocytic compartment. In parallel, the extracellular space (ECS) shrinks, presumably due to astrocytic cell swelling. With the Na+ /K+ /2Cl- cotransporter and the Kir4.1/AQP4 complex not required for the astrocytic cell swelling in the(More)
Synaptic activity results in transient elevations in extracellular K+ , clearance of which is critical for sustained function of the nervous system. The K+ clearance is, in part, accomplished by the neighboring astrocytes by mechanisms involving the Na+ /K+ -ATPase. The Na+ /K+ -ATPase consists of an α and a β subunit, each with several isoforms present in(More)
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