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Here’s why CBD oil could put current anxiolytic drugs to shame

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There is growing interest in the eCB system as a target for anxiety, trauma and stress-related disorders based on a burgeoning preclinical and clinical literature that supports a relationship between eCBs and fear, anxiety and stress. In the current mini-review, we have sought to highlight some of the main pathways to exploiting the eCB system as a means of generating novel pharmacotherapeutics for these disorders. These include the notion of augmenting the on-demand recruitment of AEA and 2-AG, either by inhibiting the hydrolyzing enzymes, fatty acid amide hydrolyze (FAAH) and monoacylglycerol lipase (MAGL), or by targeted inhibition of cyclooxygenase-2 (COX-2). Alternatively, blocking the activation of TRPV1 receptors, possibly in concert with the augmentation of AEA, could be an effective route to alleviating excessive anxiety and promoting stress-coping. Lastly, there is the possibility of utilizing the constituent of cannabis, CBD, to treat anxiety and stress-related disorders, albeit via neural mechanisms that might be independent of eCB signaling. Further basic research together with well-designed clinical studies, over the coming years will determine how successfully these various promising approaches evolve into much needed medications.

There is initial evidence supporting a functional connection between CBD and the 5-HT1A-R in regulating anxiety-like behavior. The anxiolytic-like effects produced by CBD injections into the rat infralimbic (Marinho et al., 2015) or prelimbic (Fogaca et al., 2014) cortices, BNST (Gomes et al., 2013; Gomes et al., 2012; Gomes et al., 2011) and dPAG (Campos et al., 2013a) are attenuated by concomitant 5-HT1A-R antagonism. One potential explanation for this interaction is that CBD could work as a positive allosteric enhancer of 5-HT1A-R. This would mean that for CBD to be fully effective as an anxiolytic there would need to be basal 5-HT1A-R occupancy (Rock et al., 2012). This is notable because 5-HT1A-R agonists, such as Buspirone, display also anxiolytic-like properties in assorted preclinical assays (e.g., Roncon et al., 2013; Saito et al., 2013; Zhou et al., 2014) and are clinically prescribed for various Anxiety Disorders, with reasonable response rates (Blessing et al., 2015; Chessick et al., 2006). Thus, one could envision a treatment strategy entailing the use of CBD as an adjunct that augment Buspirone efficacy via the two drugs additive or synergistic action at the 5-HT1A-R. An added benefit would be that the limited psychoactive profile of CBD, as compared to, for instance, THC, should produce fewer side-effects. The next step will be to begin testing these predictions in the clinic and parallel preclinical assays.

DISCLOSURE: The views and opinions expressed in this article are those of the authors, and do not represent the views of journaltranscript.com. Readers should not consider statements made by the author as formal recommendations and should consult their financial advisor before making any investment decisions. To read our full disclosure

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