Memantine regulates contralesional motor cortical NMDA receptor components. Western blots for (a) the NMDA receptor subunit GluN2B, which predominantly localizes in extrasynaptic NMDA receptors targeted by memantine, (b) GluN2A, which is preferentially found in synaptic NMDA receptors, and (c) PSD-95, which upon NMDA receptor binding consolidates synaptic plasticity processes, in the contralesional motor cortex of animals exposed to transient MCAO or sham-surgery. Note that in response to stroke, all three proteins are reduced at 3 d after reperfusion. Protein abundance is partly restored in vehicle-treated animals at 14 and 28 dpt. Interestingly, memantine reduces GluN2B abundance at 14 dpt and increases GluN2A and PSD-95 abundance at 28 dpt. Representative blots are also shown. Results are medians (lines inside boxes)/means (crosses inside boxes) ± IQR (boxes) and minimum/maximum data (elongation lines) (n = 4 independent blots). Data were analyzed by two-way ANOVA followed by two-tailed paired t tests for individual time-points. *p < 0.05, **p < 0.01 compared with ischemic vehicle.