Ketamine-Induced Modulation of the Thalamo-Cortical Network in Healthy Volunteers As a Model for Schizophrenia
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Updated: Apr 14, 2026
A Multimodal Imaging- and Stimulation-based Method of Evaluating Connectivity-related Brain Excitability in Patients with Epilepsy
Published on: November 13, 2016
Anna Höflich1, Andreas Hahn1, Martin Küblböck1
1Department 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).
Background:
Schizophrenia 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.
Methods:
Based 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.
Results:
Functional 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.
Conclusions:
Our 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.
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