^ Klein C, Karanges E, Spiro A, Wong A, Spencer J, Huynh T, Gunasekaran N, Karl T, Long LE, Huang XF, Liu K, Arnold JC, McGregor IS (November 2011). "Cannabidiol potentiates Δ⁹-tetrahydrocannabinol (THC) behavioural effects and alters THC pharmacokinetics during acute and chronic treatment in adolescent rats". Psychopharmacology. 218 (2): 443–457. doi:10.1007/s00213-011-2342-0. PMID 21667074.
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]
The symptoms of nicotine overdose are clearer indicators of what is happening in your body than the symptoms of withdrawal. This is because nicotine overdose has been studied a fair bit. Nicotine withdrawal has not been studied nearly as much. What has been studied a lot is cigarette withdrawal which is a different thing – it includes no longer inhaling a few thousand chemicals, not just nicotine.
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