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Cannabigerol (CBG) is one of the major phytocannabinoids present in  Cannabis sativa  L. that is attracting pharmacological interest because it is non-psychotropic and is abundant in some industrial hemp varieties. The aim of this work was to investigate in parallel the binding properties of CBG to cannabinoid CB 1  (CB 1 R) and CB 2  (CB 2 R) receptors and the effects of the compound on agonist activation of those receptors and of CB 1 –CB 2  heteroreceptor complexes. Using [ 3 H]-CP-55940, CBG competed with low micromolar  K  i  values the binding to CB 1 R and CB 2 R. Homogeneous binding in living cells, which is only technically possible for the CB 2 R, provided a 152 nM  K  i  value. Also interesting, CBG competed the binding of [ 3 H]-WIN-55,212-2 to CB 2 R but not to CB 1 R ( K  i : 2.7 versus >30 μM). The phytocannabinoid modulated signaling mediated by receptors and receptor heteromers even at low concentrations of 0.1–1 μM. cAMP, pERK, β-arrestin recruitment and label-free assays in HEK-293T cells expressing the receptors and treated with endocannabinoids or selective agonists proved that CBG is a partial agonist of CB 2 R. The action on cells expressing heteromers was similar to that obtained in cells expressing the CB 2 R. The effect of CBG on CB 1 R was measurable but the underlying molecular mechanisms remain uncertain. The results indicate that CBG is indeed effective as regulator of endocannabinoid signaling.

Cannabigerol Action at Cannabinoid CB1 and CB2 Receptors and at CB1–CB2 Heteroreceptor Complexes