Update publication information. Brain tissue is extremely sensitive to hypoxia/reoxygenation (H/R) injury, which can easily cause irreversible damage to neurons. H/R injury could induce neuronal apoptosis through glutamate-mediated excitotoxicity. N-methyl-d-aspartate receptor (NMDAR) is one of the main receptors of excitatory glutamate, and blocking NMDAR could protect brain tissue from ischemia and hypoxia injury. NMDAR hypofunction can also cause psychotic symptoms or cognitive impairment. However, there is still a lack of systematic research on the changes of the proteome and transcriptome in neuronal cells under the condition of NMDAR hypofunction and H/R injury. In this study, we compared the changes of proteome expression levels in neurons after NMDAR knockdown and H/R stimulation by isobaric tags for relative and absolute quantitation (iTRAQ).