Additionally, deficits in excitatory synaptic transmission during experimental autoimmune encephalomyelitis (EAE) correlated with disruption of PSD-95 integrity involving both AMPA and NMDA receptor-mediated currents (Ziehn et al., 2012a, b) while preserving presynaptic function in CA1 neurons. Here, DLG4 is linked to experimental autoimmune encephalomyelitis.