Endocannabinoid signalling modulates susceptibility to traumatic stress exposure

Rebecca J. Bluett, Rita Báldi, Andre Haymer, Andrew D. Gaulden, Nolan D. Hartley, Walker P. Parrish, Jordan Baechle, David J. Marcus, Ramzi Mardam-Bey, Brian C. Shonesy, Md. Jashim Uddin, Lawrence J. Marnett, Ken Mackie, Roger J. Colbran, Danny G. Winder and Sachin Patel ()
Additional contact information
Rebecca J. Bluett: Vanderbilt University Medical Center
Rita Báldi: Vanderbilt University Medical Center
Andre Haymer: Vanderbilt University Medical Center
Andrew D. Gaulden: Vanderbilt University Medical Center
Nolan D. Hartley: Vanderbilt University Medical Center
Walker P. Parrish: Vanderbilt University Medical Center
Jordan Baechle: Vanderbilt University Medical Center
David J. Marcus: Vanderbilt University Medical Center
Ramzi Mardam-Bey: Vanderbilt University Medical Center
Brian C. Shonesy: Vanderbilt University Medical Center
Md. Jashim Uddin: A.B. Hancock Jr. Memorial Laboratory for Cancer Research and Vanderbilt Institute of Chemical Biology
Lawrence J. Marnett: A.B. Hancock Jr. Memorial Laboratory for Cancer Research and Vanderbilt Institute of Chemical Biology
Ken Mackie: Indiana University
Roger J. Colbran: The Vanderbilt Brain Institute, Vanderbilt University Medical Center
Danny G. Winder: Vanderbilt University Medical Center
Sachin Patel: Vanderbilt University Medical Center

Nature Communications, 2017, vol. 8, issue 1, 1-18

Abstract: Abstract Stress is a ubiquitous risk factor for the exacerbation and development of affective disorders including major depression and posttraumatic stress disorder. Understanding the neurobiological mechanisms conferring resilience to the adverse consequences of stress could have broad implications for the treatment and prevention of mood and anxiety disorders. We utilize laboratory mice and their innate inter-individual differences in stress-susceptibility to demonstrate a critical role for the endogenous cannabinoid 2-arachidonoylglycerol (2-AG) in stress-resilience. Specifically, systemic 2-AG augmentation is associated with a stress-resilient phenotype and enhances resilience in previously susceptible mice, while systemic 2-AG depletion or CB1 receptor blockade increases susceptibility in previously resilient mice. Moreover, stress-resilience is associated with increased phasic 2-AG-mediated synaptic suppression at ventral hippocampal-amygdala glutamatergic synapses and amygdala-specific 2-AG depletion impairs successful adaptation to repeated stress. These data indicate amygdala 2-AG signalling mechanisms promote resilience to adverse effects of acute traumatic stress and facilitate adaptation to repeated stress exposure.

Date: 2017
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DOI: 10.1038/ncomms14782

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