精神分裂症作为一种神经发育疾病，与突触发生和神经可塑性的异常密切相关。神经网络的可塑性包括了成体脑中新神经元的发生和新突触连接的形成，即成体神经发生过程，其生理功能是正常的学习与记忆所必需的。成体神经发生紊乱被认为是精神分裂症发生的重要病理机制之一。Dysbindin-1的编码基因DTNBP1是一个非常重要的精神分裂症易感基因，因可变剪接产生多种不同的异构体。精神分裂症患者不同脑区，表现为dysbindin-1不同异构体的变化不一致，这些不同的异构体在精神分裂症发生中的作用是否不同，目前并不清楚。本研究利用不同dysbindin-1异构体缺乏的sdy小鼠和mu小鼠，研究其在海马成体神经发生和环路形成中的作用，以探讨不同dysbindin-1异构体在精神分裂症发生中的作用机制，有望在成体神经发生层面对精神分裂症进行药物治疗提供新的思路。

Schizophrenia is associated with the impairment of synaptogenesis and neuroplasticity. Adult neurogenesis is required for learning and memory. While compelling evidence has shown that impaired adult neurogenesis contributes to the pathogenesis of schizophrenia, the underlying mechanism is still lacking. DTNBP1, which encodes dysbindin-1, is one of the major susceptibility genes of schizophrenia. It has reported that expression of different dysbindin-1 isoforms vary in different brain regions. Whether different dysbindin-1 isoforms contribute differentially to the development of schizophrenia is unknown. In this study, we propose to study the underlying mechanism of how different dysbindin-1 isoforms are involved in hippocampal adult neurogenesis and loop integration. This may gain insights into the development of memory deficits in schizophrenia.