Gestational psychedelic exposure disrupts brain development and offspring behavior in mice.
Ya'El Courtney, Josephine M Anderson, Christian Lagares-Linares, Cody J. Wenthur, Maria K Lehtinen
bioRxiv : the preprint server for biology September 30, 2025 preprint DOI: 10.1101/2025.09.30.677638 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Experimental study |
|---|---|
| Population | Mice |
| Intervention | LSD |
| Dose | 0.3 mg kg-1 |
| Duration | Single dose at E12.5 or repeated dosing from E12.5 to E16.5; outcomes assessed at postnatal day 8 and in adulthood |
| Keywords | Maternal psychedelic exposure Prenatal hallucinogen exposure Gestational LSD Use Maternal substance use Neurodevelopmental impacts Brain development alterations Fetal neurotoxicity Embryonic brain changes Developmental neuroscience effects Neurological impacts Offspring behavioral changes Adult offspring deficits Developmental behavioral issues Sensory processing problems Lasting behavioral differences Postnatal behavioral effects Fetal brain development Embryonic brain formation Developing brain effects Prenatal brain growth Brain structure changes Cell development |
| Key findings | Maternal LSD exposure in mice alters fetal brain development and leads to lasting behavioral changes in adult offspring, including reduced prepulse inhibition and rotational stereotypy. |
Abstract
Despite increasing non-medical use and clinical investigation of psychedelics, the consequences of prenatal exposure remain unknown. In mice, maternal lysergic acid diethylamide (LSD; 0.3 mg kg -1 ) crossed the placenta, appearing in embryonic cerebrospinal fluid (CSF) within minutes at E12.5 and E16.5. Within 30 minutes, LSD and other serotonergic psychedelics induced a 5-HT 2 C agonist-like response in the choroid plexus, triggering apical remodeling and increasing CSF protein. A single E12.5 exposure altered cerebral cortical laminar organization and composition at postnatal day 8, and repeated dosing (E12.5-E16.5) amplified male-biased shifts from SATB2 + to CTIP2 + neuronal identities and increased microglia. Adult offspring showed reduced prepulse inhibition (male-predominant) and rotational stereotypy. These data identify an embryo-facing interface that detects maternal psychedelics and link CSF access to enduring neurodevelopmental and behavioral consequences.
Citations in the library
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