Calcium dynamics in cortical astrocytes and arterioles during neurovascular coupling.

Jessica A. Filosa, Adrian D. Bonev, Mark T. Nelson

    Research output: Contribution to journalArticlepeer-review


    Neuronal activity in the brain is thought to be coupled to cerebral arterioles (functional hyperemia) through Ca2+ signals in astrocytes. Although functional hyperemia occurs rapidly, within seconds, such rapid signaling has not been demonstrated in situ, and Ca2+ measurements in parenchymal arterioles are still lacking. Using a laser scanning confocal microscope and fluorescence Ca2+ indicators, we provide the first evidence that in a brain slice preparation, increased neuronal activity by electrical stimulation (ES) is rapidly signaled, within seconds, to cerebral arterioles and is associated with astrocytic Ca2+ waves. Smooth muscle cells in parenchymal arterioles exhibited Ca2+ and diameter oscillations ("vasomotion") that were rapidly suppressed by ES. The neuronal-mediated Ca2+ rise in cortical astrocytes was dependent on intracellular (inositol trisphosphate [IP3]) and extracellular voltage-dependent Ca2+ channel sources. The Na+ channel blocker tetrodotoxin prevented the rise in astrocytic [Ca2+]i and the suppression of Ca2+ oscillations in parenchymal arterioles to ES, indicating that neuronal activity was necessary for both events. Activation of metabotropic glutamate receptors in astrocytes significantly decreased the frequency of Ca2+ oscillations in parenchymal arterioles. This study supports the concept that astrocytic Ca2+ changes signal the cerebral microvasculature and indicate the novel concept that this communication occurs through the suppression of arteriolar [Ca2+]i oscillations and corresponding vasomotion. The full text of this article is available online at
    Original languageEnglish
    Pages (from-to)e73-81
    JournalCirculation research
    Issue number10
    Publication statusPublished - 12 Nov 2004


    • pharmacology: 15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid
    • Animals
    • drug effects: Arterioles
    • drug effects: Astrocytes
    • pharmacology: Boron Compounds
    • physiology: Calcium Channels
    • Calcium Signaling
    • blood supply: Cerebral Cortex
    • Cerebrovascular Circulation
    • analogs & derivatives: Cycloleucine
    • Electric Stimulation
    • physiopathology: Hyperemia
    • pharmacology: Indans
    • physiology: Inositol 1,4,5-Trisphosphate
    • Inositol 1,4,5-Trisphosphate Receptors
    • Microscopy, Video
    • metabolism: Muscle, Smooth, Vascular
    • metabolism: Myocytes, Smooth Muscle
    • physiology: Neurons
    • pharmacology: Nifedipine
    • pharmacology: Pyridines
    • Rats
    • Rats, Sprague-Dawley
    • antagonists & inhibitors: Receptors, Cytoplasmic and Nuclear
    • agonists: Receptors, Metabotropic Glutamate
    • pharmacology: Sodium Channel Blockers
    • drug effects: Sodium Channels
    • drug effects: Synaptic Transmission
    • pharmacology: Tetrodotoxin


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