Parvalbumin阳性中间神经元缺陷在精神分裂症病理机制中的作用

精神分裂症是一种多发于青壮年的重性精神病, 其原因尚不明确。经典的多巴胺缺陷理论假说在某些方面欠缺解释力; 与此同时, 关于Parvalbumin阳性的中间神经元(后简称PV+神经元)缺陷在精神分裂症病理机制中的作用逐渐明晰, 并引起了越来越多的关注。PV+神经元在绝大部分脑区中是一种快速放电的抑制性神经元, 参与了突触可塑性的调节, 兴奋/抑制平衡的维持和神经发生等。而在精神分裂症中, PV+神经元的异常在患者和动物研究中都被普遍证实, 并发现与 NMDA受体缺陷、gamma波异常和氧化应激存在某些关联。

Roles of impaired parvalbumin positive interneurons in schizophrenic pathology

Schizophrenia is a severe mental disorder typically began in late adolescence or early adulthood. To date, the cause of schizophrenia remains largely unclear. The classical dopamine hypothesis of schizophrenia is now thought to be sided. Meanwhile, the involvement of impaired Parvalbumin positive interneurons (PV+ neurons) in the pathological mechanism of schizophrenia has been realized and received increasing attention. Generally, PV+ cells is a kind of inhibitory, fast-spiking interneurons, which had been demonstrated to be involved in synaptic plasticity, excitation/inhibition balance and neurogenesis. In schizophrenia, abnormal PV+ neurons has been commonly found in patients and relevant animal models., In this article, we reviewed the roles of deficits of PV+ neurons in schizophrenic pathology combined its principal phenotypes including defective NMDA receptors, abnormal gamma oscillation and oxidative stress, hoping to contribute to further investigation and development of new drugs.