While this result is phenomenologically similar to our previous observation of preserved OD-plasticity in both young standard-cage raised mice or adult enriched mice after an S1-stroke, the underlying mechanism is clearly different: on the one hand, reduced intracortical inhibition and no changes in AMPA/NMDA excitatory postsynaptic currents (EPSCs) in young or enriched mice [9], and on the other, more silent synapses but normal inhibitory tone in the PSD-95 KO mice [20]. The gene discussed is DLG4; the disease is stroke disorder.