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Objective Long-term synaptic plasticity, including long term potentiation (LTP) and long term depression (LTD), was an eventful pattern to modulate efficiency of synaptic transmission in nervous system, and LTP was regarded as the underlying mechanism in learning and memory.LTP and LTD switched enhancement or attenuation of neural signal via adjustment the ratio of NR2A/NR2B.This study focused on the relationship between the alteration of long-term synaptic plasticity and the performance of Morris water maze (MWM), attempted to interpret the mechanism, which electrophysiological effects on the behavior.Methods Rats were randomly divided into 3 groups, MK-801 (n=16), AP-V (n=16) and control group (n=16).MK-801 (10 μg, 1 μg/μL), AP-V (10 μg, 1 μg/μL) and artificial cerebrospinal fluid (ACSF, 10 μL) were administered in dentate gyrus (DG) of hippocampus.MWM was carried, and LTP and LTD were recorded respectively.Results LTP was significantly attenuated (P<0.01), while LTD was barely influenced (P>0.05) in DG region of MK-801 group compared with control.On the contrary, LTP was barely influenced (P>0.05), while LTD was significantly attenuated (P<0.01) in DG region of AP-V group compared with control.In acquisition and retention tests, the escape latency and path length were prolonged (P<0.05; P<0.01) in MK-801 group, and were cut down (P<0.05; P<0.01) in AP-V group compared with control group.On the contrary, in reacquisition phase, the escape latency (P<0.05) was cut down in MK-801 group, and was prolonged (P<0.05) in AP-Ⅴ compared with control group.Conclusion The unbalance of long-term synaptic plasticity results in the spatial cognitive impairment in rats.