|CBDV||anti-convulsant in mice||Cannabidivarin is anticonvulsant in mouse and rat||Dec 2012|
Ingestion Method: 50-200 mg/kg|
These results indicate that CBDV is an effective anticonvulsant in a broad range of seizure models. Also it did not significantly affect normal motor function and, therefore, merits further investigation as a novel anti-epileptic in chronic epilepsy models.
|CBD,CBDV||dmd in mice via experiment||Effects of non-euphoric plant cannabinoids on muscle quality and performance of dystrophic mdx mice.||May 2019|
|In mdx mice, CBD (60 mg?kg-1 ) and CBDV (60 mg?kg-1 ) prevented the loss of locomotor activity, reduced inflammation and restored autophagy.|
|CBD,CBDV||neuroprotective in vitro||Low doses of widely consumed cannabinoids (cannabidiol and cannabidivarin) cause DNA damage and chromosomal aberrations in human-derived cells.||Jan 2019|
|Negative Both compounds induced DNA damage in single cell gel electrophoresis (SCGE) experiments in a human liver cell line (HepG2) and in buccal-derived cells (TR146) at low levels (>= 0.2 uM).|
|CBDV||rett syndrome in mice via experiment||Cannabidivarin completely rescues cognitive deficits and delays neurological and motor defects in male Mecp2 mutant mice.||May 2019|
|Positive CBDV rescues recognition memory deficits in Mecp2 mutant mice and delays the appearance of neurological defects.|
|CBD,CBDV||epilepsy in vitro via experiment||Nonpsychotropic plant cannabinoids, cannabidivarin (CBDV) and cannabidiol (CBD), activate and desensitize transient receptor potential vanilloid 1 (TRPV1) channels in vitro: potential for the treatment of neuronal hyperexcitability.||Nov 2014|
Action Pathway: TRPV1|
However, TRPV1 was strongly phosphorylated (and hence likely sensitized) in Mg(2+)-free solution-treated hippocampal tissue, and both capsaicin and CBDV caused TRPV1 dephosphorylation, consistent with TRPV1 desensitization. We propose that CBDV effects on TRP channels should be studied further in different in vitro and in vivo models of epilepsy.