N-methyl-D-aspartate receptors (NMDARs) have a pivotal role in long-term plasticity and NMDAR-mediated synaptic transmission is subject to plasticity although the mechanisms involved are little understood. Subunit composition determines the properties of NMDARs and there is evidence for subtype differences between receptors at different subcellular locations and between different neuronal cell types. NR2D-containing NMDARs are predominantly expressed at extrasynaptic locations and our previous data suggests that extrasynaptic NR2D-containing NMDARs relocate to the synapse during NMDAR-LTP. Expression of the NR2D subunit has also been demonstrated in inhibitory interneurons in hippocampus. Hippocampal slices were prepared from male Wistar rats (3-5 weeks old) and whole-cell patch-clamp recordings were performed to compare NMDAR-mediated synaptic transmission in granule cells (GCs) and interneurons (INs) in dentate gyrus. NMDAR-EPSCs were evoked by stimulation of the medial perforant path, at a test frequency of 0.033 Hz, at 34 °C. Decay kinetics were significantly slower for NMDAR-EPSCs recorded in interneurons, with a weighted decay time constant (τ_W) of 85 ± 8 ms (n = 21), compared to τ_W of 32 ± 1 ms in granule cells (n = 17, p < 0.001). NMDAR-EPSC amplitude and 10-90% rise time was similar between granule cells and interneurons (amplitude 28 ± 3 pA and 24 ± 5 pA in GCs and INs, respectively, 10-90% rise time 4.7 ± 0.3 ms and 5 ± 0.9 ms in GCs and INs, respectively). The NR2D-preferring antagonist UBP141, inhibited NMDAR-EPSCs in INs by 27 ± 4 % of control amplitude (n = 7) but had no effect on currents recorded in GCs (99 ± 3 % of control, n = 4). Ifenprodil had similar effects on NMDAR-EPSC amplitude in both cell types, inhibiting EPSCs by 28 ± 6 % of control in GCs (n = 5) and by 35 ± 9 % of control in INs ( n = 7). Our findings suggest that different NMDAR subtypes are expressed at perforant path synapses on principal cells and interneurons, and this variation may be associated with differences in spike timing and synaptic plasticity.