There is evidence of interaction between the body’s widespread endocannabinoid and monoamine neurotransmitter systems in regulation of compulsive behavior. Cannabidiol (CBD) has been shown in animal models to inhibit obsessive-compulsive behaviour, in a time-dependent manner, matching its pharmacokinetic profile.
The mechanisms of action behind this are beginning to be understood. Cannabinoid receptors are significantly expressed in most parts of the cortico-striatal-thalamic circuitry, the network related to OCD, where they are able to modulate the release of key neurotransmitters such as glutamate, dopamine, GABA, and serotonin. Preclinical studies show that enhancement of cannabinoid receptor site 1 (CB1) function by direct agonists or inhibitors modulates compulsive activity. Deletion of CB1 receptors prevents shifting from goal-directed to habitual behavior. Inhibition of endocannabinoid catabolic enzymes also elicits anxiolytic effects. Endocannabinoid analogues exacerbate compulsion in mice via the TRPV1 receptor.
A murine model has shown that CBD induces a significant decrease in the number of buried marbles compared with controls. A larger decrease was also found after co-administration of paroxetine and diazepam. The effect of the CBD was still significant after 7 days of daily repeated administration, even after the effect of the diazepam disappeared. Pretreatment with WAY100635, a 5HT1A receptor antagonist, prevented the effects of paroxetine but failed to alter those of CBD. These latter effects, however, were prevented by pretreatment with the CB1 receptor antagonist AM251.
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The foregoing is a report on trends and developments in the cannabinoid industry. No product described herein is intended to diagnose, treat, cure or prevent any disease or syndrome.
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