Interactions of CB1R and GABAergic systems provide another potential explanation for the psychotomimetic effects of Δ9-THC given the converging preclinical evidence of important interactions between endocannabinoid and GABA systems [58]. Considering the high expression of CB1R on GABAergic interneurons, the modulation of the activity of these interneurons is believed to mediate most of the effects of cannabinoids [67]. However, recent studies suggest that the loss of CB1R from GABAergic neurons does not have any significant effect on any of the major effects of cannabinoids [158].
