中文摘要：

谷氨酸作为主要的兴奋性神经递质，在脑内正常生理状态下有重要作用，但在脑缺血等多种病理状态下，谷氨酸在脑内大量释放和堆积，导致对神经元的过度刺激，引起兴奋性毒性，并成为缺血性神经元损伤的主要诱发因素。谷氨酸的兴奋性毒性主要通过与神经元细胞膜上的受体结合，引起细胞内Na＋和Ca2＋增加。胞内Ca2＋浓度增加会引起线粒体功能异常、蛋白酶激活、活性氧增加及NO的释放，从而引起神经元的死亡；胞内Na＋增加将引起过量水分进入细胞，造成神经细胞毒性水肿和细胞死亡。因此，深入了解脑缺血后上述谷氨酸通路的调控机制，并针对该通路的不同环节进行干预，将为阻止或减轻缺血性神经元损伤提供有效途径。多种针对谷氨酸通路的脑缺血治疗策略正在积极探索中，如抑制谷氨酸合成或释放、增加谷氨酸清除、阻断谷氨酸受体或抑制细胞内Ca2＋浓度增加等。本文将对缺血性脑中风后，谷氨酸引起兴奋性毒性的机制以及该系统的调控机制、相应干预策略的研究进展进行综述。

英文摘要：

Although acting as an important excitatory neurotransmitter and play roles in physiological state of mammalian brain, glutamate also play key roles under several pathological conditions, including cerebral ischemia. The extracellular glutamate was accumulated under cerebral ischemia, which leads to overexcitation of neurons, causing the exitotoxicity and injury of neurons. The eccessive glutamate stimulates the glutamate NMDA receptors on neuronal membrane, leading to influx of Na＋ and Ca2＋. The overload of intracellular Ca2＋ will lead to a variety of cell abnormalities including mitochondrial dysfunction, activation of proteases and nitric oxide synthase, accumulation of reactive oxygen species and furthermore, cell death. In addition, the elevated intracellular Na＋ will also induce cytotoxic edema and cell death. Therefore, comprehensive understanding of the regulatory mechanism of glutamatergic pathway may provide novel therapeutic target for reducing neuronal injury under cerebral ischemia. Recently, a variety of neuroprotective strategies have been explored which focus on blocking of glutamate-mediated excitotoxity, e.g. inhibiting of synthesis and release of glutamate, increasing of glutamate clearance, blocking of glutamate receptors, inhibiting of the elevation of intracellular Ca2＋ and so on. This review aims to make a general summary on the progress in regulatory mechanism of glutamatergic pathway and the intervention strategies after cerebral ischemia.