Abstract #3344

Abnormal glutamate metabolism in prefrontal cortex of post-traumatic stress disorder linked to comorbidity with major depression

Kelley M. Swanberg¹, Hetty Prinsen², Christopher L. Averill^3,4,5, Leonardo Campos¹, Abhinav V. Kurada¹, John H. Krystal^3,4, Ismene L. Petrakis^3,4, Lynnette A. Averill^3,4,5, Chadi G. Abdallah^4,5, and Christoph Juchem^1,2,6,7

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

Synopsis

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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