Cannabigerol, a minor phytocannabinoid, prevents behavioral changes induced by psychotomimetic drugs.

Pedrazzi J.; Sales A.; Hallak J.; Zuardi A.; Guimarães F.; Del Bel E.; Crippa J. · Progress in neuro-psychopharmacology & biological psychiatry · 2026

**Background & Methods** This review study investigated cannabigerol (CBG), a minor phytocannabinoid from Cannabis sativa, for antipsychotic-like effects in preclinical animal models. Male Swiss mice received intraperitoneal injections of CBG followed by psychotomimetic agents (d-amphetamine or MK-801), then underwent behavioral testing including open field, novel object recognition (NOR), social interaction, and prepulse inhibition (PPI) assays to evaluate antipsychotic potential. **Key Findings** • CBG demonstrated attenuation of d-amphetamine-induced behavioral disruptions in both the PPI and open field tests, suggesting effectiveness against amphetamine-induced hyperlocomotion and deficits. • Pre-treatment with CBG significantly attenuated MK-801-induced impairments across multiple behavioral domains: social interaction deficits, novel object recognition impairment, and PPI disruption, indicating broad antipsychotic-like effects. • Notably, these therapeutic benefits were observed at reduced/lower concentrations compared to other cannabinoids, suggesting CBG may have enhanced potency or improved therapeutic potential as an antipsychotic candidate. **Dosage & Administration** Specific dosages and concentrations of CBG are not explicitly detailed in the abstract provided. Administration was via intraperitoneal injection in the animal model. **Safety & Adverse Effects** The abstract does not report specific adverse effects or safety data from this study. However, it notes that CBG, like cannabidiol (CBD), does not cause psychotomimetic effects and that CBD has demonstrated lower induction of side effects compared to conventional antipsychotic therapy, suggesting a potentially favorable safety profile for CBG. **Evidence Quality** This is a preclinical animal study with significant limitations. The research uses only male Swiss mice and psychotomimetic drug-induced animal models, which may not fully translate to human schizophrenia pathology. The abstract provides limited methodological detail regarding sample sizes, statistical analysis, or control conditions. As an animal model study, this represents lower-level evidence (preclinical stage) and requires validation through human clinical trials before therapeutic claims can be established. The authors appropriately frame CBG as a "promising candidate for future translational and clinical investigations" rather than a proven treatment.

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