Oxygen and glucose deprivation-induced changes in astrocyte membrane potential and their underlying mechanisms in acute rat hippocampal slices.

Oxygen and glucose deprivation-induced changes in astrocyte membrane potential and their underlying mechanisms in acute rat hippocampal slices. Research Abstract Details 

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Oxygen and glucose deprivation-induced changes in astrocyte membrane potential and their underlying mechanisms in acute rat hippocampal slices. Abstract Text:

Minjie Xie,Wei Wang,Harold K Kimelberg,Min Zhou,

Accumulating evidence indicates a significant astrocytic involvement in cerebral ischemia neuropathology, but little is known about the immediate astrocytic responses to ischemia insults in terms of electrophysiology and their pathologic implications. We show that astrocytes in acute rat hippocampal slices responded reversibly to more than 30 mins oxygen and glucose deprivation (OGD) treatment with depolarized membrane potentials (V(m)) in whole-cell current clamp recording. This depolarization was multiphasic, showing an initial approximately 11 mins small-amplitude depolarization plateau, followed by a 6-mins accelerated depolarization, and then a second plateau. Oxygen and glucose deprivation-induced astrocyte V(m) depolarization was only marginally inhibited, approximately 10%, by inhibition of ionotropic glutamate, gamma-aminobutyric acid, purinergic receptors, and glutamate transporters presumed to be present on astrocytes in situ, suggesting increase in extracellular [K(+)] was primarily responsible for the astrocytic V(m) change. The V(m) depolarization was five-fold greater when glycolysis was inhibited by iodoacetate in a short 8 mins OGD treatment, suggesting glycolytic ATP is critical in maintaining extracellular K(+) homeostasis in the early phase of OGD. Addition of oxidative metabolism inhibitors had much less effect. Cessation of OGD was always followed by a rapid and transient 9 mV astrocyte V(m) hyperpolarization relative to the control V(m) that was inhibited by ouabain, indicating a reactively enhanced Na(+)/K(+)-ATPase activity in post-OGD reperfusion. Altogether, hippocampal astrocytes appear to be electrophysiologically more resistant to acute ischemia insults as compared with neurons, and this should allow astrocytes to rescue endangered neurons in the face of acute ischemia insults via their various homeostatic functions.Journal of Cerebral Blood Flow & Metabolism (2008) 28, 456-467; doi:10.1038/sj.jcbfm.9600545; published online 22 August 2007.

Oxygen and glucose deprivation-induced changes in astrocyte membrane potential and their underlying mechanisms in acute rat hippocampal slices. Publishing Authors By Initials

M Xie,W Wang,HK Kimelberg,M Zhou,

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Oxygen and glucose deprivation-induced changes in astrocyte membrane potential and their underlying mechanisms in acute rat hippocampal slices. Journal Published:

PUBLICATION TYPE: Journal Article

Journal: Journal of cerebral blood flow and metabolism : of

VOLUME: 28

Page Numbers: 456-67

Journal Abbreviation: J. Cereb. Blood Flow Metab.

ISSN: 0271-678X

DAY: 22

MONTH: 08

YEAR: 2007

Oxygen and glucose deprivation-induced changes in astrocyte membrane potential and their underlying mechanisms in acute rat hippocampal slices. Information

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LANGUAGE: eng

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AFFILIATION: [1] 1Department of Neural and Vascular Biology, Ordway Research Institute, Albany, New York, USA [2] 2Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Country: United States

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