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The Journal of Neuroscience, March 15, 2006, 26(11):2862-2870; doi:10.1523/JNEUROSCI.4048-05.2006
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Cellular/Molecular
Glial Cells Dilate and Constrict Blood Vessels: A Mechanism of Neurovascular Coupling
Monica R. Metea andEric A. Newman Department of Neuroscience, University of Minnesota, Minneapolis, Minnesota 55455
Correspondence should be addressed to Dr. Eric A. Newman, Department of Neuroscience, University of Minnesota, Jackson Hall, 6-145, 321 Church Street Southeast, Minneapolis, MN 55455. Email: ean{at}umn.edu
Neuronal activity evokes localized changes in blood flow. Although this response, termed neurovascular coupling, is widely used to monitor human brain function and diagnose pathology, the cellular mechanisms that mediate the response remain unclear. We investigated the contribution of glial cells to neurovascular coupling in the acutely isolated mammalian retina. We found that light stimulation and glial cell stimulation can both evoke dilation or constriction of arterioles. Light-evoked and glial-evoked vasodilations were blocked by inhibitors of cytochrome P450 epoxygenase, the synthetic enzyme for epoxyeicosatrienoic acids. Vasoconstrictions, in contrast, were blocked by an inhibitor of
-hydroxylase, which synthesizes 20-hydroxyeicosatetraenoic acid. Nitric oxide influenced whether vasodilations or vasoconstrictions were produced in response to light and glial stimulation. Light-evoked vasoactivity was blocked when neuron-to-glia signaling was interrupted by a purinergic antagonist. These results indicate that glial cells contribute to neurovascular coupling and suggest that regulation of blood flow may involve both vasodilating and vasoconstricting components.
Key words: blood flow; glia; arachidonic acid metabolites; calcium; retina; ATP
Received Sept. 23, 2005; revised Feb. 1, 2006; accepted Feb. 1, 2006.
Correspondence should be addressed to Dr. Eric A. Newman, Department of Neuroscience, University of Minnesota, Jackson Hall, 6-145, 321 Church Street Southeast, Minneapolis, MN 55455. Email: ean{at}umn.edu
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