• Anna Höflich, Andreas Hahn, Martin Küblböck, Georg S Kranz, Thomas Vanicek, Christian Windischberger, Alois Saria, Siegfried Kasper, Dietmar Winkler, and Rupert Lanzenberger.
• Department of Psychiatry and Psychotherapy (Drs Höflich, Hahn, Kranz, Vanicek, Kasper, Winkler, and Lanzenberger), and MR Center of Excellence and Center for Biomedical Engineering and Physics (Mr Küblböck and Dr Windischberger), Medical University of Vienna, Vienna, Austria; Experimental Psychiatry Unit, Center for Psychiatry and Psychotherapy, Medical University of Innsbruck, Innsbruck, Austria (Dr Saria).
• Int. J. Neuropsychopharmacol. 2015 Apr 19; 18 (9).

BackgroundSchizophrenia has been associated with disturbances of thalamic functioning. In light of recent evidence suggesting a significant impact of the glutamatergic system on key symptoms of schizophrenia, we assessed whether modulation of the glutamatergic system via blockage of the N-methyl-D-aspartate (NMDA)-receptor might lead to changes of thalamic functional connectivity.MethodsBased on the ketamine model of psychosis, we investigated changes in cortico-thalamic functional connectivity by intravenous ketamine challenge during a 55-minute resting-state scan. Thirty healthy volunteers were measured with pharmacological functional magnetic resonance imaging using a double-blind, randomized, placebo-controlled, crossover design.ResultsFunctional connectivity analysis revealed significant ketamine-specific changes within the thalamus hub network, more precisely, an increase of cortico-thalamic connectivity of the somatosensory and temporal cortex.ConclusionsOur results indicate that changes of thalamic functioning as described for schizophrenia can be partly mimicked by NMDA-receptor blockage. This adds substantial knowledge about the neurobiological mechanisms underlying the profound changes of perception and behavior during the application of NMDA-receptor antagonists.© The Author 2015. Published by Oxford University Press on behalf of CINP.

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