干细胞移植的功能机制一直备受关注。本研究拟追踪BMSCs与神经元间功能性突触样结构形成,探讨G蛋白偶联受体激酶结合蛋白1(GIT1)介导细胞外调节蛋白激酶(ERK)1/2调控BMSCs与神经元间突触可塑性及神经元轴突定向迁移的关联性。通过低渗蒸馏水裂解GFP标记的BMSCs,收集细胞碎片后模拟BMSCs移植过程死亡的细胞与细胞共培养及体内移植观察宿主细胞表达GFP,评判GFP标记细胞的非特异性;模拟BMSCs颅内移植,建立BMSCs与神经元体外共培养体系。采用慢病毒载体和RNA干扰技术使BMSCs中GIT1过表达和沉默,分析GIT1上下调对BMSCs与神经元间突触可塑性及神经元轴突定向迁移能力的影响,探讨GIT1促进突触可塑性及神经元轴突定向迁移机制：GIT1过表达引起ERK1/2磷酸化促进BMSCs与神经元间功能性突触形成及神经元轴突定向迁移。

To evaluate the nonspecificity of green fluorescent protein (GFP), we constructed a model to investigate the interaction between the host and the GFP labeled BMSCs cracking by Sterile hypotonic distilled water in vivo after transplanted via tail vein. In order to trace the functional synapses formation between BMSCs and cortical neurons and explore the G protein-coupled receptor kinase-binding protein 1(GIT1) regulate the synaptic plasticity between BMSCs and cortical neurons and the directional migration of axons via extracellular regulated protein kinase 1/2(ERK1/2). To mimic the intracranial transplantation of BMSCs, we constructed a co-culture system that was combination of BMSCs and cortical neurons. We applied lentiviral vector and RNA interference technology to establish the GIT1 expression and silence model of BMSCs, and analyze the influences of functional synapses formation between BMSCs and cortical neurons and the directional migration of axons after the GIT1 of BMSCs was upregulation and downregulation, to confirm the potential mechanism of synaptic plasticity and directional migration of axons regulated bu GIT1. It is likely that the overexpress of GIT1 in BMSCs induce the phosphorylation of ERK1/2 to promote the functional synapse formation and directional migration of axons. We raise a new target for central nervous system diseases for establishing communication with host cells by BMSCs transplantation.