Related resources
Full-text held externally
- DOI: 10.1073/pnas.0914722107
- PMID: 20133576
- UKPMCID: 20133576
Search for item elsewhere
University researcher(s)
Academic department(s)
Astrocytic endfoot Ca2+ and BK channels determine both arteriolar dilation and constriction.
Girouard, Hélène; Bonev, Adrian D; Hannah, Rachael M; Meredith, Andrea; Aldrich, Richard W; Nelson, Mark T
Proceedings of the National Academy of Sciences of the United States of America. 2010;107(8):3811-3816.
Access to files
Full-text and supplementary files are not available from Manchester eScholar. Full-text is available externally using the following links:
Full-text held externally
- DOI: 10.1073/pnas.0914722107
- PMID: 20133576
- UKPMCID: 20133576
Abstract
Neuronal activity is thought to communicate to arterioles in the brain through astrocytic calcium (Ca(2+)) 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 Ca(2+) was elevated, modest increases in Ca(2+) induced dilation, whereas larger increases switched dilation to constriction. Large-conductance, Ca(2+)-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 Ca(2+) and perivascular K(+).