Functional Redundancy Between Canonical Endocannabinoid Signaling Systems in the Modulation of Anxiety

摘要

BackgroundIncreasing the available repertoire of effective treatments for mood and anxiety disorders represents a critical unmet need. Pharmacological augmentation of endogenous cannabinoid (eCB) signaling has been suggested to represent a novel approach to the treatment of anxiety disorders; however, the functional interactions between two canonical eCB pathways mediated via anandamide (AEA) and 2-arachidonoylglycerol (2-AG) in the regulation of anxiety are not well understood.