缺血性脑卒中（ischemic stroke, IS）发生率高，是成年人致残的主要原因之一，目前尚无有效的药物治疗手段和外科干预措施。最新研究表明，IS后可引起神经元大量凋亡和坏死，尤其是神经元突起的损伤，可导致神经传导束路结构、功能破坏，但其确切的分子病理机制尚不清楚，这是导致IS后残、死率高的根本原因。我们的前期研究发现，突触后支架蛋白Homer在神经元树突棘和轴浆内特异性表达，参与IS后神经元损伤过程，是其分子调控网络的关键点。本课题拟在以往工作基础上，深入研究Homer对IS后神经元突起结构和功能重塑的调控作用与机制，阐明Homer参与IS后运动、感觉、认知功能损伤与修复过程的分子机制与重要信号途径，进而以Homer为核心揭示IS后神经元突起损伤与功能重塑的分子调控网络，为设计和验证IS的预防和治疗新策略提供理论依据。

Ischemic stroke (IS), with high incidence, is still one of the most common causes of long-term disability in adulthood. Effects of drug treatment and surgical intervention on IS are limited. Recent studies demostrated that IS induced massive apoptosis and necrosis in brain. Especially, neurite damage can lead to disruption in structure and function of nerve conduction. But, its molecular pathological mechanism is not clear, which is the essential reason for high morbidity and mortality. Our previous studies found that Homer, a postsynaptic scaffold protein expressed in the dendritic spines and axon of neurons, was associated with neuronal injury and served as the key point of the molecular network after IS. On the basis of previous studies, this subject is to investigate the mechanism underlying structure and function remodelings of neurite following IS and to elucidate the molecular network and crucial signal pathways related to Homer during repairment of motor, sensory, and cognitive function. Furthermore, our investigation would clarify the molecular network of neurite structure and function remodeling, in which Homer act as a core molecular, and provide a provide a theoretical basis for the design and verification of new strategy on prevention and treatment of IS.