Schizophrenia is a major debilitating psychiatric disorder with a lifetime prevalence of ~1%, and its clinical presentation encompasses positive, negative, and cognitive symptoms. Despite decades of research, the underlying neurophysiology has remained elusive.Here, we examine the large-scale neurophysiology underlying schizophrenia by employing multiple, simultaneous Neuropixel recordings in rodents carrying a rare genetic variant implicated in the disease. Three or four Neuropixel probes were simultaneously targeted to prefrontal cortices, motor cortices, striatum, hippocampus, auditory cortex, and a range of thalamic nuclei. Head-fixed mice performed a self-paced sensory predictive coding task aimed at taxing the differentiation between self-generated and externally-generated sensory stimuli. During training and recording, transgenic and wildtype mice were able to perform thousands of trials containing self-generated or external, expected or unexpected, stimuli. Preliminary evidence suggests broad and graded attenuation of self-generated sensory stimuli compared to external sensory stimuli across the brains of wildtype mice. Analyses are underway for comparison between transgenic mice and wildtype littermates in large-scale cellular physiology, neuronal co-activity motifs, and population dynamics.Together, these examinations will provide crucial insight into the complex large-scale neurophysiology underlying schizophrenia.