谷氨酸和ATP作为信号递质在神经系统的功能活动中起着重要的作用。在诸如脑缺血再灌注等情况下，星形胶质细胞和神经细胞均可通过不同的途径向细胞外液中释放过多谷氨酸和ATP。我们的研究证明在低渗和缺血条件下，星形胶质细胞主要通过大阴离子通道和VSOR氯离子通道释放谷氨酸；同时大阴离子通道在低渗和缺氧缺糖条件下是星形胶质细胞释放ATP的主要途径。谷氨酸和ATP在脑缺血再灌注发展过程中的作用是相辅相成的，为了阐明谷氨酸对ATP释放及ATP信号途径的作用，我们设计利用培养的细胞体系和急性分离的大鼠海马切片及整体大鼠，通过电生理，分子生物学，药理学和免疫组化等方法详细探讨在细胞外液高谷氨酸刺激下星形胶质细胞和神经细胞释放ATP的途径，并在缺血再灌注大鼠模型中通过相应药理干预，寻求调控谷氨酸引起的ATP释放和ATP受体的有效方法，为减少该条件下神经功能损伤开辟新途径。

As signal transmitters, glutamate and ATP play important roles in central nervous system. In cases such as ischemia reperfusion, astroyctes and neurons may release excessive glutamate into the extracellular spaces via different pathways. Our previous studies demonstrated: in hypotonicity or ischemia condition, astrocytes mainly release glutamate through maxi-anion channel and VSOR chloride channel; and maxi-anion channel is the main pathway for ATP release from astrocytes in oxygen-glucose deprivation condition. Glutamate and ATP function and affect mutually in the process of ischemia reperfusion and its development.We degign using cultured cell systems and ischemia reperfusion rat model to explore in detail the pathways for ATP release from astrocytes and neurons on the effects of different concentration of glutamate. And further study in ischemia reperfusion rat model by pharmacological intervention of glutamate-induced ATP release pathways and ATP receptors to explore effective methods to protect the nervous function during and after ischemia reperfusion process.