Abstract: N-methyl-D-aspartic acid receptor(NMDAR) is a glutamatergic excitatory neuroreceptor, which is transformed into a mandatory heterotetramer by a variety of subgroups. Excitatory glutamatergic neurotransmission of NMDAR is essential for synaptic plasticity and survival of neurons. Synaptic plasticity in hippocampus and striatum is closely related to learning and memory. Long-term potentiation(long-term potentiation, LTP), the prototype form of synaptic plasticity in cavernous body, is involved in the maintenance and consolidation of learning and memory, while synaptic plasticity in striatum is the cellular basis of learning and memory. The subunits of NMDAR in physiological state can promote the production of learning and memory. However, excessive activation of NMDAR subunit can cause learning and memory impairment, induce excitatory neurotoxicity and promote nerve cell death. In addition, the normal activation of NMDAR in synapses initiates synaptic plasticity and stimulates cell survival. On the contrary, the overactivation of extracellular NMDAR can induce Ca²⁺ overload, mediate excitatory neurotoxicity and promote neuronal death. However, more and more studies have shown that NMDAR in synapses can also induce excitatory neurotoxicity and cause neuronal death while promoting neuronal survival. The mainstream view is that excitatory neurotoxicity is mainly mediated by Ca²⁺ overload, while some think that NMDAR can also mediate excitatory neurotoxicity through Ca²⁺ overload and Nonionic channels at the same time. This paper mainly reviews the research progress of the promoting and inhibitory effect of NMDAR on learning and memory and its excitatory neurotoxicity.