Mice exposed to THC during adolescence developed persistent social interaction deficits, sensorimotor gating problems, and long-lasting changes in cortico-striatal brain connectivity and dopamine receptor balance that persisted into adulthood.
Neuroscientists studying adolescent brain vulnerability, psychiatrists concerned about youth cannabis use, and policymakers evaluating age restrictions for cannabis.
What the researchers found
Adolescent THC exposure impaired social interaction and increased vulnerability to sensorimotor gating deficiencies (similar to those in heavy cannabis users). Long-term cortico-striatal dysconnectivity correlated with impaired social interactions in adulthood. Lasting molecular changes were found in the balance between dopamine D2, adenosine A2A, and cannabinoid CB1 receptors in the striatum.
Why it matters
This provides neurobiological evidence for why adolescent cannabis use is associated with increased psychosis risk. The combination of brain connectivity changes, receptor imbalances, and behavioral deficits creates a plausible mechanistic pathway from adolescent exposure to adult psychiatric vulnerability.
The numbers in context
Persistent effects found in: social interaction, sensorimotor gating, cortico-striatal connectivity, and D2/A2A/CB1 receptor balance in striatum. Social interaction deficits correlated with connectivity changes.
How the study worked
Mice treated with THC during adolescence were assessed for behavioral, connectivity, and molecular changes persisting into adulthood. Included social interaction testing, sensorimotor gating, brain connectivity imaging, and receptor expression analysis.
What this study cannot tell us
Mouse model may not fully translate to human adolescent brain development. THC dosing and exposure patterns may not match typical human use. Only assessed a limited set of behaviors and brain regions.
How to read the evidence
Multi-level evidence (behavioral, circuit, molecular) providing mechanistic insight, though limited to one animal model and dosing regimen.
When this study was published
2025 publication.
The bigger picture
Human epidemiological studies associate adolescent cannabis use with psychosis risk, but demonstrating mechanism requires animal models. This study provides three levels of evidence, behavioral, circuit, and molecular, all pointing to lasting mesolimbic dopamine system disruption.
Questions still open
- Are the cortico-striatal connectivity changes reversible with extended abstinence?
- Do specific genetic backgrounds make adolescent brains more vulnerable to these THC-induced changes?
Common questions
Why is the adolescent brain more vulnerable to THC?
Do these findings apply to humans?
Read the original research
Long-lasting behavioral, molecular and functional connectivity alterations after chronic THC exposure during adolescence in mice.
Progress in neuro-psychopharmacology & biological psychiatry, 140, 111422
Citation
Gómez-Acero, Laura; Varriano, Federico; Sánchez-Fernández, Nuria; Ciruela, Francisco; Soria, Guadalupe; Aso, Ester. (2025). Long-lasting behavioral, molecular and functional connectivity alterations after chronic THC exposure during adolescence in mice.. Progress in neuro-psychopharmacology & biological psychiatry, 140, 111422. https://doi.org/10.1016/j.pnpbp.2025.111422
Explore the wider topic
- How to Talk to Your Teenager About Weed (Without Losing Them)
- My Kid's Friends Smoke Weed: A Parent's Guide
- I Smoke Weed But Don't Want My Kids To: Navigating the Hypocrisy
- Quitting Weed as a Parent: Why It Is the Hardest and Most Important Quit
- Quitting Weed as a Teen or Young Adult
- My Kid Is Smoking Weed: A Parent's Guide