Atypical cannabinoid targets
Cannabinoids effects on the central and peripheral nervous systems are primarily attributed to two G-protein-coupled receptors; cannabinoid receptors type 1 and type 2 (CB1 and CB2, respectively). Phytocannabinoids show different affinities for CB1 and CB2 receptors. Cannabidiol or CBD has a low affinity for the CB1 and CB2 receptors and acts as an antagonist of CB1 and CB2 agonists.
In many cases, the pharmacological effects of cannabinoids cannot be explained by their interactions with CB1 and CB2 receptors. A growing body of evidence supports the interaction of cannabinoids with additional novel receptors.
For example, the cannabidiol may be an antagonist of GPR55, an inverse agonist of GPR3, GPR6, and GPR12 and a serotonin 5-HT1A receptor, partial agonist. It is also an allosteric modulator of the μ- and δ-opioid receptors and agonist of PPARγ.