Abnormal glutamate metabolism in prefrontal cortex of post-traumatic stress disorder linked to comorbidity with major depression
Kelley M. Swanberg1, Hetty Prinsen2, Christopher L. Averill3,4,5, Leonardo Campos1, Abhinav V. Kurada1, John H. Krystal3,4, Ismene L. Petrakis3,4, Lynnette A. Averill3,4,5, Chadi G. Abdallah4,5, and Christoph Juchem1,2,6,7
1Biomedical Engineering, Columbia University School of Engineering and Applied Science, New York, NY, United States, 2Radiology and Biomedical Imaging, Yale University School of Medicine, New Haven, CT, United States, 3Clinical Neuroscience Division, Department of Veterans Affairs National Center for Posttraumatic Stress Disorder, Veterans Affairs Connecticut Healthcare System, West Haven, CT, United States, 4Psychiatry, Yale University School of Medicine, New Haven, CT, United States, 5Psychiatry and Behavioral Sciences, Baylor College of Medicine, Houston, TX, United States, 6Radiology, Columbia University Medical Center, New York, NY, United States, 7Neurology, Yale University School of Medicine, New Haven, CT, United States
Post-traumatic stress disorder (PTSD) is an anxiety condition evidenced by wide-ranging emotional and cognitive dysfunction. While prefrontal glutamatergic excitotoxicity is thought to contribute to its presentation, no 1H-MRS studies of PTSD have yet been conducted at 7-Tesla field strength facilitating separation of glutamate from metabolic partner glutamine. Here we apply 7-T 1H MRS to investigate medial prefrontal (mPFC) concentrations of glutamate and glutamine with GABA, glutathione, and other metabolites in both PTSD and comorbid major depressive disorder (MDD). We show several PTSD-associated abnormalities in mPFC glutamate metabolism that appear to be driven by MDD status when this comorbidity is considered.
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