孕期免疫激活已被证实与子代出生后患精神分裂症有关，但具体分子机制尚不清楚。研究表明母体免疫激活诱导子代脑内小胶质细胞向M1型极化，同时分泌大量炎症因子。我们预实验结果发现抗炎抑制剂能够降低脑内神经炎症，且M2型蛋白标记物精氨酸酶（Arginase1，Arg1）的表达水平显著升高，因此推测小胶质细胞可能由M1型向M2型极化，在治疗精神分裂症模型中起关键作用。本项目拟通过前脉冲抑制试验、旷场试验、免疫荧光染色、Western blot和qRT-PCR等方法，旨在探讨小胶质细胞M2极化这一事件在治疗孕期免疫激活所致精神分裂症中的关键作用。进一步采用Arg1基因敲除小鼠及小胶质细胞条件性敲除Arg基因小鼠（Arg1+/-小鼠模型及CX3CR1-Arg1-/-小鼠模型），有望揭示小胶质细胞源的Arg1在防治精神分裂症中发挥的作用及潜在机制，为确立Arg1作为精神障碍治疗的新靶点提供更充分的科学依据。

It has been proved that the maternal immune activation is highly related to offspring’s development of schizophrenia, but the molecular mechanism remains elusive. The previous studies have found that the maternal immune activation cause microglia to skew toward M1- polarization, accompanied with high expression of inflammatory factors in the brain. Our findings showed that the neuroinflammation was attenuated after treatment of minocycline, and that the levels of Arginase1, a marker of M2 microglial phenotype, was obviously increased. Thus, we purpose the hypothesis that the polarization of M1/M2 phenotypes may play a crucial role in the treatment of the schizophrenia models. In the present study. Pre-Pulse Inhabitation (PPI), Open Field Test, Immunofluorescence technique, Western blot and qRT-PCR were adopted to explore that whether atM2- microglia polarization contribute to vital effect in the treatment of schizophrenia related to material immune activation. In the models of Arg1 gene knockout/conditional knockout mice (Arg1+/- and CX3C1-Arg1-/- mice), the present will reveal the important effect of microglia-producing Arg1 in the prevention and cure of schizophrenia, and provide a solid scientific evidence for the new target of Arg1 in the further clinical cure of mental disorders.