Cannabidiol has a very low affinity for CB1 and CB2 receptors but acts as an indirect antagonist of their agonists. While one would assume that this would cause cannabidiol to reduce the effects of THC, it may potentiate THC’s effects by increasing CB1 receptor density or through another CB1-related mechanism. It may also extend the duration of the effects of THC via inhibition of the cytochrome P-450-3A and 2C enzymes.
Recently, it was found to be an antagonist at the putative new cannabinoid receptor, GPR55, a GPCR expressed in the caudate nucleus and putamen Cannabidiol has also been shown to act as a 5-HT1A receptor partial agonist, an action which may be involved in its antidepressant, anxiolytic, and neuroprotective effects. Cannabidiol is an allosteric modulator of μ and δ-opioid receptors. Cannabidiol’s pharmacological effects have also been attributed to PPAR-γ receptor agonism and intracellular calcium release.
Research suggests that CBD may exert some of its pharmacological action through its inhibition of FAAH, which may in turn increase the levels of endocannabinoids, such as anandamide, produced by the body.
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