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The Negative BOLD Response in Monkey V1 is Associated with Decreases in Neuronal Activity

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Shmuel,  A
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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Augath,  M
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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Oeltermann,  A
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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Pauls,  J
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
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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Citation

Shmuel, A., Augath, M., Oeltermann, A., Pauls, J., & Logothetis, N. (2003). The Negative BOLD Response in Monkey V1 is Associated with Decreases in Neuronal Activity. Poster presented at 33rd Annual Meeting of the Society for Neuroscience (Neuroscience 2003), New Orleans, LA, USA.


Cite as: https://hdl.handle.net/11858/00-001M-0000-0013-DB09-9
Abstract
Negative BOLD responses (NBRs) are pervasive in human fMRI, but commonly ignored. A recent study (Shmuel et al., Neuron 2002) characterized a robust sustained NBR in the human occipital cortex associated with decreases in cerebral blood flow (CBF) and oxygen consumption, corroborating that the NBR could be triggered by decreases in neuronal activity (DsiNA).
Aims
1) Is the NBR associated with DsiNA?
2) Is the origin of the DsiNA vascular (e.g. from hypoxia due to blood steal) or neuronal?
Monkeys were visually stimulated with iso-eccentricity rings composed of rotating checkers. A blank gray stimulus was used to measure the baseline cortical signal.
Similar to the findings in humans, NBR was observed in monkeys: 1) in V1, V2, and V3, 2) in response to stimulation of part of the visual-field (VF), and 3) with a time course anti-correlated to that of the PBR.
To determine the neuronal correlates of the NBR, electrical recordings were obtained from the central VF representation in V1 simultaneously with fMRI. Central/peripheral VF stimulus elicited PBR/NBR in the vicinity of the electrode (Fig. 1). Note that: 1) the NBR was associated with DsiNA, 2) the onsets of the increases and DsiNA were approximately concurrent, and 3) the onset of the DsiNA preceded the corresponding onset of the NBR. The NBR was associated with comparable decreases in both the local-field potential and the multi-unit activity.
Conclusions
The NBR in monkey V1 is associated with DsiNA that could not be caused by blood steal. Most plausibly, the DsiNA trigger reductions in CBF that cause the NBR.