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The hemodynamic initial-dip consists of both volumetric and oxymetric changes correlated to localized spiking activity

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Zaidi,  AD
Department Physiology of Cognitive Processes, Max Planck Institute for Biological Cybernetics, Max Planck Society;
Max Planck Institute for Biological Cybernetics, Max Planck Society;

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Logothetis,  NK
Max Planck Institute for Biological Cybernetics, Max Planck Society;
Department Physiology of Cognitive Processes, Max Planck Institute for Biological Cybernetics, Max Planck Society;

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Sitaram,  R
Max Planck Institute for Biological Cybernetics, Max Planck Society;
Department Physiology of Cognitive Processes, Max Planck Institute for Biological Cybernetics, Max Planck Society;

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Zaidi, A., Birbaumer, N., Fetz, E., Logothetis, N., & Sitaram, R. (submitted). The hemodynamic initial-dip consists of both volumetric and oxymetric changes correlated to localized spiking activity.


Cite as: http://hdl.handle.net/21.11116/0000-0001-7D1E-3
Abstract
The initial-dip is a transient decrease frequently observed in functional neuroimaging signals, immediately after stimulus onset, and is believed to originate from a rise in deoxy-hemoglobin (HbR) caused by local neural activity. It has been shown to be more spatially specific than the hemodynamic response, and is believed to represent focal neuronal activity. However, despite being observed in various neuroimaging modalities (such as fMRI, fNIRS, etc), its origins are disputed and its neuronal correlates unknown. Here, we show that the initial-dip is dominated by a decrease in total-hemoglobin (HbT). We also find a biphasic response in HbR, with an early decrease and later rebound. However, HbT decreases were always large enough to counter spiking-induced increases in HbR. Moreover, the HbT-dip and HbR-rebound were strongly coupled to highly localized spiking activity. Our results suggest that the HbT-dip helps prevent accumulation of spiking-induced HbR concentration in capillaries by flushing out HbT, probably by active venule dilation.