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dasasgue.bsky.social

@dasasgue.bsky.social
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Alessandro Gozzi @gozziale.bsky.social · 18/03/2026
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
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Alessandro Gozzi @gozziale.bsky.social · 18/03/2026
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
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Alessandro Gozzi @gozziale.bsky.social · 18/03/2026
Thus our work suggests that 1️⃣ cortical excitability inversely modulates fMRI connectivity 2️⃣ fMRI coupling rests on distributed, slow neuronal fluctuations (i.e. QPPs, CAPs, neuromodulation pulses..) 3️⃣cortical excitability gates local coupling by weakening or facilitating that slow synchrony 15/n
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Alessandro Gozzi @gozziale.bsky.social · 18/03/2026
Notably, biophysical modelling supports this framework. Using a simple three-node model we found that local excitability changes are sufficient to reproduce the direction of the low-frequency coherence effects across perturbations. This offers a plausible mechanistic account of our results! 14/n
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Alessandro Gozzi @gozziale.bsky.social · 18/03/2026
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
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Alessandro Gozzi @gozziale.bsky.social · 18/03/2026
By comparing fMRI to LFP coherence one thing stood out ▶️ low-frequency coherence (<4 Hz) consistently tracked fMRI effects across all manipulations! Higher frequencies also change (sometimes a lot), but they don’t covary with fMRI. So slow neuronal coupling is the common denominator of fMRI! 12/n
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Alessandro Gozzi @gozziale.bsky.social · 18/03/2026
Given that fMRI is a measure of how synchronous fMRI fluctuations are across regions, we thougth measures of interareal electrophysiological (LFP) coherence could shed light into rhythms underlying large-scale fMRI coupling 11/n
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Alessandro Gozzi @gozziale.bsky.social · 18/03/2026
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
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Alessandro Gozzi @gozziale.bsky.social · 18/03/2026
However, fMRI revealed something very consistent ▶️higher excitability →reduced fMRI connectivity ▶️lower excitability →increased fMRI connectivity So in our datasets more local activity ≠ more fMRI connectivity! Rather, fMRI connectivity is inversely related to cortical excitability. 9/n
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Alessandro Gozzi @gozziale.bsky.social · 18/03/2026
As expected, these manipulations look very different spectrally. So if fMRI connectivity depended on a complex mix of neuronal rhythms, we should see divergent effects once we map the effect of these manipulations on large-scale fMRI coupling. 8/n
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Alessandro Gozzi @gozziale.bsky.social · 18/03/2026
Using these manipulations we sought to push cortical circuits into different firing-rate regimes. ▶️↑Excitation → higher firing ▶️↓Inhibition → higher firing ▶️ Silencing → lower firing So we can now map what happens when we manipulate excitability via different circuit mechanisms 7/n
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Alessandro Gozzi @gozziale.bsky.social · 18/03/2026
We considered three manipulations (through novel or existing datasets) 1️⃣ increasing pyramidal-cell excitability (↑Excitation) 2️⃣ reducing PV interneuron activity (↓Inhibition) 3️⃣ pan-neuronal suppression (Silencing) 6/n
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Alessandro Gozzi @gozziale.bsky.social · 18/03/2026
To test our hypothesis, we combined (in the mouse PFC) ▶️Chemogenetics to manipulate excitability ▶️Electrophysiology (spikes + LFP) ▶️fMRI connectivity But crucially: we combined the result of multiple manipulations into one unified framework, instead of interpreting each one in isolation 5/n
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Alessandro Gozzi @gozziale.bsky.social · 18/03/2026
In our work, cortical excitability = mean population firing. This is because in recurrent cortical networks, excitatory and inhibitory activity change in a coordinated way: if excitatory neurons fire more, inhibitory neurons also fire more (& viceversa - we show this using a simple model) 4/n
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Alessandro Gozzi @gozziale.bsky.social · 18/03/2026
The key idea here is 👉Cortical *excitability" might be a key hidden physiological variable controlling fMRI connectivity. This hypothesis stems from the observation that cortical excitability closely regulates rhythmic interareal coupling. So we thought this could apply to fMRI connectivity too 3/n
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Alessandro Gozzi @gozziale.bsky.social · 18/03/2026
fMRI connectivity is often interpreted as a proxy for direct interareal communication, but its physiology remains debated. In particular, it is unclear how local circuit activity maps onto fMRI connectivity. 2/n
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Alessandro Gozzi @gozziale.bsky.social · 18/03/2026
📢 New preprint from the lab🧠 ▶️doi.org/10.64898/2026.03.12.710517 What does fMRI connectivity actually reflect at the neural level? The natural intuition is: more neural activity = more connectivity! Using cortical perturbations we show this is not necessarily the case: sometimes less is more! 👇🧵
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dasasgue.bsky.social @dasasgue.bsky.social · 17/03/2026
🧠What if increasing neuronal firing could actually reduce fMRI connectivity? 📡What drives long-range fMRI connectivity? I’m very excited to share that my PhD work is now out as a preprint Check this out! 👇 doi.org/10.64898/202...
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Chiara Pepe @chiarapepe.bsky.social · 11/02/2026
🐭🧠 Can fUSI truly map canonical mouse resting-state networks — and how does it compare to fMRI? I’m excited to share the work of my PhD in our new preprint!👉 doi.org/10.64898/202... Go check it out — it’s time to expand your neuroimaging toolkit 🧠🚀
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Nature @nature.com · 02/10/2025
Jane Goodall, known for her pioneering work with chimpanzees, has passed away aged 91 go.nature.com/46K10ja
go.nature.com
Jane Goodall’s legacy: three ways she changed science
The primatologist challenged what it meant to be a scientist.
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