Dynamic causal modelling revisited
This paper revisits the dynamic causal modelling of fMRI timeseries by replacing the usual (Taylor) approximation to neuronal dynamics with a neural mass model of the canonical microcircuit. This provides a generative or dynamic causal model of laminar specific responses that can generate haemodynam...
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| Vydáno v: | NeuroImage (Orlando, Fla.) Ročník 199; s. 730 - 744 |
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| Hlavní autoři: | , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
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United States
Elsevier Inc
01.10.2019
Elsevier Limited Academic Press |
| Témata: | |
| ISSN: | 1053-8119, 1095-9572, 1095-9572 |
| On-line přístup: | Získat plný text |
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| Abstract | This paper revisits the dynamic causal modelling of fMRI timeseries by replacing the usual (Taylor) approximation to neuronal dynamics with a neural mass model of the canonical microcircuit. This provides a generative or dynamic causal model of laminar specific responses that can generate haemodynamic and electrophysiological measurements. In principle, this allows the fusion of haemodynamic and (event related or induced) electrophysiological responses. Furthermore, it enables Bayesian model comparison of competing hypotheses about physiologically plausible synaptic effects; for example, does attentional modulation act on superficial or deep pyramidal cells – or both? In this technical note, we describe the resulting dynamic causal model and provide an illustrative application to the attention to visual motion dataset used in previous papers. Our focus here is on how to answer long-standing questions in fMRI; for example, do haemodynamic responses reflect extrinsic (afferent) input from distant cortical regions, or do they reflect intrinsic (recurrent) neuronal activity? To what extent do inhibitory interneurons contribute to neurovascular coupling? What is the relationship between haemodynamic responses and the frequency of induced neuronal activity? This paper does not pretend to answer these questions; rather it shows how they can be addressed using neural mass models of fMRI timeseries.
•This paper describes a DCM for fMRI based on neural mass models and canonical microcircuits.•This enables the (Bayesian) fusion of EEG and fMRI data.•That encompasses the formal modelling of neurovascular coupling.•Offers a surprising insight into the relationship between haemodynamic and electrophysiological responses. |
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| AbstractList | This paper revisits the dynamic causal modelling of fMRI timeseries by replacing the usual (Taylor) approximation to neuronal dynamics with a neural mass model of the canonical microcircuit. This provides a generative or dynamic causal model of laminar specific responses that can generate haemodynamic and electrophysiological measurements. In principle, this allows the fusion of haemodynamic and (event related or induced) electrophysiological responses. Furthermore, it enables Bayesian model comparison of competing hypotheses about physiologically plausible synaptic effects; for example, does attentional modulation act on superficial or deep pyramidal cells – or both? In this technical note, we describe the resulting dynamic causal model and provide an illustrative application to the attention to visual motion dataset used in previous papers. Our focus here is on how to answer long-standing questions in fMRI; for example, do haemodynamic responses reflect extrinsic (afferent) input from distant cortical regions, or do they reflect intrinsic (recurrent) neuronal activity? To what extent do inhibitory interneurons contribute to neurovascular coupling? What is the relationship between haemodynamic responses and the frequency of induced neuronal activity? This paper does not pretend to answer these questions; rather it shows how they can be addressed using neural mass models of fMRI timeseries.
•
This paper describes a DCM for fMRI based on neural mass models and canonical microcircuits.
•
This enables the (Bayesian) fusion of EEG and fMRI data.
•
That encompasses the formal modelling of neurovascular coupling.
•
Offers a surprising insight into the relationship between haemodynamic and electrophysiological responses. This paper revisits the dynamic causal modelling of fMRI timeseries by replacing the usual (Taylor) approximation to neuronal dynamics with a neural mass model of the canonical microcircuit. This provides a generative or dynamic causal model of laminar specific responses that can generate haemodynamic and electrophysiological measurements. In principle, this allows the fusion of haemodynamic and (event related or induced) electrophysiological responses. Furthermore, it enables Bayesian model comparison of competing hypotheses about physiologically plausible synaptic effects; for example, does attentional modulation act on superficial or deep pyramidal cells - or both? In this technical note, we describe the resulting dynamic causal model and provide an illustrative application to the attention to visual motion dataset used in previous papers. Our focus here is on how to answer long-standing questions in fMRI; for example, do haemodynamic responses reflect extrinsic (afferent) input from distant cortical regions, or do they reflect intrinsic (recurrent) neuronal activity? To what extent do inhibitory interneurons contribute to neurovascular coupling? What is the relationship between haemodynamic responses and the frequency of induced neuronal activity? This paper does not pretend to answer these questions; rather it shows how they can be addressed using neural mass models of fMRI timeseries. This paper revisits the dynamic causal modelling of fMRI timeseries by replacing the usual (Taylor) approximation to neuronal dynamics with a neural mass model of the canonical microcircuit. This provides a generative or dynamic causal model of laminar specific responses that can generate haemodynamic and electrophysiological measurements. In principle, this allows the fusion of haemodynamic and (event related or induced) electrophysiological responses. Furthermore, it enables Bayesian model comparison of competing hypotheses about physiologically plausible synaptic effects; for example, does attentional modulation act on superficial or deep pyramidal cells – or both? In this technical note, we describe the resulting dynamic causal model and provide an illustrative application to the attention to visual motion dataset used in previous papers. Our focus here is on how to answer long-standing questions in fMRI; for example, do haemodynamic responses reflect extrinsic (afferent) input from distant cortical regions, or do they reflect intrinsic (recurrent) neuronal activity? To what extent do inhibitory interneurons contribute to neurovascular coupling? What is the relationship between haemodynamic responses and the frequency of induced neuronal activity? This paper does not pretend to answer these questions; rather it shows how they can be addressed using neural mass models of fMRI timeseries. •This paper describes a DCM for fMRI based on neural mass models and canonical microcircuits.•This enables the (Bayesian) fusion of EEG and fMRI data.•That encompasses the formal modelling of neurovascular coupling.•Offers a surprising insight into the relationship between haemodynamic and electrophysiological responses. This paper revisits the dynamic causal modelling of fMRI timeseries by replacing the usual (Taylor) approximation to neuronal dynamics with a neural mass model of the canonical microcircuit. This provides a generative or dynamic causal model of laminar specific responses that can generate haemodynamic and electrophysiological measurements. In principle, this allows the fusion of haemodynamic and (event related or induced) electrophysiological responses. Furthermore, it enables Bayesian model comparison of competing hypotheses about physiologically plausible synaptic effects; for example, does attentional modulation act on superficial or deep pyramidal cells - or both? In this technical note, we describe the resulting dynamic causal model and provide an illustrative application to the attention to visual motion dataset used in previous papers. Our focus here is on how to answer long-standing questions in fMRI; for example, do haemodynamic responses reflect extrinsic (afferent) input from distant cortical regions, or do they reflect intrinsic (recurrent) neuronal activity? To what extent do inhibitory interneurons contribute to neurovascular coupling? What is the relationship between haemodynamic responses and the frequency of induced neuronal activity? This paper does not pretend to answer these questions; rather it shows how they can be addressed using neural mass models of fMRI timeseries.This paper revisits the dynamic causal modelling of fMRI timeseries by replacing the usual (Taylor) approximation to neuronal dynamics with a neural mass model of the canonical microcircuit. This provides a generative or dynamic causal model of laminar specific responses that can generate haemodynamic and electrophysiological measurements. In principle, this allows the fusion of haemodynamic and (event related or induced) electrophysiological responses. Furthermore, it enables Bayesian model comparison of competing hypotheses about physiologically plausible synaptic effects; for example, does attentional modulation act on superficial or deep pyramidal cells - or both? In this technical note, we describe the resulting dynamic causal model and provide an illustrative application to the attention to visual motion dataset used in previous papers. Our focus here is on how to answer long-standing questions in fMRI; for example, do haemodynamic responses reflect extrinsic (afferent) input from distant cortical regions, or do they reflect intrinsic (recurrent) neuronal activity? To what extent do inhibitory interneurons contribute to neurovascular coupling? What is the relationship between haemodynamic responses and the frequency of induced neuronal activity? This paper does not pretend to answer these questions; rather it shows how they can be addressed using neural mass models of fMRI timeseries. |
| Author | Zeidman, Peter Heinzle, Jakob Cagnan, Hayriye Razi, Adeel Mathys, Chris Preller, Katrin H. Friston, K.J. |
| AuthorAffiliation | f Department of Electronic Engineering, NED University of Engineering and Technology, Karachi, Pakistan d MRC Brain Network Dynamics Unit (BNDU), Department of Pharmacology and Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK c Max Planck UCL Centre for Computational Psychiatry and Ageing Research, University College London, United Kingdom b Neuropsychopharmacology and Brain Imaging, Department of Psychiatry, Psychotherapy and Psychosomatics, University Hospital for Psychiatry Zurich, 8032 Zurich, Switzerland a The Wellcome Trust Centre for Neuroimaging, University College London, United Kingdom e Translational Neuromodeling Unit, Institute for Biomedical Engineering, University of Zurich and ETH Zurich, 8032 Zürich, Switzerland |
| AuthorAffiliation_xml | – name: f Department of Electronic Engineering, NED University of Engineering and Technology, Karachi, Pakistan – name: a The Wellcome Trust Centre for Neuroimaging, University College London, United Kingdom – name: c Max Planck UCL Centre for Computational Psychiatry and Ageing Research, University College London, United Kingdom – name: b Neuropsychopharmacology and Brain Imaging, Department of Psychiatry, Psychotherapy and Psychosomatics, University Hospital for Psychiatry Zurich, 8032 Zurich, Switzerland – name: d MRC Brain Network Dynamics Unit (BNDU), Department of Pharmacology and Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK – name: e Translational Neuromodeling Unit, Institute for Biomedical Engineering, University of Zurich and ETH Zurich, 8032 Zürich, Switzerland |
| Author_xml | – sequence: 1 givenname: K.J. surname: Friston fullname: Friston, K.J. email: k.friston@ucl.ac.uk organization: The Wellcome Trust Centre for Neuroimaging, University College London, United Kingdom – sequence: 2 givenname: Katrin H. surname: Preller fullname: Preller, Katrin H. email: preller@bli.uzh.ch organization: The Wellcome Trust Centre for Neuroimaging, University College London, United Kingdom – sequence: 3 givenname: Chris surname: Mathys fullname: Mathys, Chris email: c.mathys@ucl.ac.uk organization: The Wellcome Trust Centre for Neuroimaging, University College London, United Kingdom – sequence: 4 givenname: Hayriye surname: Cagnan fullname: Cagnan, Hayriye email: hayriye.cagnan@ndcn.ox.ac.uk organization: The Wellcome Trust Centre for Neuroimaging, University College London, United Kingdom – sequence: 5 givenname: Jakob surname: Heinzle fullname: Heinzle, Jakob email: heinzle@biomed.ee.ethz.ch organization: The Wellcome Trust Centre for Neuroimaging, University College London, United Kingdom – sequence: 6 givenname: Adeel surname: Razi fullname: Razi, Adeel email: a.razi@ucl.ac.uk organization: The Wellcome Trust Centre for Neuroimaging, University College London, United Kingdom – sequence: 7 givenname: Peter surname: Zeidman fullname: Zeidman, Peter email: peter.zeidman@ucl.ac.uk organization: The Wellcome Trust Centre for Neuroimaging, University College London, United Kingdom |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/28219774$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
| Copyright | 2017 The Authors Copyright © 2017 The Authors. Published by Elsevier Inc. All rights reserved. 2017. The Authors 2017 The Authors 2017 |
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| DOI | 10.1016/j.neuroimage.2017.02.045 |
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| Keywords | Haemodynamic models Neural mass models Bayesian Dynamic causal modelling Effective connectivity |
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| SubjectTerms | Adult Attention Bayesian Bayesian analysis Blood Brain - diagnostic imaging Brain - physiology Cortex Dynamic causal modelling Effective connectivity Electroencephalography Functional magnetic resonance imaging Functional Neuroimaging - methods Haemodynamic models Hemodynamics Hemodynamics - physiology Humans Interneurons Magnetic Resonance Imaging Mathematical models Models, Biological Motion detection Motion Perception - physiology Nerve Net - diagnostic imaging Nerve Net - physiology Neural mass models Neurovascular Coupling - physiology Population Pyramidal cells Sensory neurons Time series Visual perception |
| Title | Dynamic causal modelling revisited |
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