Prolonged Ketamine Effects in Sp4 Hypomorphic Mice: Mimicking Phenotypes of Schizophrenia

摘要: It has been well established that schizophrenia patients display impaired NMDA receptor (NMDAR) functions as exacerbation of symptoms in response to NMDAR antagonists. Abnormal signaling presumably contributes cognitive deficits which substantially contribute functional disability schizophrenia. Establishing a mouse genetic model will help investigate molecular mechanisms hypoglutmatergic neurotransmission Here, we examined the responses Sp4 hypomorphic mice antagonists electroencephalography and various behavioral paradigms. mice, previously reported have reduced NMDAR1 expression LTP deficit hippocampal CA1, displayed increased sensitivity prolonged Molecular studies demonstrated glutamic acid decarboxylase 67 (GAD67) both cortex hippocampus, consistent with abnormal gamma oscillations mice. On other hand, human SP4 gene was be deleted Several suggested association psychiatric disorders. Therefore, elucidation pathway may provide novel insights our understanding