Nature neuroscience
July 1, 2025
Ya'El Courtney, Joshua P Head, Neil Dani et al.
10 citations
The choroid plexus (ChP) regulates cerebrospinal fluid (CSF) composition, providing essential molecular cues for brain development. Apocrine secretion by embryonic ChP epithelial cells is a key regulator of the CSF proteome and neurodevelopment in male and female mice. Activation of serotonergic 5-HT2C receptors triggers sustained calcium signaling, driving high-volume apocrine secretion in mouse and human ChP. This secretion alters the CSF proteome, stimulating neural progenitors and shifting their developmental trajectory. Inducing ChP secretion in utero disrupts neural progenitor dynamics, cerebral cortical architecture, and offspring behavior. Illness or lysergic acid diethylamide exposure during pregnancy provokes coordinated ChP secretion in mouse embryos. The findings reveal a fundamental secretory pathway in the ChP that shapes brain development, and its disruption can have lasting consequences for brain health.
bioRxiv : the preprint server for biology
January 16, 2024
Ya'El Courtney, Joshua P Head, Elizabeth D Yimer et al.
9 citations
preprint
Apocrine secretion by embryonic choroid plexus (ChP) epithelial cells contributes to the cerebrospinal fluid (CSF) proteome and influences brain development in mice. This process depends on sustained intracellular calcium signaling and calpain-mediated cytoskeletal remodeling, rapidly altering the CSF proteome and activating neural progenitors lining the brain's ventricles. Overactivation of this secretion—triggered by maternal administration of a serotonergic 5HT2C receptor agonist, maternal illness, or the psychedelic drug LSD during pregnancy—dysregulates cerebral cortical development, alters the fate of CSF-contacting neural progenitors, and changes adult social behaviors. These findings demonstrate a mechanism by which diverse maternal stressors disrupt in utero brain development.
Neuroscience letters
May 23, 2025
Diane Joss, Gunes Sevinc, John W Denninger et al.
1 citation
Among 94 chronically stressed but otherwise healthy adults randomized to eight weeks of meditation, yoga, or stress education, only the meditation group showed a significant reduction in resting-state functional connectivity between the posterior cingulate cortex and the left hippocampus. Changes in this brain connectivity were correlated with improvements in perceived stress, allostatic load, and anti-inflammatory gene expression, suggesting that meditation's neural effects are closely linked to physical wellness biomarkers. No such changes occurred in the yoga or stress education groups, indicating this neurobiological mechanism may be unique to meditation training.