Figure 1. In mice, subchronic treatment with THC leads to the downregulation of presynaptic cannabinoid CB₁ receptors expressed by parallel fibers that project onto Purkinje cells.

Cutando et al. (9) show that the loss of CB₁ receptors, either due to TCH-induced downregulation or genetic deletion, triggers a neuroinflammatory response typified by changes in microglial cell morphology and CB₂ receptor expression. This adaptive response underlies THC-induced deficits in cerebellar-associated learning functions.