卒中导致的后天致残迄今尚无有效的药物治疗。GABA张力（tonic）抑制负调控卒中后功能修复，而GABA相位（phasic）抑制的作用则相反。GAT1（GABA transporter 1）介导GABA再摄取，其功能缺失增强GABA tonic抑制，同时减弱GABA phasic抑制。Syntaxin 1A与GAT1相互作用导致GAT1功能下调。我们推测：如在卒中后阻断Syntaxin 1A与GAT1耦联，有望通过压制GABA tonic抑制，同时增强GABA phasic抑制的双重作用促进神经功能修复。本项目拟研究Syntaxin 1A-GAT1耦联在卒中恢复期的如下作用：（1）对运动功能、学习记忆能力的影响；（2）对神经可塑性和结构重构的影响；（3）作用的分子机制和信号通路。预期研究结果将阐明Syntaxin 1A-GAT1耦联在卒中神经功能重建中的意义，为卒中恢复期治疗提供新靶标。

Stroke is a major cause of aquired disability, but no pharmacological therapy is available. Reducing GABA tonic inhibition promotes functional recovery from stroke, while GABA phasic inhibition enhancement improves motor function. GAT1 is responsible for GABA uptake and GAT1 knockout has been shown increased GABA tonic inhibition and reduced GABA phasic inhibition. It has been demonstrated that Syntaxin 1A interacts with GAT1 and decreases transport rates of GAT1. Thus we suppose that dissociating Syntaxin 1A-GAT1 interaction promotes stroke recovery via reducing GABA tonic inhibition and increasing GABA phasic inhibition. In this project, we will investigate the effects of delayed disrupting Syntaxin 1A-GAT1 interaction after stroke on motor function, spatial learning and memory, neural circuit plasticity and remodeling and the underlying mechanisms. So this project will reveal the role of Syntaxin 1A-GAT1 interaction in functional rebuilding after stroke and provide a novel target for neural repair.