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Molecular Physiology & Biophysics

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

AUTHORS

Bedse G , Hartley ND , Neale E , Gaulden AD , Patrick TA , Kingsley PJ , Uddin MJ , Plath N , Marnett LJ , Patel S , . Biological psychiatry. 2017 10 1; 82(7). 488-499

ABSTRACT

Increasing 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 (N-arachidonylethanolamine [AEA]) and 2-arachidonoylglycerol (2-AG) in the regulation of anxiety are not well understood.

Increasing 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 (N-arachidonylethanolamine [AEA]) and 2-arachidonoylglycerol (2-AG) in the regulation of anxiety are not well understood.

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