Earlier versions did! There are word limitations that make mentioning everything quite hard.

And I want to thank the wonderful reviewers (among them was @theborislab.bsky.social )who made the paper all that much stronger

All of this work was made possible by the wonderful team. @AdamBauer @jordacular.bsky.social @realjoshsiegel.bsky.social @oliverk28.bsky.social @washumedicine.bsky.social @washumedmir.bsky.social

8/ So now what!?

Next steps:
• Validate in humans 🧍‍♂️
• Build “vascular correction” models
• Revisit classic fMRI psychedelic studies

7/ Serotonin is vasoactive—it affects blood vessels, not just neurons (it’s right there in the etymology!). 🩸
Yet most imaging studies barely account for that.

6/ Take-home: neuronal and hemodynamic measures of brain function can dissociate under psychedelics, which has huge implications for interpreting human imaging data when under the influence of psychedelics.

5/ And here's a little mechanistic clue: blocking 5-HT₂A receptors (with MDL100907) predominantly reversed the dissociated reports of brain function → receptor-specific!?

4/ fMRI (BOLD) signals depend on blood flow.
So, some “functional” effects in psychedelic imaging may reflect vascular—not neuronal—changes. We observe divergent patterns across multiple functional measures, including FC, modularity, power, and stimulus response (
@every
figure)

3/ Even tripper: we saw similar shifts in human psilocybin fMRI data.

2/ After DOI (blue trace, right), neurovascular coupling (the link between brain ⚡️and blood 🩸signals) went off script.
The hemodynamic response got tighter—and even sprouted an acausal feature (suggesting an emergent vasculo-neuronal relation!). Wild stuff. 🤯

1/ We concurrently tracked pan-cortical neural ⚡️and hemodynamic 🩸signals before and after psychedelic intoxication in mice. SURPRISE: these signals reported different effects!