Journal
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM
Volume 33, Issue 7, Pages 996-999Publisher
SAGE PUBLICATIONS INC
DOI: 10.1038/jcbfm.2013.63
Keywords
AQP4; astrocytes; glia; NADH; metabolic
Categories
Funding
- US National Institutes of Health [NS075177, NS078304]
- Research Council of Norway
- Letten Foundation
- Fulbright Foundation
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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.
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