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Identifying genetic factors that in uence electrophysiological signatures associated with disordered behavior will reveal mechanisms of cognitive dysfunction relevant to disease. Homer1 is a reproducible gene candidate for synaptic and cognitive function. Alternative splicing produces activity-dependent isoforms including the circular RNA, circHomer1. While dysregulation of circHomer1 expression has been identi ed across multiple psychiatric and neurodegenerative disorders and is associated with impaired cognitive exibility, it is unknown whether circHomer1 can induce electrophysiological signatures relevant to cognitive dysfunction in these disorders. Using in vivo microarray recordings within the orbitofrontal cortex (OFC) of awake, behaving mice during a translational touchscreen task, we demonstrate that reduction of circHomer1 within the OFC induces robust changes in multiunit ring rate and local eld potential (LFP) coordination and power to salient stimuli. Further, these electrophysiological changes are associated with transcriptional downregulation of glutamatergic signaling effectors and behavioral alterations leading to impaired cognitive exibility.