Citation

Michels L, Schulte-Vels T, Schick M, O'Gorman RL, Zeffiro T, Hasler G, Mueller-Pfeiffer C. Psychiatry Res. 2014; 224(3): 288-295.

Affiliation

Department of Psychiatry and Psychotherapy, University Hospital Zurich, Zurich, Switzerland; Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; Center of Education and Research (COEUR), Psychiatric Services of the County of St. Gallen-North, Wil, Switzerland.

Copyright

(Copyright © 2014, Elsevier Publishing)

DOI

10.1016/j.pscychresns.2014.09.007

PMID

25448399

Abstract

Although posttraumatic stress disorder (PTSD) is associated with a variety of structural and functional brain changes, the molecular pathophysiological mechanisms underlying these macroscopic alterations are unknown. Recent studies support the existence of an altered excitation-inhibition balance in PTSD. Further, there is preliminary evidence from blood-sample studies suggesting heightened oxidative stress in PTSD, potentially leading to neural damage through excessive brain levels of free radicals. In this study we investigated PTSD (n=12) and non-PTSD participants (n=17) using single-voxel proton magnetic resonance spectroscopy (MRS) in dorsolateral prefrontal cortex (DLPFC) and anterior cingulate cortex (ACC). We found significantly higher levels of γ-amino butyric acid (GABA) (a primary inhibitory neurotransmitter) and glutathione (a marker for neuronal oxidative stress) in PTSD participants. Atypically high prefrontal inhibition as well as oxidative stress may be involved in the pathogenesis of PTSD.

Language: en