They may also have implications for brain stimulation. For example: if we increase excitability in a cortical area (with TMS) we may see a decrease in its fMRI connectivity. What we like here is that these are testable hypotheses: and so we will soon see if (any of) this holds in humans!
17/n
This seem to hold across different manipulations, and different cortical areas. Which raises the obvious question: what neural signals/mechanism track the observed fMRI connectivity changes?
10/n
Alessandro Gozzi
We believe our results may (partly) reframe how we interpret fMRI connectivity
▶️ fMRI connectivity ≠direct communication strength
▶️ fMRI connectivity is supported by distributed slow neuronal coupling
▶️ Hyper/hypoconnectivity (eg., in brain disorders) may reflect cortical hypo/hyperexcitability
16/n
So these results suggest that
▶️slow, shared LFP fluctuations provide a neuronal scaffold for fMRI connectivity
▶️cortical excitability gates how strongly regions participate on this process: shifts in cortical excitability weaken or facilitate this coupling, leading to
hypo/hyperconnectivity
13/n
