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 CB1 (CB1R) and CB2 (CB2R) receptors and the effects of the compound on agonist activation of those receptors and of CB1–CB2 heteroreceptor complexes. Using [3H]-CP-55940, CBG competed with low micromolar Ki values the binding to CB1R and CB2R. Homogeneous binding in living cells, which is only technically possible for the CB2R, provided a 152 nM Ki value. Also interesting, CBG competed the binding of [3H]-WIN-55,212-2 to CB2R but not to CB1R (Ki: 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 CB2R. The action on cells expressing heteromers was similar to that obtained in cells expressing the CB2R. The effect of CBG on CB1R was measurable but the underlying molecular mechanisms remain uncertain. The results indicate that CBG is indeed effective as regulator of endocannabinoid signaling.

Δ -THCA shows potent neuroprotective activity, which is worth considering for the treatment of Huntington's disease and possibly other neurodegenerative and neuroinflammatory diseases.

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Plum shoot proliferation was investigated in terms of two distinct processes: axillary bud differentiation and axillary shoot development. Results showed that light quality influenced bud differentiation and interacted with apical dominance in determining shoot outgrowth, resulting in a differentiated structure of shoot clusters and type of branching. Results suggested that blue light, acting through its photoreceptor, increased the number of axillary buds differentiated from apical meristem, but did not remove the apical dominance. Red light removed apical dominance, while reducing the formation of axillary buds; both events appeared to be dependent on the putative amount of phytochrome active form, and independent of light photon fluence rate. On the contrary, blue light action appeared to be dependent on photon fluence rate. In addition, apparent blue±red interactions related to photomorphogenic events fit an antagonistic model for branching regulated by light via cryptochrome and phytochrome photoreceptors. Our results show that the dynamics of shoot cluster development is the product of two events: the formation of new axillary buds and their release from apical dominance.

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