During acute ischemia, (i) vesicular release from neurons constitutes a crucial component of extracellular Glu increase [11]; (ii) the expression of Glu transporter EAAT1 or EAAT2 decreases rapidly after ischemia and hypoxia, leading to ineffective removal of extracellular Glu [12, 13]; severe ischemia even leads to reverse transport of Glu via EAATs. Here, SLC1A2 is linked to ischemia.