Journal
NATURE NEUROSCIENCE
Volume 6, Issue 1, Pages 43-50Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nn980
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- Telethon [1095] Funding Source: Medline
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The cellular mechanisms underlying functional hyperemia-the coupling of neuronal activation to cerebral blood vessel responses-are not yet known. Here we show in rat cortical slices that the dilation of arterioles triggered by neuronal activity is dependent on glutamate-mediated [Ca2+](i) oscillations in astrocytes. Inhibition of these Ca2+ responses resulted in the impairment of activity-dependent vasodilation, whereas selective activation-by patch pipette-of single astrocytes that were in contact with arterioles triggered vessel relaxation. We also found that a cyclooxygenase product is centrally involved in this astrocyte-mediated control of arterioles. In vivo blockade of glutamate-mediated [Ca2+](i) elevations in astrocytes reduced the blood flow increase in the somatosensory cortex during contralateral forepaw stimulation. Taken together, our findings show that neuron-to-astrocyte signaling is a key mechanism in functional hyperemia.
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