Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 107, Issue 8, Pages 3811-3816Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0914722107
Keywords
inwardly rectifying potassium channel; large-conductance calcium-sensitive potassium channel neurovascular coupling
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Funding
- National Institutes of Health [R01 HL44455, HL098243-01, 2R37DK 053832, P01 HL077378, P20 RR016435, HL098243, T32 HL07944]
- Canadian Institutes in Health Research
- Fonds de la Recherche en Sante du Quebec
- Totman Trust for Medical Research
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Neuronal activity is thought to communicate to arterioles in the brain through astrocytic calcium (Ca2+) signaling to cause local vasodilation. Paradoxically, this communication may cause vasoconstriction in some cases. Here, we show that, regardless of the mechanism by which astrocytic endfoot Ca2+ was elevated, modest increases in Ca2+ induced dilation, whereas larger increases switched dilation to constriction. Large-conductance, Ca2+-sensitive potassium channels in astrocytic endfeet mediated a majority of the dilation and the entire vasoconstriction, implicating local extracellular K+ as a vasoactive signal for both dilation and constriction. These results provide evidence for a unifying mechanism that explains the nature and apparent duality of the vascular response, showing that the degree and polarity of neurovascular coupling depends on astrocytic endfoot Ca2+ and perivascular K+.
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