How do cortical perturbations affect fMRI connectivity? Not necessarily as one would expect! Our new work @NatureComms shows that cortical inactivation may unexpectedly INCREASE fMRI connectivity! https://t.co/Bhs9ulbn6N 🧵below explains how. Spoiler: δ oscillations are key! 1/n

The outsized role of our brain astrocytes https://t.co/aWeuurgdNh @Nature feature

Over-active excitatory neurons in the cortex in infant mice lead to social deficits, according to a new preprint that study researchers claim can sway the debate over how signaling imbalances contribute to autism. By @DeWeerdt_Sarah https://t.co/DRrx4PiJA3

Interested in the mechanisms shaping the extraordinary complexity of the connectome? Then check out our new preprint, lead by @_francisnormand with a stellar team showing how geometry constrains connectome architecture: https://t.co/xKWm5R6x3N Peep the 🧵

Huge congrats to @StueferAlexia for steadily leading this tour-de-force 🥳, and to all the collaborators who generously contributed to this study. Special thanks also to @SimonsFdn @ERC_Research and @IITalk for funding this effort!

Chicken–egg solved? 🐣🥚 A brief early-life E:I imbalance ⚡ → transcriptional reprogramming 🧬 → disrupted social circuits 🧠 → lasting autism-relevant traits. Bottom line: early *developmental* E:I imbalance *is sufficient* to cause autism-related phenotypes!

Are these connectivity changes behaviorally relevant? Yes! In controls, PFC–dopaminergic (VTA, NAcc) connectivity tightly predicted sociability. But in manipulated mice, this relationship broke down → linking network dysfunction to social deficits.

But what’s happening at the circuit level? fMRI revealed selective hypoconnectivity between PFC & social brain hubs, sparing sensory networks. Intriguingly, dysregulated genes were spatially enriched in the hypoconnected regions → pointing to why social circuits are hit hardest!

How do these synaptic changes affect brain function? 🧠 EEG showed persistent cortical hyperexcitability in adult mice ⚡Strikingly, boosting inhibition with GABAergic drugs (R-baclofen, bumetanide) rescued sociability 💊

Why these persistent behavioral changes? We suspected activity-dependent transcriptional dysregulation might be at play. We indeed found evidence of lasting dysregulation of 530 genes. Notably this gene list is robustly enriched for synaptic autism-risk transcripts!

To this end, we boosted excitability in newborn mouse cortex (P1–P14) using chemogenetics. Result: manipulated mice showed persistent, autism-like social deficits 🐭 but not major motor, sensory, or memory issues. Crucially: no effect when manipulation was done in adolescence.

We thought, maybe these two opposing views can be reconciled using a developmental perspective: a short-lived imbalance during a critical early window might permanently derail circuit formation and produce autism-like phenotypes. This is exactly what we set out to test!

But critics note ↕️ E:I changes go both ways in autism 🧬 Evidence skewed to rare mutations 🐭 Research in autism models in fact suggests E:I imbalance may be compensatory (👉 https://t.co/1Fphcqiyfq) So, chicken or egg? 🐣🥚

Evidence: 🧬 Many autism genes (SHANK3, FMR1, TSC2…) regulate E:I 🐭 Mouse models show seizures & hyperexcitability 👩‍⚕️ 30% of autistic individuals show epileptiform activity

The E:I imbalance theory posits that too much excitation / too little inhibition destabilize circuits, leading to hyperexcitability & autism-related dysfunction

Excited to share our new preprint led by our mighty @StueferAlexia Here we tackle a classic chicken/egg 🐣🥚 question in #autism and dev. neuroscience 👉Is excitation–inhibition (E:I) imbalance a "cause" or a "consequence of autism? 👉 https://t.co/VsbzK14lXK Find out below🧵

Developmental excitation-inhibition imbalance permanently reprograms autism-relevant social brain circuits https://t.co/nF6KAAqV36 #biorxiv_neursci

Excited to share our new PNAS paper! 🎉 We examined the neural source of rs-fMRI FC using patterned optogenetic manipulation in mice 🧲🧠. A step toward answering a long-standing question. Fantastic work by @HnSk_Moon @hong_seok_jun @CNIR_IBS

Scientists have uncovered how puberty reshapes brain connectivity in 22q11.2 deletion syndrome, a genetic condition linked to autism and schizophrenia. The findings highlight how changes in synapses and brain connections may shape social behavior and…

First tweet on an exciting new manuscript online @NatureNeuro - in collab with @LucinaUddin and Catie Chang. We take a fresh look at the physiological dynamics associated with the global signal 🧠... #neuroscience #neuroimaging #fMRI Read here: https://t.co/KrLrLYOTUf

🚀 I will be presenting about our 🧠 🧲 BrainCAP toolbox at #OHBM in two weeks! 🎉 I'm on the job ⚡ market this year for a tenure-track assistant professor position in #psychiatry and relevant depts, and would love to meet you and chat about research and opportunities! 👇👇👇