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The Journal of Neuroscience, March 7, 2007, 27(10):2468-2471; doi:10.1523/JNEUROSCI.3204-06.2007

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Brief Communications
Neurovascular Coupling Is Not Mediated by Potassium Siphoning from Glial Cells

Monica R. Metea, Paulo Kofuji, and Eric 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, 6-145 Jackson Hall, 321 Church Street Southeast, Minneapolis, MN 55455. Email: ean{at}umn.edu

Neuronal activity evokes localized changes in blood flow, a response termed neurovascular coupling. One widely recognized hypothesis of neurovascular coupling holds that glial cell depolarization evoked by neuronal activity leads to the release of K⁺ onto blood vessels (K⁺ siphoning) and to vessel relaxation. We now present two direct tests of this glial cell-K⁺ siphoning hypothesis of neurovascular coupling. Potassium efflux was evoked from glial cells in the rat retina by applying depolarizing current pulses to individual cells. Glial depolarizations as large as 100 mV produced no change in the diameter of adjacent arterioles. We also monitored light-evoked vascular responses in Kir4.1 knock-out mice, where functional Kir K⁺ channels are absent from retinal glial cells. The magnitude of light-evoked vasodilations was identical in Kir4.1 knock-out and wild-type animals. Contrary to the hypothesis, the results demonstrate that glial K⁺ siphoning in the retina does not contribute significantly to neurovascular coupling.

Key words: blood flow; glia; astrocytes; Müller cells; Kir4.1; potassium siphoning; retina

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Received July 26, 2006; revised Dec. 29, 2006; accepted Jan. 21, 2007.

Correspondence should be addressed to Dr. Eric A. Newman, Department of Neuroscience, University of Minnesota, 6-145 Jackson Hall, 321 Church Street Southeast, Minneapolis, MN 55455. Email: ean{at}umn.edu

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