Light controls cerebral blood flow in naive animals
Optogenetics is increasingly used to map brain activation using techniques that rely on functional hyperaemia, such as opto-fMRI. Here we test whether light stimulation protocols similar to those commonly used in opto-fMRI or to study neurovascular coupling modulate blood flow in mice that do not ex...
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Published in: | Nature communications Vol. 8; no. 1; p. 14191 |
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Main Authors: | , , , , |
Format: | Journal Article |
Language: | English |
Published: |
London
Nature Publishing Group UK
31-01-2017
Nature Publishing Group Nature Portfolio |
Subjects: | |
Online Access: | Get full text |
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Summary: | Optogenetics is increasingly used to map brain activation using techniques that rely on functional hyperaemia, such as opto-fMRI. Here we test whether light stimulation protocols similar to those commonly used in opto-fMRI or to study neurovascular coupling modulate blood flow in mice that do not express light sensitive proteins. Combining two-photon laser scanning microscopy and ultrafast functional ultrasound imaging, we report that in the naive mouse brain, light per se causes a calcium decrease in arteriolar smooth muscle cells, leading to pronounced vasodilation, without excitation of neurons and astrocytes. This photodilation is reversible, reproducible and energy-dependent, appearing at about 0.5 mJ. These results impose careful consideration on the use of photo-activation in studies involving blood flow regulation, as well as in studies requiring prolonged and repetitive stimulations to correct cellular defects in pathological models. They also suggest that light could be used to locally increase blood flow in a controlled fashion.
Combination of optogenetics and BOLD fMRI is routinely used to map neuronal activity upon photostimulation. Here the authors show that light, shone at intensities used in optogenetic studies, dilates vessels and increases blood flow independently of exogenous light-sensitive proteins in the mouse brain. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 These authors contributed equally to this work |
ISSN: | 2041-1723 2041-1723 |
DOI: | 10.1038/ncomms14191 |