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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
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.
2
1] Centre National de la Recherche Scientifique (CNRS), UMR 7203, Paris, France. [2] Laboratory of Biomolecules, Université Pierre et Marie Curie, Paris, France.
3
The Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
4
CNRS UPR 3212, University of Strasbourg, Institute of Cellular and Integrative Neurosciences (INCI), Strasbourg, France.

Abstract

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.

PMID:
25531572
PMCID:
PMC4651918
DOI:
10.1038/nn.3906
[Indexed for MEDLINE]
Free PMC Article

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