Abstract
Epilepsy contributes to approximately 1% of the global disease burden. By affecting especially young children as well as older persons of all social and racial variety, epilepsy is a present disorder worldwide. Currently, only 65% of epileptic patients can be successfully treated with antiepileptic drugs. For this reason, alternative medicine receives more attention. Cannabis has been cultivated for over 6000 years to treat pain and insomnia and used since the 19th century to suppress epileptic seizures. The two best described phytocannabinoids, (−)-trans-Δ9-tetrahydrocannabinol (THC) and cannabidiol (CBD) are claimed to have positive effects on different neurological as well as neurodegenerative diseases, including epilepsy. There are different cannabinoids which act through different types of receptors and channels, including the cannabinoid receptor 1 and 2 (CB1, CB2), G protein-coupled receptor 55 (GPR55) and 18 (GPR18), opioid receptor µ and δ, transient receptor potential vanilloid type 1 (TRPV1) and 2 (TRPV2), type A γ-aminobutyric acid receptor (GABAAR) and voltage-gated sodium channels (VGSC). The mechanisms and importance of the interaction between phytocannabinoids and their different sites of action regarding epileptic seizures and their clinical value are described in this review.
Highlights
Epilepsy is a chronic neurological disease affecting approximately 50 million people of all ages and sexes worldwide
These findings show that the effects of CBDV in different ages and epilepsy models are TRPV1-dependent [138]
Cannabis sativa L. stepped in the main focus of present research and reached an approximately 2400-fold publication rate since the first official cannabis report in 1939
Summary
Epilepsy is a chronic neurological disease affecting approximately 50 million people of all ages and sexes worldwide. Lorazepam and other benzodiazepines increase GABAAR-mediated inhibition and display a decent medication for symptomatic seizures [12,13] Other medications such as phenytoin and carbamazepine prevent voltage-gated Na+ channels from activation and reduce the firing of action potentials [14,15]. Its structure was taken as a lead compound for the development of increasingly active synthetic cannabinoids Such synthetic cannabinoids have different chemical structures like classical (e.g., nabilones) [30], non-classical (e.g., WIN55212-2) [31], aminoalkylindoles (e.g., JWH-018) [32] and endogenous arachidonic acid derivatives including endocannabinoids such as 2-arachidonoylglycerol (2-AG) and N-arachidonylethanolamide The mechanism and function of inhibition of endocannabinoid hydrolysis in epileptogenesis requires further investigation
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