Abstract  Schizophrenia is a severe mental illness that afflicts nearly 1% of the world population. Although the exact pathophysiology of schizophrenia is unknown, the N-methyl-d-aspartate receptor (NMDAR), a major glutamate receptor subtype, has received great attention. The NR1 subunit is often considered indispensable for functional NMDAR assemblies, abnormal modulation of which is found in patients with schizophrenia. In this review, we discuss how disrupted function of NR1 subunits in NMDAR leads to the progression and development of symptoms of schizophrenia-like behaviors in a variety of genetically modified mouse models. We also discuss some of the susceptible genes and shared signaling pathways among the schizophrenia, and how their mutations lead to NR1 subunits hypofunction. Finally, we suggest that the subunit-selective modulators of NR1 subunits in NMDA receptors may be promising tools for the therapy of schizophrenia.

Keywords   NR1 subunits; NMDA receptor; schizophrenia

Received   2015-5-25　　
Accepted  2015-10-26

Funding  This work was supported by the grants from the Natural Science Foundation of Shanghai, China (No. 14ZR1435900), Qihang Personnel Training Program of Shanghai Mental Health Center (No. 2013-QH-01 & 2013-QH-01-X), the National Natural Science Foundation of

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