The Glycine Transport Inhibitor Bi 425809 Restores Translatable EEG Deficits in an Acute Mouse Model for Schizophrenia-Related Sensory Processing and Cortical Network Dysfunction

      Patients with schizophrenia show alterations in cortical network function and processing of sensory information, which can be monitored by electroencephalography (EEG), particularly auditory event-related potentials (AERP) and auditory steady-state response (ASSR). There is growing evidence that N-methyl-D-aspartate (NMDA) receptor dysfunction contributes to the pathophysiology of schizophrenia. Hence, NMDA receptor antagonists like MK-801 or ketamine can induce symptoms in animals and humans, which resemble those of patients with schizophrenia including cortical network dysfunction. Inhibition of the glycine transporter-1 (GlyT1) is an approach to facilitate NMDA receptor function via increasing its co-agonist glycine. In this study, we tested the ability of the novel GlyT1 inhibitor BI425809 to reverse MK-801 induced deficits on AERPs, ASSR and basal gamma oscillation.
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