精神分裂症可引起认知功能和海马神经发生的改变，但其病理机制尚未明确。研究证实少突胶质细胞及其转录因子与精神分裂症的发生密切相关。转录因子Olig2是少突胶质细胞成熟、分化的必要因子。项目组前期在Olig2表达异常的动物模型中发现海马神经发生降低，因此我们推测转录因子Olig2可能参与了精神分裂症海马神经发生的调控。本项目拟用精神分裂症动物模型和CPZ介导小鼠急性脱髓鞘模型，以Olig2和海马神经发生为研究靶点，采用形态学、分子生物学等技术，通过在体与活细胞水平开展系列研究。在明确海马各区Olig2表达的基础上，阐明Olig2对精神分裂症海马神经细胞凋亡、增殖及分化的调控作用；利用条件性基因敲除和Olig2质粒重建转染等技术，探讨Olig2对精神分裂症海马神经发生的调控机制。本项目不仅有望为精神分裂症认知功能及海马神经发生调控机制的阐明提供新思路，同时为精神分裂症的临床防治提供新靶点。

Schizophrenia can cause cognitive dysfunction and hippocampal neurogenesis changes, but the mechanism is still unclear. Study showed that oligodendrocyte and its transcription factors are closely related with schizophrenia. The transcription factor Olig2 is necessary for oligodendrocyte differentiation. Our early study found that in the Olig abnormally expressed animal model of schizophrenia, hippocampal neurogenesis decreased obviously. Therefore, we speculate that dysfunction of oligodendrocyte and its transcription factor Olig may be a factor causing changes of hippocampal neurogenesis in schizophrenia. This project aims to use animal models of schizophrenia and CPZ mediated acute demyelinating mouse model, with Olig2 and the hippocampal neurogenesis as the research targets, based on the explicit expression of Olig2 in hippocampus, to study the effect of Olig2 on the apoptosis, proliferation and differentiation of hippocampal neural cells, and clarify the regulation mechanism of Olig2 on schizophrenia hippocampus neurogenesis by in vivo and in vitro experiments through morphology and molecular biology techniques. We expect to provide the theory basis to clarify the regulation mechanism of oligodendrocytes and myelin on hippocampus neurogenesis in schizophrenia and provide new targets for clinical prevention and treatment of schizophrenia.