脑缺血/低氧预适应(I/HPC)是缺血/低氧预刺激诱发神经细胞产生的内源性保护现象，但其发生发展机制尚不清楚。从分子水平探明其细胞信号转导机制，可为临床防治脑缺血/低氧性损伤药物的研发提供有效靶点。本研究是在我们已借助功能性蛋白质组学技术发现经典型蛋白激酶C(cPKC)gamma及其底物分子突触蛋白参与I/HPC发生发展过程的基础上，拟利用cPKCgamma基因敲除小鼠，制备小鼠整体HPC、大脑中动脉阻塞(MCAO)和原代皮层神经元氧-糖剥夺(OGD)等模型，借助行为学、形态学、分子生物学和生物化学等学科研究技术，进一步探讨缺血/低氧条件下，cPKCgamma激活对突触蛋白特定亚型的调控机制，以及cPKCgamma-突触蛋白信号通路在脑I/HPC中的作用。所获成果将进一步丰富人们对脑缺血/低氧预适应分子机制的认识，并为临床防治脑卒中等缺血/低氧性脑损伤药物的开发提供实验依据。

Cerebral ischemic/hypoxic preconditioning (I/HPC) is an endogenous neuroprotective strategy which is induced by ischemic/hypoxic pretreatment, but its molecular mechanism is unclear. The profound molecular signal transduction mechanism makes it an attractive target for potential clinical therapeutic approaches. Previously, we have found the involvement of conventional protein kinase C (cPKC) gamma and its substrate synapsin in the development of I/HPC by functional proteomics. In this study, we established I/HPC and middle cerebral artery occlusion (MCAO)-induced mouse stroke models, and oxygen-glucose deprivation (OGD)-induced cellular ischemic model by using cPKCgamma knockout mice. The techniques of behavior, morphology, molecular biology and biochemistry were applied to explore the regulatory mechanism of synapsin by cPKCgamma activation under ischemic/hypoxic condition, and their roles in cerebral I/HPC. The achievements will further expand our understanding of the molecular mechanisms underlying cerebral I/HPC, and may provide new molecular targets for the treatment of cerebral ischemic/hypoxic injury-related diseases such as stroke in clinical practice.