In previous study, electrophysiological patch-clamp recording showed that uncoupling of an activated DAPK1 from the NMDA receptor complex protects against brain damage in stroke without affecting the physiological actions of the NMDA receptors (Tu et al., 2010); our results show that after the interaction between DAPK1 and NR2B was blocked by Tat-NR2B, the number and morphology of synapse did not change, which were consistent with above electrophysiological results. Here, TAT is linked to stroke disorder.