In this study, we investigate the vascular contribution to the BOLD signal by comparing purely non-neuronal-related changes in the BOLD signal induced by gas manipulations with neuronal-related hemodynamic changes in the BOLD signal for different vascular compartments. Different vascular compartments were targeted by employing gradient-echo and spin-echo in combination with cortical depth estimations and pial vein segmentations. Our findings suggest that the increase in macro-vascular baseline venous blood volume (CBVv0) is the main contributor to the large GE-BOLD signal increase towards the pial surface and that normalization for this CBVv0-dependence is possible using a hyperoxia breathing task.
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