It has been reported that ketamine as an uncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist has also non-NMDA receptor antagonist properties. We recently found that ketamine (20 ?M) affected differently induction of NMDA receptor-mediated long-term potentiation (LTP) when administered 30 min prior to tetanic Primed-Bursts (PBs) stimulation. On the other hand, ketamine also influenced non-NMDA-mediated synaptic transmission in different manner. In the present study, in order to find the cause of different effects of ketamine on NMDA-mediated responses, we examined the probable relationship between the effects of ketamine on non-NMDA-mediated baseline responses and NMDA-mediated responses. Population spikes amplitude (PSA) was measured before and after tetanic stimulation in ketamine (1-100 µM) treated slices. We found that ketamine failed to inhibit NMDA receptor-mediated LTP, when baseline PSA enhanced in presence of ketamine. On the other hand, when ketamine not changed or decreased beseline PSA, caused LTP inhibition or even LTD induction. These findings indicated that ketamine effects on NMDA receptor-mediated responses depends on, ketamine effects on non-NMDA receptor-mediated synaptic transmission.