Thus, in animal models of temporal lobe epilepsy, the GluN2B/GluN2A ratio increased in several forebrain regions (Amakhin et al., 2017; Zubareva et al., 2018), and synapses enriched in GluN2B subunits favored seizure susceptibility (Okuda et al., 2017), whereas blockade of GluN2B receptors during experimental status epilepticus with compounds that included the rapid acting antidepressant ketamine (a non-selective NMDA-R antagonist) reduced neuronal damage (Loss et al., 2019). The gene discussed is GRIN2A; the disease is temporal lobe epilepsy.