Cannabidiol (CBD) is a non-psychotomimetic compound from Cannabis sativa plant that produces antipsychotics effects in rodents and humans. CBD reduced catalepsy induced by typical antipsychotic haloperidol, a dopamine D2 receptor antagonist. CBD has been proposed to act as an atypical antipsychotic. Cannabigerol (CBG) is another non-psychoactive molecule from Cannabis sativa, a potential pharmaceutical for several neuropsychiatric conditions. In this study we investigated if CBG could have beneficial effects on motor related striatal disorders. We evaluated if CBG would prevent catalepsy induced by haloperidol (0.3mg/kg; s.c) and the c-Fos protein induction in the dorsal striatum. For this adult male Swiss mice received acute preatment with CBG (0.3, 1.0, 3.0 or 10mg/kg; i.p) 15min prior to the haloperidol treatment. CBG was not able to attenuate haloperidol-induced catalepsy and the expression of the induced c-Fos protein. No study of the combination of no-psychoactive cannabinoids is available. We evaluate the possible effects of the two lowest doses of CBG (1 and 3mg/kg) and CBD (15mg/kg), sub-effective doses given in combination. This combination attenuated haloperidol-induced catalepsy. A 5-HT1A-receptor blocker (WAY100635, 0.1mg/kg) inhibited the anticataleptical effects of CBD-CBG low dose. In contrast, high dose CBG (10mg/kg) blocked the anticataleptic effect of CBD (30mg/kg), at its effective dose. In conclusion, the results suggest an interaction dose dependent between both cannabinoids. The benefits shared by CBD and CBG are enhanced when they are combined, making the overall compound more effective at the dose of 3 and 15mg already. CBG and CBD exert their activity at multiple molecular sites. The CBG in high dose possibly blocks 5-HT1A-receptor inhibiting the CBD action.