Abstract
Over the last several years, there has been increased interest in cannabidiol (CBD) to treat various ailments such as pain, anxiety, insomnia, and inflammation. The potential for CBD as an anti-inflammatory therapy has come, in part, from its demonstrated ability to suppress neuroinflammation in autoimmune diseases, such as the mouse model of multiple sclerosis, experimental autoimmune encephalomyelitis (EAE). The increased use of CBD strongly suggests that more research is necessary to elucidate its safety and efficacy and determine the mechanisms by which it acts. Thus, we conducted two separate studies. In the first, RNA sequencing (RNA-Seq) analysis of brains of female mice undergoing EAE in the presence and absence of CBD was conducted to identify potential genes that mediated its neuroprotective effects when efficacious. In the second, we assessed some of the same genes in male and female mice treated with CBD in the absence of an immune stimulus. Together, these data showed that CBD modestly increased oxytocin (Oxt) and arginine vasopressin (vasopressin, Avp) gene expression in the brains of mice, regardless of whether there was active inflammation. Overall, these data suggest that Oxt and Avp might act as biomarkers for CBD exposure.