These findings highlight the complexity of interpreting effects of disease-causing NMDA receptor missense mutations in the context of neuronal function.
Particularly, GluN2B GoF and LoF mutants show similar phenotypes in the presence of GluN1/2A/2B triheteromers, while the LoF mutation, C456Y, shows much less rescue effect than GoF mutation in the absence of both GluN2A and GluN2B.