Journal
BIOLOGICAL PSYCHIATRY
Volume 70, Issue 11, Pages 1033-1038Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.biopsych.2011.07.003
Keywords
Amygdala; neuroimaging; positron emission tomography; posttraumatic stress disorder; serotonin; serotonin transporter
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Funding
- National Institutes of Health [R21 MH085627]
- Department of Veterans Affairs
- Clinical Neurosciences Division of the VA National Center for PTSD
- VA Merit Review Grant
- National Alliance for Research on Schizophrenia and Depression (NARSAD)
- Mount Sinai School of Medicine (MSSM)
- AstraZeneca
- Janssen Research Foundation
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Background: The amygdala is a key site where alterations in the regulation of the serotonin transporter (5-HTT) may alter stress response. Deficient 5-HTT function and abnormal amygdala activity have been hypothesized to contribute to the pathophysiology of posttraumatic stress disorder (PTSD), but no study has evaluated the 5-HTT in humans with PTSD. On the basis of translational models, we hypothesized that patients diagnosed with PTSD would exhibit reduced amygdala 5-HTT expression as measured with positron emission tomography and the recently developed 5-HTT-selective radiotracer [C-11]AFM. Methods: Fifteen participants with PTSD and 15 healthy control (HC) subjects without trauma history underwent a resting-state positron emission tomography scan. Results: [C-11] AFM binding potential (BP ND) within the combined bilateral amygdala region of interest was significantly reduced in the PTSD group compared with the HC group (p = .027; 16.3% reduction), which was largely driven by the between-group difference in the left amygdala (p = .008; 20.5% reduction). Furthermore, amygdala [C-11]AFM BP ND was inversely correlated with both Hamilton Rating Scale for Anxiety scores (r = -.55, p = .035) and Montgomery-Asberg Depression Rating Scale scores (r = -.56, p = .029). Conclusions: Our findings of abnormally reduced amygdala 5-HTT binding in PTSD and its association with higher anxiety and depression symptoms in PTSD patients support a translational neurobiological model of PTSD directly implicating dysregulated 5-HTT signaling within neural systems underlying threat detection and fear learning.
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