神经胶质细胞包括星形细胞、寡突细胞及小胶质细胞，其主要表达的离子通道为两类钾离子通道，包括内向整流钾离子通道(Kir)和电压门控钾离子通道(Kv) 。胶质细胞上表达的钾离子通道决定了细胞静息膜电位，并能够调节细胞外的K+浓度，谷氨酸的清除，细胞容积，细胞增殖和细胞死亡等多种病理生理进程。在前期研究中，人的成纤维细胞被成功转化成诱导性干细胞，并能够分化成人的星形胶质细胞，该项目从细胞和分子水平，特别是离子通道功能性(电生理)的角度，系统研究：1）离子通道在人的诱导性干细胞分化成的星形胶质细胞上的功能性表达及其分子基础，2）在缺血性中风发生条件下，其主要离子通道的功能性变化和变化的机制，3）特定离子通道的功能性变化与缺血性中风病理进程的相关机制研究。 研究成果不仅有助于深化对在人脑中缺血性中风病理机制的认识，也为研发有效的多潜能的中风神经保护剂提供新靶标。

K+ channels including the inward-rectifier K+ (Kir) channels and the voltage-gated K+ (Kv) channels have been found ubiquitously expressed in the neuroglia including oligodendrocytes, astrocytes and microglia. K+ channels play crucial role in many pathophysiologic processes in astrocytes such as potassium spatial buffering, glutamate clearance, cell volume regulation and cell proliferation. Our primary study generated induced pluripotent stem cells from human fibroblasts and successfully differentiate them to astrocytes (i.e., human IPSC-Derived astrocytes). In the present study, we intend to use human IPSC-Derived astrocytes to explore the molecular and cellular mechanism, particularly the roles of K+ ion channels in the pathologic process of stroke. We will perform the functional characterization of variable types of ion channels expressed in human astrocytes. We will also examine the altered ion channel function under ischemic conditions (oxygen and/or glucose deprivation and/or extracellular acidification). Furthermore, we will study the mechanism underlying the altered function of ion channels and their correlation to the pathophysiologic processes in stroke. These works will give us a novel insight into the pathologic mechanisms of ischemic stroke in human glial cells, and potential targets for anti-stroke therapeutics.