Chronic epilepsy can cause a persistent shift in NMDA receptor subtype composition. Such an alteration may underlie changes in the propensity of synaptic plasticity. Therefore, we compared rats that have experienced a pilocarpine-induced status epilepticus (SE) with controls using extracellular field potential recordings. Here we focused on NMDA receptor-dependent synaptic plasticity in the CA1 region of hippocampal slices. In controls, theta-burst stimulation induced robust LTP. Likewise, LTD could also be elicited by 1 Hz stimulation for 15 min. LTP levels were significantly enhanced after SE compared to controls, but no differences in LTD were found. Therefore, we asked whether this discrepancy is due to differential alteration of the NMDA receptor subtypes NR2A and NR2B. We found that application of zinc (10 mM), a modulator of NR2A, virtually abolished LTP in controls, whereas in epileptic rats significant LTP was still observed. At a higher zinc concentration (100 mM), LTP was inhibited in both groups. In contrast, using the specific NR2B inhibitor Ro 25 6981 (1 mM) LTP remained inducible in controls, but was completely lost after SE suggesting a dominant role of NR2B in LTP induction in epileptic rats. In conclusion, SE leads to persistent enhancement of LTP without any alteration of LTD, probably due to differential changes of the NMDA receptor subtypes.