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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© 2021 Published by Elsevier Inc.
