GRIN2D and tuberous sclerosis: In addition, compound 2i shows a time-dependent enhancementof inhibitory actions at GluN2C- and GluN2D-containing NMDARs in thepresence of the agonist glutamate, which could attenuate hypersynchronousactivity driven by high-frequency excitatory synaptic transmission.Consistent with this finding, compound 2i significantlyreduced the number of epileptic events in a murine model of tuberoussclerosis complex (TSC)-induced epilepsy that is associated with upregulationof the GluN2C subunit.