Milan Scheidegger1, Simone Grimm2, Martin Walter3, Heinz Boeker2, Peter Boesiger1, Erich Seifritz2, Anke Henning1
1Institute for Biomedical Engineering, University and ETH Zurich, Zurich, Switzerland; 2Clinic of Affective Disorders and General Psychiatry, University Hospital of Psychiatry Zurich, Zurich, Switzerland; 3Department of Psychiatry, Otto-von-Guericke University, Magdeburg, Germany
Many neuroimaging findings are compatible with the hypothesis that limbic hyperactivity during evaluation of emotional stimuli, combined with prefrontal hypoactivity, might cause negative emotional biases in patients suffering from major depressive disorder (MDD) and that this imbalance can be reversed by antidepressant drug treatment. Our findings show that in healthy subjects an antidepressant intravenous dose of ketamine reduces limbic reactivity in the amygdalo-hippocampal complex during an emotional processing task, which is in support of the hypothesis that pharmacologically modulating limbic neurocircuits might be an important therapeutic strategy to restore parts of the disrupted neurobehavioural homeostasis in MDD.