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Nat Neurosci. 2015 Feb;18(2):210-8. doi: 10.1038/nn.3906. Epub 2014 Dec 22.

Calcium dynamics in astrocyte processes during neurovascular coupling.

Author information

1] Institut National de la Santé et de la Recherche Médicale (INSERM), U1128, Paris, France. [2] Laboratory of Neurophysiology and New Microscopies, Université Paris Descartes, Paris, France.
1] Centre National de la Recherche Scientifique (CNRS), UMR 7203, Paris, France. [2] Laboratory of Biomolecules, Université Pierre et Marie Curie, Paris, France.
The Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
CNRS UPR 3212, University of Strasbourg, Institute of Cellular and Integrative Neurosciences (INCI), Strasbourg, France.


Enhanced neuronal activity in the brain triggers a local increase in blood flow, termed functional hyperemia, via several mechanisms, including calcium (Ca(2+)) signaling in astrocytes. However, recent in vivo studies have questioned the role of astrocytes in functional hyperemia because of the slow and sparse dynamics of their somatic Ca(2+) signals and the absence of glutamate metabotropic receptor 5 in adults. Here, we reexamined their role in neurovascular coupling by selectively expressing a genetically encoded Ca(2+) sensor in astrocytes of the olfactory bulb. We show that in anesthetized mice, the physiological activation of olfactory sensory neuron (OSN) terminals reliably triggers Ca(2+) increases in astrocyte processes but not in somata. These Ca(2+) increases systematically precede the onset of functional hyperemia by 1-2 s, reestablishing astrocytes as potential regulators of neurovascular coupling.

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