Recently, it has been found that extrasynaptic NMDAR subunits GluN2A and GluN2B form a complex with transient receptor potential cation channel subfamily M member 4 (TRPM4) and that this complex is accountable for ischemia-related excitotoxicity, since disruption of the complex provides neuroprotection without disturbing physiological NMDAR-induced calcium signals [31]. Here, TRPM4 is linked to ischemia.