Collin, C., Ehler, E., Waberzinek, G., Alsindi, Z., Davies, P., Powell, K., Notcutt, W., O'Leary, C., Ratcliffe, S., Novakova, I., Zapletalova, O., Pikova, J., and Ambler, Z. A double-blind, randomized, placebo-controlled, parallel-group study of Sativex, in subjects with symptoms of spasticity due to multiple sclerosis. Neurol.Res. 2010;32(5):451-459. View abstract.
Cannabidiol has low affinity for the cannabinoid CB1 and CB2 receptors,[26][27] although it can act as an antagonist of CB1/CB2 agonists despite this low affinity.[27] Cannabidiol may be an antagonist of GPR55, a G protein-coupled receptor and putative cannabinoid receptor that is expressed in the caudate nucleus and putamen in the brain.[28] It also may act as an inverse agonist of GPR3, GPR6, and GPR12.[29] CBD has been shown to act as a serotonin 5-HT1A receptor partial agonist.[30] It is an allosteric modulator of the μ- and δ-opioid receptors as well.[31] The pharmacological effects of CBD may involve PPARγ agonism and intracellular calcium release.[7] cannabidiol
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