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