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

View ORCID ProfileAli Danish Zaidi, Niels Birbaumer, Eberhard Fetz, Nikos Logothetis, Ranganatha Sitaram
doi: https://doi.org/10.1101/259895
Ali Danish Zaidi
1Max Planck Institute for Biological Cybernetics, Tübingen, Germany.
2Institute for Medical Psychology and Behavioral Neurobiology, University of Tübingen, Germany.
3Wyss Center for Bio and Neuroengineering, Geneva, Switzerland.
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  • ORCID record for Ali Danish Zaidi
Niels Birbaumer
2Institute for Medical Psychology and Behavioral Neurobiology, University of Tübingen, Germany.
3Wyss Center for Bio and Neuroengineering, Geneva, Switzerland.
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Eberhard Fetz
4Department of Physiology and Biophysics and Washington National Primate Research Center, University of Washington, Seattle, USA.
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Nikos Logothetis
1Max Planck Institute for Biological Cybernetics, Tübingen, Germany.
5Center for Imaging Sciences, Biomedical Imaging Institute, University of Manchester, UK.
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Ranganatha Sitaram
2Institute for Medical Psychology and Behavioral Neurobiology, University of Tübingen, Germany.
6Institute of Biological and Medical Engineering, and Department of Psychiatry and Section of Neuroscience, Pontificia Universidad Católica de Chile, Santiago, Chile.
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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.

Footnotes

  • ↵⋆ Lead contact

  • Abbreviations

    BOLD
    blood-oxygen level dependent signal
    CPVs
    Capillary and Peri-capillary Vessels (precapillary-arterioles, capillaries and post-capillary venules)
    fMRI
    functional Magnetic Resonance Imaging
    fNIRS
    functional Near Infra-Red Spectroscopy
    HbO
    concentration of oxy-hemoglobin
    HbR
    concentration of deoxy-hemoglobin
    HbT
    concentration of total hemoglobin
    LFP
    local field potential
    R
    Wilcoxon’s one-tailed rank-sum test
    Š
    Wilcoxon’s two-tailed signed rank test
    T1
    Tetrode 1 (0.55mm from emitter)
    T2
    Tetrode 2 (1.75mm from emitter)
    T3
    Tetrode 2 (2.95mm from emitter)
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    Posted February 22, 2018.
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    The hemodynamic initial-dip consists of both volumetric and oxymetric changes correlated to localized spiking activity
    Ali Danish Zaidi, Niels Birbaumer, Eberhard Fetz, Nikos Logothetis, Ranganatha Sitaram
    bioRxiv 259895; doi: https://doi.org/10.1101/259895
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    The hemodynamic initial-dip consists of both volumetric and oxymetric changes correlated to localized spiking activity
    Ali Danish Zaidi, Niels Birbaumer, Eberhard Fetz, Nikos Logothetis, Ranganatha Sitaram
    bioRxiv 259895; doi: https://doi.org/10.1101/259895

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