Li_2007_Neurosci.Lett_426_192

In this study, we investigated the interactions between synapse adhesion molecules neurexin, neuroligin1, neuroligin2 and postsynaptic density protein 95 (PSD-95) in transient cerebral ischemia and possible regulatory mechanism of these interactions. Our data show that preconditioning ischemia can down-regulate the increased neurexin-neuroligin1-PSD-95 interaction induced by ischemia injury and exerts a neuroprotective effect. Pre-treatment of N-methyl-D-aspartate (NMDA) receptor antagonist ketamine can demolish this neuroprotective effect of preconditioning by increasing neurexin-neuroligin1-PSD-95 interaction. These results indicate that the neurexin-neuroligin1-PSD-95 is an important signalling module in ischemic injury and a novel possible target in therapeutics of brain ischemia.