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Task-free fMRI is governed by high-amplitude BOLD coactivations (termed "CAPs"). But how do these patterns emerge and what do they mean?
New collaborative work conceived by #Diego_Fasoli and #Stefano_Panzeri provides possible explanations 👉tinyurl.com/2p8un5kp
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New collaborative work conceived by #Diego_Fasoli and #Stefano_Panzeri provides possible explanations 👉tinyurl.com/2p8un5kp
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In this work, we developed a large-scale network model of the mouse cortex that combines *directed* axonal connectivity (👉tinyurl.com/mryub799) with *non-linear* firing rate dynamics.
PS: “we” in this thread mostly stands for “Diego & Stefano”
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PS: “we” in this thread mostly stands for “Diego & Stefano”
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Our model reproduces remarkably well (ρ = 0.55) the topography of empirical 🐁 rsfMRI activity: simulated data show robust inter-hemispheric symmetry, and delineate well-characterized network systems of the mouse such a default-mode network, latero-cortical system etcetera.
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Wondering whether axonal input *drives* fMRI-based functional connectivity? Us too!
Here is what we found using #chemogenetic deconstruction of rsfMRI in the mouse🐁🐭
➡️Cortical silencing results in paradoxical fMRI overconnectivity tinyurl.com/yy269j92
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Here is what we found using #chemogenetic deconstruction of rsfMRI in the mouse🐁🐭
➡️Cortical silencing results in paradoxical fMRI overconnectivity tinyurl.com/yy269j92
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Computational and empirical evidence suggest that structural and functional connectivity are robustly related
➡️ this recent review from @richardfbetzel @misicbata summarizes it all tinyurl.com/yyy5u3zm
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➡️ this recent review from @richardfbetzel @misicbata summarizes it all tinyurl.com/yyy5u3zm
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⚠️A key prediction of structurally based models of fMRI coupling is that *inactivation* of a brain node would result in reduced rsfMRI connectivity with its targets⚠️
But is that really the case?
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But is that really the case?
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