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Neuropsychopharmacology. 2018 Jan;43(1):80-102. doi: 10.1038/npp.2017.162. Epub 2017 Jul 26.

Integrating Endocannabinoid Signaling and Cannabinoids into the Biology and Treatment of Posttraumatic Stress Disorder.

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Departments of Cell Biology and Anatomy & Psychiatry, Hotchkiss Brain Institute and Mathison Center for Mental Health Research and Education, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada.
Department of Physiology and Pharmacology, Sapienza University of Rome, Rome, Italy.
Traumatic Stress Studies Division, Mount Sinai School of Medicine, James J Peters VA Medical Center, Bronx, NY, USA.
Department of Psychiatry and Behavioral Sciences, Nashville, TN, USA.
Department of Pharmacology, Nashville, TN, USA.
Department of Molecular Physiology & Biophysics, Nashville, TN, USA.
The Vanderbilt Brain Institute, Vanderbilt University Medical Center, Nashville, TN, USA.


Exposure to stress is an undeniable, but in most cases surmountable, part of life. However, in certain individuals, exposure to severe or cumulative stressors can lead to an array of pathological conditions including posttraumatic stress disorder (PTSD), characterized by debilitating trauma-related intrusive thoughts, avoidance behaviors, hyperarousal, as well as depressed mood and anxiety. In the context of the rapidly changing political and legal landscape surrounding use of cannabis products in the USA, there has been a surge of public and research interest in the role of cannabinoids in the regulation of stress-related biological processes and in their potential therapeutic application for stress-related psychopathology. Here we review the current state of knowledge regarding the effects of cannabis and cannabinoids in PTSD and the preclinical and clinical literature on the effects of cannabinoids and endogenous cannabinoid signaling systems in the regulation of biological processes related to the pathogenesis of PTSD. Potential therapeutic implications of the reviewed literature are also discussed. Finally, we propose that a state of endocannabinoid deficiency could represent a stress susceptibility endophenotype predisposing to the development of trauma-related psychopathology and provide biologically plausible support for the self-medication hypotheses used to explain high rates of cannabis use in patients with trauma-related disorders.

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