Abstract
Using in vivo two-photon imaging, we show that mice deficient in aquaporin-4 (AQP4) display increased fluorescence of nicotinamide adenine dinucleotide (NADH) when subjected to cortical spreading depression. The increased NADH signal, a proxy of tissue hypoxia, was restricted to microwatershed areas remote from the vasculature. Aqp4 deletion had no effects on the hyperemia response, but slowed [K(+)]o recovery. These observations suggest that K(+) uptake is suppressed in Aqp4(-/-) mice as a consequence of decreased oxygen delivery to tissue located furthest away from the vascular source of oxygen, although increased oxygen consumption may also contribute to our observations.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Aquaporin 4 / genetics
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Aquaporin 4 / physiology*
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Cerebrovascular Circulation / drug effects
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Cerebrovascular Circulation / physiology
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Cortical Spreading Depression / drug effects
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Cortical Spreading Depression / genetics
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Cortical Spreading Depression / physiology*
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Female
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Gene Deletion
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Hypoxia, Brain / metabolism*
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Male
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Mice
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Mice, Knockout
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Microscopy, Fluorescence, Multiphoton / methods*
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Models, Biological
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NAD / chemistry
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NAD / metabolism*
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Oxygen / metabolism*
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Oxygen Consumption / physiology
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Potassium Chloride / metabolism
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Potassium Chloride / pharmacology
Substances
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Aqp4 protein, mouse
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Aquaporin 4
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NAD
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Potassium Chloride
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Oxygen