AMPAR过度激活引起胞内钙超载诱发的兴奋毒性是脑缺血损伤的重要机制，而利用其拮抗剂减弱兴奋毒性的临床试验，却因阻断AMPAR的生理作用，以失败告终。申请者前期研究发现，电针预处理可上调缺血后神经元上决定AMPAR钙离子通透性的GluR2亚基表达水平，诱导脑缺血耐受，相关结果已被Scientific Reports(IF=5.078)接收。然而电针如何调控GluR2的表达，通过何种机制减轻脑缺血损伤尚未了解。文献报道MicroRNA-223(miR-223)可影响脑内GluR2蛋白表达，改善脊髓缺血损伤。本课题假设：电针通过抑制MicroRNA-223，上调GluR2的表达，减少钙调蛋白(calmodulin，CaM)介导脑缺血耐受。本项目拟应用功能、形态和分子生物学等方法，阐明电针调节GluR2诱导脑缺血耐受的具体机制，为提出脑卒中防治新策略带来新的视角与契机，具有重要的临床意义。

Calcium overload is induced by excessive activation of AMPA-type glutamate receptors (AMPAR), and excitotoxicity mediated by this play a critical role in cerebral ischemic insults. However, the clinical application of AMPAR antagonist is limited due to directly blocking receptor physiological function. Our previous study reveals that electric acupuncture (EA) pretreatment enhances GluR2 protain expression, the subunit adjusted the permeability of AMPAR to calcium ion, to protect against global cerebral ischemia. The relevant article was accepted by Scientific Reports. However, the underlying mechanisms of GluR2 regulated by EA pretreatment were incomletely understood. GluR2 has been reported as one target of MicroRNA-223(miR-223), and miR-223 could effectively ameliorate the pathologic hallmarks of spinal cord injury(SCI) via increasing GluR2 expression. Therefore, we will investigate whether inhibition of miR-223 is involved in neuroprotection induced by EA pretreatment via GluR2, which may be related to calmodulin(CaM) signaling pathway after transient global cerebral ischemia in mice. The aim of the study was to clarify the mechanism of neuroprotection induced by EA through regulating GluR2 with comprehensive methods such as morphology and molecular biology and to bring a new perspective of stroke.