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

Fig. 4.

Fig. 4.

The late inhibitory period induced by PF bursts depends on NMDA receptors and the prolonged increase in firing induced by LFS depends on group II mGluRs. (A) To explore whether changes at the PF-IN synapse could account for the changes in spike output of the circuit, the extracellular experiments were repeated in the presence of antagonists to block specific forms of PF-IN plasticity. (B-D) Recordings performed in the presence of 10 μM CPP, an NMDA receptor antagonist that blocks PF-IN LTP. Example cells (B), PSTHs (C), and summary bar graphs (D) show that the late inhibitory period in the PSTH that was observed under control conditions (Fig. 1) is blocked by this drug, which also blocks LTP at the PF-IN synapse (Fig. 3). (E-G) Recordings performed in the presence of 200 μM EGLU, a group II mGlu receptor antagonist that blocks PF-IN LTD. Example cells (E), PSTHs (F) and summary bar graphs (G) show that the prolonged excitatory response in the PSTH that was observed under control conditions (Fig. 1) is blocked by this drug, which also blocks LTD at the PF-IN synapse (Fig. 3).