Mice lacking the GluN2A subunit do not exhibit depression-like behavior after LPS treatment, which indicates an important regulatory role of the GluN2A subunit in neuroinflammation-related depression [116] In line with the complex regulatory mechanisms of NMDARs in anxiety studies, antidepressant studies involving NMDARs also have shown contradictory conclusions from different subunits in different brain regions. This evidence concerns the gene GRIN2A and depressive symptom measurement.