ArticleImaging neuroscience (Cambridge, Mass.)2024
The contribution of the vascular architecture and cerebrovascular reactivity to the BOLD signal formation across cortical depth.
Article in Imaging neuroscience (Cambridge, Mass.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- A synthetic 3D human cerebrovascular model informed by histology for simulating the cortical depth-dependent BOLD fMRI signal.PLoS computational biology · 2026Article
- FMRI Approaches to Mapping Cerebrovascular Reactivity: Comparison of Gradient Echo BOLD and Spin Echo BOLD With Arterial Spin Labeling.Magnetic resonance in medicine · 2026Article
- Impact of thermal and physiological denoising on laminar functional connectivity.Scientific reports · 2026Article
- Article
- Impact of vascular architecture, oxygen saturation, and hematocrit on human cortical depth-dependent GE- and SE-BOLD fMRI signals: A simulation approach using realistic 3D vascular networks.Imaging neuroscience (Cambridge, Mass.) · 2025Article
- A fully synthetic three-dimensional human cerebrovascular model based on histological characteristics to investigate the hemodynamic fingerprint of the layer BOLD fMRI signal formation.bioRxiv : the preprint server for biology · 2024Article
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Authors and funding
8 authors.
Funding
Abstract
Assessment of neuronal activity using blood oxygenation level-dependent (BOLD) is confounded by how the cerebrovascular architecture modulates hemodynamic responses. To understand brain function at the laminar level, it is crucial to distinguish neuronal signal contributions from those determined by the cortical vascular organization. Therefore, our aim was to investigate the purely vascular contribution in the BOLD signal by using vasoactive stimuli and compare that with neuronal-induced BOLD responses from a visual task. To do so, we estimated the hemodynamic response function (HRF) across cortical depth following brief visual stimulations under different conditions using ultrahigh-field (7 Tesla) functional (f)MRI. We acquired gradient-echo (GE)-echo-planar-imaging (EPI) BOLD, containing contributions from all vessel sizes, and spin-echo (SE)-EPI BOLD for which signal changes predominately originate from microvessels, to distinguish signal weighting from different vascular compartments. Non-neuronal hemodynamic changes were induced by hypercapnia and hyperoxia to estimate cerebrovascular reactivity and venous cerebral blood volume (
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