The potentiation of synaptic AMPA receptors induced by the deletion of NMDA 2 receptors requires the GluA 2 subunit

27 Deletion of NMDA receptors (NMDARs) early in development results in an increase in 28 the number of synaptic AMPA receptors (AMPARs), suggesting a role for NMDARs in 29 negatively regulating AMPAR trafficking at developing synapses. Substantial evidence 30 has shown that AMPAR subunits function differentially in AMPAR trafficking. 31 However, the role of AMPAR subunits in the enhancement of AMPARs following 32 NMDAR ablation remains unknown. We have now performed single-cell genetic 33 deletions in double-floxed mice in which the deletion of GluN1 is combined with the 34 deletion of GluA1 or GluA2. We find that the AMPAR enhancement following NMDAR 35 deletion requires the GluA2 subunit, but not the GluA1 subunit, indicating a key role for 36 GluA2 in the regulation of AMPAR trafficking in developing synapses. 37