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Cannabidiol (CBD), the main non-psychotomimetic component of the plant Cannabis sativa, exerts therapeutically promising effects on human mental health such as inhibition of psychosis, anxiety and depression. However, the mechanistic bases of CBD action are unclear. Here we investigate the potential involvement of hippocampal neurogenesis in the anxiolytic effect of CBD in mice subjected to 14 d chronic unpredictable stress (CUS). Repeated administration of CBD (30 mg/kg i.p., 2 h after each daily stressor) increased hippocampal progenitor proliferation and neurogenesis in wild-type mice. Ganciclovir administration to GFAP-thymidine kinase (GFAP-TK) transgenic mice, which express thymidine kinase in adult neural progenitor cells, abrogated CBD-induced hippocampal neurogenesis. CBD administration prevented the anxiogenic effect of CUS in wild type but not in GFAP-TK mice as evidenced in the novelty suppressed feeding test and the elevated plus maze. This anxiolytic effect of CBD involved the participation of the CB1 cannabinoid receptor, as CBD administration increased hippocampal anandamide levels and administration of the CB1–selective antagonist AM251 prevented CBD actions. Studies conducted with hippocampal progenitor cells in culture showed that CBD promotes progenitor proliferation and cell cycle progression and mimics the proliferative effect of CB1 and CB2 cannabinoid receptor activation. Moreover, antagonists of these two receptors or endocannabinoid depletion by fatty acid amide hydrolase overexpression prevented CBD-induced cell proliferation. These findings support that the anxiolytic effect of chronic CBD administration in stressed mice depends on its proneurogenic action in the adult hippocampus by facilitating endocannabinoid-mediated signalling.
Experimenting with sublingual CBD/THC blend oil causes my benign PVCs to subside. I would be very interested in any reputable clinical trial on the effects of CBD on cardiac PVCs to determine if there is some mechanistic basis for my personal experience regarding the cardiac nervous system.
@HeartyVegan Above average neurogenesis in the hippocampus has also been shown to be responsible for the disruption of the short-term memory, and adding another piece to the puzzle another study recently showed that amyloid beta actually plays a functional role in short-term memory (not sure if you saw the paper a while back that showed that THC prevented the aggregation of amyloid beta).
Amyloid beta aggregates, of course, is the stuff more well known for the fact that it causes alzheimer’s.
So it’s sort of interesting that this effect of abnormal levels of neurogenesis (which causes short-term memory impairment) also happens to be the cause of the anti-anxiety effects. Neuroscience is complicated. :)
@HeartyVegan actually, here’s a fresh PR piece on the alzheimers-cannabinoid connection… glad to see there’s still research going on: