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View Article and Find Full Text PDFImportance: Exposure to trauma increases the risk for developing threat (ie, fear) symptoms, such as reexperiencing and hyperarousal symptoms, and loss (ie, dysphoria) symptoms, such as emotional numbing and depressive symptoms. While preclinical data have implicated the activated dynorphin/κ-opioid receptor (KOR) system in relation to these symptoms, the role of the KOR system in mediating these phenotypes in humans is unknown. Elucidation of molecular targets implicated in threat and loss symptoms is important because it can help inform the development of novel, mechanism-based treatments for trauma-related psychopathology.
View Article and Find Full Text PDFAttentional bias to threat is a key endophenotype that contributes to the chronicity of trauma-related psychopathology. However, little is known about the neurobiology of this endophenotype and no known in vivo molecular imaging study has been conducted to evaluate candidate receptor systems that may be implicated in this endophenotype or the phenotypic expression of trauma-related psychopathology that comprises threat (ie, re-experiencing, avoidance, and hyperarousal) and loss (ie, emotional numbing, depression/dysphoria, generalized anxiety) symptomatology. Using the radioligand [(11)C]OMAR and positron emission tomography (PET), we evaluated the relationship between in vivo cannabinoid receptor type 1 (CB1) receptor availability in the amygdala, and performance on a dot-probe measure of attentional bias to threat, and clinician interview-based measures of trauma-related psychopathology.
View Article and Find Full Text PDFIntroduction: Recent confirmatory factor analytic studies of the dimensional structure of posttraumatic stress disorder (PTSD) suggest that this disorder may be best characterized by five symptom dimensions-re-experiencing, avoidance, numbing, dysphoric arousal, and anxious arousal. Hypothalamic-pituitary-adrenal (HPA) axis dysregulation in PTSD and has been attributed to enhanced glucocorticoid responsiveness. However, little is known about how altered HPA-axis function is related to this contemporary phenotypic model of PTSD.
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