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Abstract
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.
Highlights
Optogenetics is increasingly used to map brain activation using techniques that rely on functional hyperaemia, such as opto-fMRI
These results suggest that blue light itself is capable of increasing cerebral blood flow (CBF), in naive brain tissue
This work shows that light per se, delivered in trains and at intensities commonly used to trigger functional hyperaemia and/ or fMRI signals in rodents, decreases smooth muscle cells (SMCs) calcium, either directly or via endothelial cells, leading to dilation of arterioles
Summary
Optogenetics is increasingly used to map brain activation using techniques that rely on functional hyperaemia, such as opto-fMRI. 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. Two-photon Ca2 þ imaging of GCaMP6f in different transgenic mouse lines reveals that light causes a Ca2 þ decrease in arteriolar smooth muscle cells that precedes the onset of dilation in the absence of neuronal or astrocyte excitation, suggesting a direct action of light on SMCs
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