Long-term potentiation (LTP),one of the major forms of synaptic plasticity,is thought to be an important cellular model for learning and memory.It has been shown from many experiments that an activation of N-methyl-D-aspartate subtype of glutamate receptors (NMDARs) plays an important role in an induction of LTP at hippocampal CA1 synapse.NMDARs are assembled from NMDAR subunit 1 (NR1) and at least one type of NR2.NR1 is an essential and basic functional subunit.NR2,as contrast,serves as an assistant subunit to lead to the diversity of NMDA receptors.With different subtypes of NR2 subunit,including NR2A,NR2B,NR2C and NR2D,NMDARs vary in their functions.In adult mice hippocampus,NR2A and NR2B are the predominant NR2 Subunits.As once reported by Yu Tian Wang s group,NR2A is required for an induction of LTP and NR2B for LTD,but many other reports are also available to contradict this view.All these results have suggested that the role of NR2A and NR2B on synaptic plasticity is complicated.In 1996,Wickliffe C.Abraham and Mark E Bear brought us a concept of metaplasticity,viz.the plasticity of plasticity.It is shown from the experiments at the hippocampal CA1 area that a "Priming" stimulus prior to tetanic stimulus shall change the amplitude of LTP.Effective duration of "Priming" stimulus may stay for one hour.In this study we investigated the role of NR2A and NR2B in the induction of metaplasticity in mice hippocampal CA1 neurons.The evidences are provided here that NR2B is involved in the regulation of metapasticity.We have made further study of its functional mechanism.