More on cannabis use disorder

    November 29, 2022 2 min read

    More on cannabis use disorder

    We have written elsewhere about the fairly well established ability of cannabidiol (CBD) to counteract certain effects of tetrahydrocannabinol (THC), and in a related vein to have a possible application in treatment of cannabis use disorder (and other dependency syndromes). More has been learned recently* about the synaptic changes that can accompany chronic cannabinoid use, notably those associated with agonists for the CB1 receptor, which participates in short- and long-term brain plasticity. THC is a partial agonist at CB1. Vexingly, its actions are inconsistent, being inhibitory at some synapses but not others. This may be a function of varying CB1 density in different places. Chronic exposure to THC, in any case, degrades presynaptic CB1 actions in several brain regions. This in turn gives rise to deficient endocannabinoid-mediated synaptic plasticity, which disrupts cognitive functions, in particular those pertaining to reward processing. This has been observed in animal models and in humans. There is still work ahead to identify the molecular mechanisms behind this loss of CB1 function, and to ascertain where in the brain it is likely to arise. 

    *See for example, Augustin SM, et al., Neurobiology of Disease 167 (2022), 105670;

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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.