We uncovered a new serotonergic axis — from the ChP to the CSF — that sculpts the developing brain. It’s powerful, fast, and vulnerable to disruption. This work opens a new window into how maternal environments influence lifelong brain function.
📖 Full paper: rdcu.be/eoaSY

Maternal exposure to the psychedelic LSD triggered the same ChP secretory response. Within 30 minutes, nearly 70% of embryonic ChP cells formed aposomes.
This suggests serotonergic drugs in pregnancy may directly alter brain development via the CSF.

When we triggered ChP secretion during neurogenesis, the consequences were striking.
We saw shifts in neuronal fate:
⬆️ SATB2+ callosal projection neurons
⬇ TBR1+ corticothalamic neurons
These changes were layer-specific — reorganizing cortical architecture at its foundation.

Apocrine secretion changes the composition of the CSF in minutes. We found a surge of key developmental signals including IGF2, Sonic Hedgehog (SHH), insulin, & transthyretin (TTR). Each of these proteins is known to shape how neural progenitors divide and differentiate.

So what sets off this secretory burst? Among other things, activation of the serotonin receptor 5-HT2C. We showed that stimulating 5-HT2C triggers a wave of calcium signaling followed by apocrine secretion in the embryonic ChP, flooding the CSF with key developmental signals.

Balloon-like structures, called aposomes, form at the surface of ChP cells & release huge amounts of protein directly into the CSF. This is a high-volume, coordinated secretion mechanism, & it massively expands our understanding of how the ChP contributes to brain development.

We discovered the choroid plexus (ChP) doesn’t just secrete tiny vesicles & exosomes. It also unleashes large apocrine secretory structures packed with proteins that flood cerebrospinal fluid (CSF) during brain development. This changes how we think about embryonic brain signaling.