The involvement of NMDA receptors and voltage-dependent calcium channels in augmentation of long-term potentiation (LTP) was investigated at the Schaffer collateral CA1 pyramidal cell synapses in hippocampal slices of morphine dependent rats, using primed-burst tetanic simulation. The amplitude of the population spike and its delay were measured as indices of increase in postsynaptic excitability. D,L-APV and nifedipine were used as an NMDA receptor antagonist and a voltage-dependent calcium channel blocker, respectively. The amount of LTP of the orthodromic population spike (OPS) was higher in slices from dependent rats. Perfusion of slices from control and dependent rats with ACSF containing D,L-APV (25 µ M) and delivering tetanic simulation showed that D,L- APV completely blocked the LTP of OPS in slices from both control and dependent rats, while nifedipine (10 µ M) attenuated the amount of LTP of OPS in dependent slices and had no effect on controls. The results suggest that the enhanced LTP of OPS in the CA1 area of hippocampal slices from morphine-dependent rats is primarily induced by NMDA receptor activity, and the voltage-dependent calcium channels may also be partially involved in this phenomenon.