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dc.contributor.authorNeumeister, Alexanderen_US
dc.contributor.authorNormandin, Marc D.en_US
dc.contributor.authorPietrzak, Robert H.en_US
dc.contributor.authorPiomelli, Danieleen_US
dc.contributor.authorZheng, Ming-Qiangen_US
dc.contributor.authorGujarro-Anton, Anaen_US
dc.contributor.authorPotenza, Marc N.en_US
dc.contributor.authorBailey, Christopher R.en_US
dc.contributor.authorLin, Shu-feien_US
dc.contributor.authorNajafzadeh, Soheilaen_US
dc.contributor.authorRopchan, Jimen_US
dc.contributor.authorHenry, Shannanen_US
dc.contributor.authorCorsi-Travali, Stefanien_US
dc.contributor.authorCarson, Richard E.en_US
dc.contributor.authorHuang, Yiyunen_US
dc.date.accessioned2014-04-11T14:13:12Z
dc.date.issued2013en_US
dc.identifier.citationNeumeister, A., M. D. Normandin, R. H. Pietrzak, D. Piomelli, M. Zheng, A. Gujarro-Anton, M. N. Potenza, et al. 2013. “Elevated Brain Cannabinoid CB1 Receptor Availability in Posttraumatic Stress Disorder: A Positron Emission Tomography Study.” Molecular psychiatry 18 (9): 1034-1040. doi:10.1038/mp.2013.61. http://dx.doi.org/10.1038/mp.2013.61.en
dc.identifier.issn1359-4184en
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:12064549
dc.description.abstractEndocannabinoids and their attending cannabinoid type 1 receptor (CB1) have been implicated in animal models of posttraumatic stress disorder (PTSD). However, their specific role has not been studied in people with PTSD. Herein, we present an in vivo imaging study using positron emission tomography (PET) and the CB1-selective radioligand [11C]OMAR in individuals with PTSD, and healthy controls with lifetime histories of trauma (trauma controls [TC]) and those without such histories (healthy controls [HC]). Untreated individuals with PTSD (N=25) with non-combat trauma histories, and TC (N=12) and HC (N=23) participated in a magnetic resonance (MR) imaging scan and a resting PET scan with the CB1 receptor antagonist radiotracer [11C]OMAR, which measures volume of distribution (VT) linearly related to CB1 receptor availability. Peripheral levels of anandamide, 2-arachidonoylglycerol (2-AG), oleoylethanolamide (OEA), palmitoylethanolamide (PEA), and cortisol were also assessed. In the PTSD group, relative to the HC and TC groups, we found elevated brain-wide [11C]OMAR VT values (F(2,53)=7.96, p=.001; 19.5% and 14.5% higher, respectively) which were most pronounced in women (F(1,53)=5.52, p=.023). Anandamide concentrations were reduced in the PTSD relative to the TC (53.1% lower) and HC (58.2% lower) groups. Cortisol levels were lower in the PTSD and TC groups relative to the HC group. Three biomarkers examined collectively—OMAR VT, anandamide, and cortisol—correctly classified nearly 85% of PTSD cases. These results suggest that abnormal CB1 receptor-mediated anandamide signaling is implicated in the etiology of PTSD, and provide a promising neurobiological model to develop novel, evidence-based pharmacotherapies for this disorder.en
dc.language.isoen_USen
dc.relation.isversionofdoi:10.1038/mp.2013.61en
dc.relation.hasversionhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC3752332/pdf/en
dash.licenseLAAen_US
dc.subjectPTSDen
dc.subjectCannabinoid receptorsen
dc.subjectbrain imagingen
dc.subjectPETen
dc.subjectOMARen
dc.titleElevated Brain Cannabinoid CB1 Receptor Availability in Posttraumatic Stress Disorder: A Positron Emission Tomography Studyen
dc.typeJournal Articleen_US
dc.description.versionVersion of Recorden
dc.relation.journalMolecular psychiatryen
dash.depositing.authorNormandin, Marc D.en_US
dc.date.available2014-04-11T14:13:12Z
dc.identifier.doi10.1038/mp.2013.61*
dash.authorsorderedfalse
dash.contributor.affiliatedNormandin, Marc


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