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==== Functional MRI ====
[[File:DCM for fMRI.svg|alt=DCM for fMRI neural circuit|thumb|The neural model in DCM for fMRI. z1 and z2 are the mean level of activity in each region. Parameters A are the connection strengths, B is the modulatory input and C is the driving input. ]]
The neural model in DCM for fMRI uses a simple mathematical device - a [[Taylor series|Taylor approximation]] - to capture the gross causal causal influences between brain regions and their change due to experimental inputs. This is coupled with a detailed biophysical model of the generation of the BOLD response and the MRI signal, based on the Balloon model of Buxton et al.<ref>{{Cite journal|last=Buxton|first=Richard B.|last2=Wong|first2=Eric C.|last3=Frank|first3=Lawrence R.|date=1998-06|title=Dynamics of blood flow and oxygenation changes during brain activation: The balloon model|url=http://dx.doi.org/10.1002/mrm.1910390602|journal=Magnetic Resonance in Medicine|volume=39|issue=6|pages=855–864|doi=10.1002/mrm.1910390602|issn=0740-3194}}</ref> and extended for use in DCM for fMRI <ref>{{Cite journal|last=Friston|first=K.J.|last2=Mechelli|first2=A.|last3=Turner|first3=R.|last4=Price|first4=C.J.|date=2000-10|title=Nonlinear Responses in fMRI: The Balloon Model, Volterra Kernels, and Other Hemodynamics|url=http://dx.doi.org/10.1006/nimg.2000.0630|journal=NeuroImage|volume=12|issue=4|pages=466–477|doi=10.1006/nimg.2000.0630|issn=1053-8119}}</ref><ref>{{Cite journal|last=Stephan|first=Klaas Enno|last2=Weiskopf|first2=Nikolaus|last3=Drysdale|first3=Peter M.|last4=Robinson|first4=Peter A.|last5=Friston|first5=Karl J.|date=2007-11|title=Comparing hemodynamic models with DCM|url=http://dx.doi.org/10.1016/j.neuroimage.2007.07.040|journal=NeuroImage|volume=38|issue=3|pages=387–401|doi=10.1016/j.neuroimage.2007.07.040|issn=1053-8119}}</ref>. Additions to the basic neural model enable the inclusion of interactions between excitatory and inhibitory neural populations <ref>{{Cite journal|last=Marreiros|first=A.C.|last2=Kiebel|first2=S.J.|last3=Friston|first3=K.J.|date=2008-01|title=Dynamic causal modelling for fMRI: A two-state model|url=https://doi.org/10.1016/j.neuroimage.2007.08.019|journal=NeuroImage|volume=39|issue=1|pages=269–278|doi=10.1016/j.neuroimage.2007.08.019|issn=1053-8119}}</ref> and non-linear influences of neural populations on the coupling between other populations<ref name=":3">{{Cite journal|last=Stephan|first=Klaas Enno|last2=Kasper|first2=Lars|last3=Harrison|first3=Lee M.|last4=Daunizeau|first4=Jean|last5=den Ouden|first5=Hanneke E.M.|last6=Breakspear|first6=Michael|last7=Friston|first7=Karl J.|date=2008-08|title=Nonlinear dynamic causal models for fMRI|url=https://doi.org/10.1016/j.neuroimage.2008.04.262|journal=NeuroImage|volume=42|issue=2|pages=649–662|doi=10.1016/j.neuroimage.2008.04.262|issn=1053-8119|pmc=PMC2636907|pmid=18565765}}</ref>.
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==== EEG / MEG / LFP ====
EEG and MEG data support more biologically detailed neural models than fMRI, as their higher temporal resolution provide access to richer neural dynamics. These can be classed into phenomenological models, which focus on reproducing particular data features, and physiological models, which recapitulate neural circuity. The physiological models can be further subdivided into two classes. [http://www.scholarpedia.org/article/Conductance-based_models Conductance-based models] derive from the equivalent circuit representation of the cell membrane developed by Hodgkin and Huxley in the 1950s<ref name=":5">{{Cite journal|last=Hodgkin|first=A. L.|last2=Huxley|first2=A. F.|date=1952-04-28|title=The components of membrane conductance in the giant axon ofLoligo|url=http://dx.doi.org/10.1113/jphysiol.1952.sp004718|journal=The Journal of Physiology|volume=116|issue=4|pages=473–496|doi=10.1113/jphysiol.1952.sp004718|issn=0022-3751}}</ref> . Convolution models derive from work by [[Wilson–Cowan model|Wilson & Cowan]]<ref>{{Cite journal|last=Wilson|first=H. R.|last2=Cowan|first2=J. D.|date=1973-09|title=A mathematical theory of the functional dynamics of cortical and thalamic nervous tissue|url=http://dx.doi.org/10.1007/bf00288786|journal=Kybernetik|volume=13|issue=2|pages=55–80|doi=10.1007/bf00288786|issn=0340-1200}}</ref> and Freeman <ref>{{Cite journal|date=1975|title=Mass Action in the Nervous System|url=http://dx.doi.org/10.1016/c2009-0-03145-6|doi=10.1016/c2009-0-03145-6}}</ref> in the 1970s and involve a convolution of pre-synaptic input by a synaptic kernel function. The specific models are as follows:
[[File:DCM for ERP and CMC.svg|thumb|Models of the cortical column used in EEG/MEG/LFP analysis. Self-connections on each population are present but not shown for clarity. Left: DCM for ERP. Right: Canonical Microcircuit (CMC). 1=spiny stellate cells (layer IV), 2=inhibitory interneurons, 3=(deep) pyramidal cells and 4=superficial pyramidal cells.]]
* Physiological models:
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