Partial NR2B inhibition blocks conversion of synaptic plasticity direction after recovery from MK-801 block. A, Partial NR2B inhibition by a low concentration of ifenprodil (0.6 μm) blocks conversion of synaptic plasticity direction. Top, Sample of evoked NMDAR-mediated currents showing partial inhibition by the NR2B antagonist ifenprodil (0.6 μm), which elevates the NR2A/NR2B ratio to close to control level. Bottom, After partial recovery of sEPSC amplitude and full recovery of sEPSC frequency from MK-801 (10 μm) block, a low concentration of ifenprodil (0.6 μm) was immediately applied, and an STP instead of LTD was induced with LTP-producing stimulus protocol (2 Hz, 200 pulses during a 2.5 min depolarization to 0 mV). B, Similar NMDAR EPSC amplitude inhibition by AP-5 at a concentration of 8–10 μm could not block conversion of synaptic plasticity direction. Top, Sample of evoked NMDAR-mediated currents showing similar partial inhibition by AP-5 (8–10 μm) as ifenprodil (0.6 μm) did. Bottom, After partial recovery of sEPSC amplitude and full recovery of sEPSC frequency from MK-801 (10 μm) block, a low concentration of AP-5 (8–10 μm) was immediately applied, and LTD was still induced with LTP-producing stimulus protocol (2 Hz, 200 pulses during a 2.5 min depolarization to 0 mV).