Accordingly, CB1R activation has been suggested as a target for anxiolytic drug development [15, 43, 44]. Proposed agents for enhancing CB1R activation include THC, which is a potent and direct agonist; synthetic CB1R agonists; FAAH inhibitors and other agents that increase eCB availability, as well as nonpsychoactive cannabis phytocannabinoids, including CBD. While CBD has low affinity for the CB1R, it functions as an indirect agonist, potentially via augmentation of CB1R constitutional activity, or via increasing AEA through FAAH inhibition (reviewed in ).
Cannabidiol, or CBD for short, is a phyto-cannabinoid found in cannabis plants. However, it does not cause the same psychoactive effects as other naturally occurring cannabinoids (such as tetrahydrocannabinol, or THC). CBD induces feelings of sleepiness and tranquility, making it suitable for insomnia and other sleep disorders; CBD can be used to alleviate symptoms of epilepsy, diabetes, and anxiety disorders, as well. Legality is an issue for some; all 50 states have laws governing the sale, possession, and use of CBD, and they vary significantly (see the table below for a full analysis).