Abstract

.Significance: Having a clear understanding of functional hyperemia is crucial for functional brain imaging and neurological disease research. Vasodilation induced by sensory stimulus propagates from the arterioles to the upstream pial arteries in a retrograde fashion. As retrograde vasodilation occurs briefly in the early stage of functional hyperemia, an imaging technique with a high temporal resolution is required for its measurement.Aim: We aimed to present an imaging method to measure stimulus-induced retrograde vasodilation in awake animals.Approach: An imaging method based on optical coherence tomography angiography, which enables a high-speed and label-free vessel diameter measurement, was developed and applied for the investigation.Results: The propagation speed of retrograde vasodilation of pial artery was measured in awake mice. Other characteristics of functional hyperemia such as temporal profile and amplitude of the vascular response were also investigated.Conclusions: Our results provide detailed information of stimulus-induced hemodynamic response in the brain of awake mice and suggest the potential utility of our imaging method for the study of functional hyperemia in normal and diseased brain.

Highlights

  • Neurovascular coupling, a close interplay between neural activity and cerebral blood flow (CBF), regulates the blood supply of corresponding brain regions

  • Our results provide detailed information of stimulus-induced hemodynamic response in the brain of awake mice and suggest the potential utility of our imaging method for the study of functional hyperemia in normal and diseased brain

  • A representative charge coupled device (CCD) image of the mouse cranial window and the corresponding optical intrinsic signal imaging (OISI) images are shown in Figs. 2(a) and 2(b)

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Summary

Introduction

Neurovascular coupling, a close interplay between neural activity and cerebral blood flow (CBF), regulates the blood supply of corresponding brain regions. The regulation is mediated by dilation and/or constriction of cerebral vessels. In order to effectively perfuse blood upon stimuli, the dilation of arterioles should be accompanied by the dilation of upstream pial arteries.[1,2,3] Dilation of arterioles induced by neural activation propagates to the pial arteries in a retrograde fashion.[2] A detailed mechanism of this coordinated vascular adjustment remains elusive; accumulating evidence indicates that such may be due to the signal transduction through endothelial and smooth muscle cell gap junctions in vessel walls.[4,5] This

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