Affiliation:
1. From the Department of Pharmacology, College of Medicine, University of Vermont, Burlington.
Abstract
Neuronal activity in the brain is thought to be coupled to cerebral arterioles (functional hyperemia) through Ca
2+
signals in astrocytes. Although functional hyperemia occurs rapidly, within seconds, such rapid signaling has not been demonstrated in situ, and Ca
2+
measurements in parenchymal arterioles are still lacking. Using a laser scanning confocal microscope and fluorescence Ca
2+
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 Ca
2+
waves. Smooth muscle cells in parenchymal arterioles exhibited Ca
2+
and diameter oscillations (“vasomotion”) that were rapidly suppressed by ES. The neuronal-mediated Ca
2+
rise in cortical astrocytes was dependent on intracellular (inositol trisphosphate [IP
3
]) and extracellular voltage-dependent Ca
2+
channel sources. The Na
+
channel blocker tetrodotoxin prevented the rise in astrocytic [Ca
2+
]
i
and the suppression of Ca
2+
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 Ca
2+
oscillations in parenchymal arterioles. This study supports the concept that astrocytic Ca
2+
changes signal the cerebral microvasculature and indicate the novel concept that this communication occurs through the suppression of arteriolar [Ca
2+
]
i
oscillations and corresponding vasomotion. The full text of this article is available online at http://circres.ahajournals.org.
Publisher
Ovid Technologies (Wolters Kluwer Health)
Subject
Cardiology and Cardiovascular Medicine,Physiology
Cited by
222 articles.
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