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. 2005 Sep 30;102(41):14901–14906. doi: 10.1073/pnas.0505028102

Fig. 3.

Fig. 3.

PF-IN synapses are potentiated by PF burst stimulation through an NMDA-dependent mechanism and are depressed by LFS through a group II mGluR-dependent mechanism. (A-F) Data from control experiments (A-C) and experiments in the presence of 10 μM CPP (D-F), an NMDA receptor antagonist, show that conditioning with PF burst induces NMDA-dependent LTP. Results are summarized by example traces (A and D), averaged data (B and E), and summary bar graphs (C and F). (G-L) By contrast, data from control experiments (G-I) and experiments in the presence of 200 μM EGLU (J-L), a group II mGluR antagonist, show that conditioning with LFS induces mGluR-dependent LTD. Results are summarized by example traces (G and J), averaged data (H and K), and summary bar graphs (I and L).