We found that 1) sepsis selectively decreased the levels of GluN2A, GluN2B andGluN1 but not synaptophysin or neuron number in the hippocampus of mice during the first 7days after sepsis; and 2) the NMDA receptor co-agonist D-serine significantly improved the brain dysfunction and the neuropathology of the hippocampus in septic survivors. The gene discussed is GRIN2B; the disease is Sepsis.