Cannabidiol inhibits sucrose self-administration by CB1 and CB2 receptor mechanisms in rodents.


A rising variety of research recommend therapeutic functions of cannabidiol (CBD), a not too long ago U.S. Meals and Drug Administration (FDA)-approved treatment for epilepsy, in remedy of many different neuropsychological issues. Nonetheless, pharmacological motion and the mechanisms by which CBD exerts its results aren’t totally understood. Right here, we examined the results of CBD on oral sucrose self-administration in rodents and explored the receptor mechanisms underlying CBD-induced behavioral results utilizing pharmacological and transgenic approaches. Systemic administration of CBD (10, 20, and 40 mg/kg, ip) produced a dose-dependent discount in sucrose self-administration in rats and in wild-type (WT) and CB1-/- mice however not in CB2-/- mice. CBD seemed to be extra efficacious in CB1-/- mice than in WT mice. Equally, pretreatment with AM251, a CB1R antagonist, potentiated, whereas AM630, a selective CB2R antagonist, blocked CBD-induced discount in sucrose self-administration, suggesting the involvement of CB1 and CB2 receptors. Moreover, systemic administration of JWH133, a selective CB2R agonist, additionally produced a dose-dependent discount in sucrose self-administration in WT and CB1-/- mice, however not in CB2-/- mice. Pretreatment with AM251 enhanced, whereas AM630 blocked JWH133-induced discount in sucrose self-administration in WT mice, suggesting that CBD inhibits sucrose self-administration possible by CB1 receptor antagonism and CB2 receptor agonism. Taken collectively, the current findings recommend that CBD could have therapeutic potential in decreasing binge consuming and the event of weight problems.


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