期刊
NATURE NEUROSCIENCE
卷 18, 期 2, 页码 210-218出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/nn.3906
关键词
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资金
- INSERM
- Agence Nationale de la Recherche (Project Angioneurins) [R11036KK]
- Leducq Foundation
- Human Frontier Science Program Organization [RGP008912009-C]
- Fondation pour la Recherche Medicale (equipe FRM)
- US National Institutes of Health [MH084020]
- Agence Nationale de la Recherche
- ERC Advanced Grant Imaging-in-the-magnet
- Ecole des Neurosciences de Paris (Paris School of Neuroscience)
- Fondation pour la Recherche Medicale [FDT20130928252]
Enhanced neuronal activity in the brain triggers a local increase in blood flow, termed functional hyperemia, via several mechanisms, including calcium (Ca2+) 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 Ca2+ 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 Ca2+ sensor in astrocytes of the olfactory bulb. We show that in anesthetized mice, the physiological activation of olfactory sensory neuron (OSN) terminals reliably triggers Ca2+ increases in astrocyte processes but not in somata. These Ca2+ increases systematically precede the onset of functional hyperemia by 1-2 s, reestablishing astrocytes as potential regulators of neurovascular coupling.
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