Disrupting the cannabinoid system in newborn mice led to vocal tics, hyperactivity, and learning deficits resembling a combined ADHD/Tourette syndrome phenotype, particularly in males.
Neurodevelopment researchers, clinicians treating ADHD/Tourette syndrome, endocannabinoid system scientists
What the researchers found
Postnatal exposure to the CB1 blocker rimonabant in wild-type, CB1 knockout, and CB2 knockout mice produced distinct behavioral outcomes. Wild-type pups developed vocal-like tics and learning deficits; as adults, they showed hyperactivity, motor tics, and risky behavior. Vocal tics required both disrupted CB1 signaling and functional CB2 receptors. The findings suggest ADHD/Tourette syndrome may share a common origin in early cannabinoid system disruption.
Why it matters
If the endocannabinoid system plays a foundational role in neurodevelopment, disruptions during critical early periods could have lasting behavioral consequences. The sex-specific patterns (males more affected) mirror the clinical epidemiology of ADHD and Tourette syndrome.
The numbers in context
Three genotypes tested (wild-type, CB1 KO, CB2 KO); rimonabant administered postnatally; males showed vocal tics, hyperactivity, and learning deficits; females showed hyperactivity but no vocal tics in CB2 knockouts
How the study worked
Postnatal wild-type, CB1 knockout, and CB2 knockout mouse pups were exposed to rimonabant (CB1 antagonist/inverse agonist). Behavioral assessments tracked vocal tics, motor activity, learning, rearing, and risk-taking from postnatal period through adulthood. Sex-specific outcomes were analyzed across all genotypes.
What this study cannot tell us
Mouse behavioral models have limited translational value for complex human neurodevelopmental disorders. Pharmacological disruption of cannabinoid signaling does not replicate naturally occurring developmental variations. Small sample sizes typical of transgenic mouse studies.
How to read the evidence
Preliminary: animal study using pharmacological and genetic manipulation, limited translational applicability.
When this study was published
2025 publication
The bigger picture
ADHD and Tourette syndrome frequently co-occur in clinical practice but are typically treated as separate conditions. This research proposes they may represent a single phenotype arising from early endocannabinoid system dysfunction.
Questions still open
- Could variations in endocannabinoid system development contribute to ADHD/Tourette risk in humans?
- Would early cannabinoid system support reduce the severity of these phenotypes?
Read the original research
A Tourette Syndrome/ADHD-like Phenotype Results from Postnatal Disruption of CB1 and CB2 Receptor Signalling.
International journal of molecular sciences, 26(13)
Citation
Gorberg, Victoria; Harpaz, Tamar; Shamir, Emilya Natali; Karminsky, Orit Diana; Fride, Ester; Pertwee, Roger G; Greig, Iain R; McCaffery, Peter; Anavi-Goffer, Sharon. (2025). A Tourette Syndrome/ADHD-like Phenotype Results from Postnatal Disruption of CB1 and CB2 Receptor Signalling.. International journal of molecular sciences, 26(13). https://doi.org/10.3390/ijms26136052
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