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Decipher the concurrent bidirectional regulation of the fMRI signal by astrocytes

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Wang,  H
Research Group Translational Neuroimaging and Neural Control, Max Planck Institute for Biological Cybernetics, Max Planck Society;
Max Planck Institute for Biological Cybernetics, Max Planck Society;

/persons/resource/persons192829

He,  Y
Research Group Translational Neuroimaging and Neural Control, Max Planck Institute for Biological Cybernetics, Max Planck Society;
Max Planck Institute for Biological Cybernetics, Max Planck Society;

/persons/resource/persons133486

Yu,  X
Research Group Translational Neuroimaging and Neural Control, Max Planck Institute for Biological Cybernetics, Max Planck Society;
Max Planck Institute for Biological Cybernetics, Max Planck Society;

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Wang, H., He, Y., Sejnowski, T., & Yu, X. (2017). Decipher the concurrent bidirectional regulation of the fMRI signal by astrocytes. In 47th Annual Meeting of the Society for Neuroscience (Neuroscience 2017).


Cite as: http://hdl.handle.net/21.11116/0000-0000-C524-9
Abstract
Astrocytic Ca2+-mediated gliovascular interactions regulate the neurovascular network in situ and in vivo. However, it is difficult to measure directly both the astrocytic activity and fMRI to relate the various forms of BOLD signaling to brain states under normal and pathological conditions. In this study, fMRI and GCaMP-mediated Ca2+ optical fiber recordings revealed distinct evoked astrocytic Ca2+ signals that were coupled with positive BOLD signals and intrinsic astrocytic Ca2+ signals that were coupled with negative BOLD signals (Fig 1). Furthermore, the evoked and intrinsic astrocytic Ca2+ signal could occur concurrently to mediate positive or negative BOLD signal changes respectively. Unlike propagating Ca2+ waves in spreading depolarization/depression, the intrinsic Ca2+ spikes occurred simultaneously in both hemispheres and were initiated upon the activation of the central thalamus and midbrain reticular formation (Fig 2). These results reveal a crucial role for astrocytes in mediating bidirectional fMRI signals based on the thalamic regulation of cortical states, providing a better understanding of how the BOLD signal is linked to brain activity at the cellular, circuit, and systems levels.