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Calcium dynamics in cortical astrocytes and arterioles during neurovascular coupling.
Filosa J, Bonev A, Nelson MT
Circulation Research. 2004;95( 10):e73-81.
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Abstract
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 http://circres.ahajournals.org.
Keyword(s)
Animals; Calcium Signaling; Cerebrovascular Circulation; Electric Stimulation; Inositol 1,4,5-Trisphosphate Receptors; Microscopy, Video; Rats; Rats, Sprague-Dawley; agonists: Receptors, Metabotropic Glutamate; analogs & derivatives: Cycloleucine; antagonists & inhibitors: Receptors, Cytoplasmic and Nuclear; blood supply: Cerebral Cortex; drug effects: Arterioles; drug effects: Astrocytes; drug effects: Sodium Channels; drug effects: Synaptic Transmission; metabolism: Muscle, Smooth, Vascular; metabolism: Myocytes, Smooth Muscle; pharmacology: 15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid; pharmacology: Boron Compounds; pharmacology: Indans; pharmacology: Nifedipine; pharmacology: Pyridines; pharmacology: Sodium Channel Blockers; pharmacology: Tetrodotoxin; physiology: Calcium Channels; physiology: Inositol 1,4,5-Trisphosphate; physiology: Neurons; physiopathology: Hyperemia