Fig. 7: Model summarising how different molecular defects can converge on similar NMDAR-mediated EPSCs.
From: Common synaptic phenotypes arising from diverse mutations in the human NMDA receptor subunit GluN2A
a WT GluN2A and GluN2B mostly contribute to NMDA-EPSCs in CA1 pyramidal neurons. GluN2B-containing NMDARs have more prolonged time course and cation influx as illustrated by the bold purple arrows. b GluN2A mutants with defects culminating in low levels of GluN2A at synapses result in NMDA-EPSCs that are dominated by residual GluN2B-containing NMDARs. c GluN2A mutants that traffic to the synapse but are functionally defective result in NMDA-EPSCs that are dominated by residual GluN2B-containing NMDARs. d GluN2A mutants that traffic to the synapse but have slower deactivation kinetics directly contribute to prolonging NMDA-EPSCs. b–d The effect of mutations may result in a combination of these different mechanisms.
