Cerebral ischemia is accompanied with a cascade of damage, including excitotoxicity, calcium overload, inflammation and apoptosis. In the early phase of brain ischemia, huge amount of glutamate released from nerve terminals over stimulate glutamate receptors. Then the increasing extracellular concentration of calcium induce acute necrosis, delayed cell necrosis and apoptosis and inflammatory response after ischemia. Glutamate is mainly cleared by glutamate circulation. Activation of glutamate transporters can attenuate the ischemic brain damage and may be neuroprotective. In this paper, the latest progress on the relationship between glutamate transporters and ischemic brain damage is summarized.