It is widely believed that synaptic plasticity may be the underlying process behind learning and memory. One form of plasticity, long-term depression (LTD), is known to be down-regulated during development, though the purpose of this remains unclear. During development, it has been shown that there is a relative increase in the expression of type 2A NMDA receptors relative to 2B, and that these receptors are targeted to the synapse. We have previously demonstrated that LTD in adult perirhinal cortex is primarily mediated by extrasynaptic NR2B receptors, while LTP and depotentiation are mediated by NR2A receptors (Massey et al. 2004). In this report, we have investigated further the developmental roles of these NMDA receptor subtypes. Perirhinal cortex slices were prepared from humanely killed juvenile (P14) rats. Extracellular field recordings were made from layer II/III in response to stimuli delivered to either side of the recording electrode. LTD was induced using the low-frequency stimulation (LFS, 900 stimuli at 1Hz) protocol (70 ± 9% of baseline, n=6). Application of the NMDA receptor antagonist AP5 (50 μM) blocked this LTD (103 ± 18%, n=3). Antagonists of NR2A and NR2B receptors were then applied during LTD induction to determine subtype specificity. Ro 25-6981 (3 μM), a NR2B inhibitor, had a small effect upon LTD (81 ± 3%, n=4) whereas the NR2A inhibitor NVP-AAM077 (0.5 μM) blocked the majority of LTD (93 ± 3%, n=5). These results, when compared with findings in adults, suggest that there are changes during development in the role of these two NMDA receptor subtypes in mediating synaptic plasticity.