Fig. 2.

A single interneuron integrates eCB signaling with its own firing to express eCB-mediated LTD. (A and B) Individual experiments where unitary IPSCs (uIPSCs) were recorded from synaptically connected INs and PCs. In each case, transient eCB release was triggered with a 10-min bath application of the mGluR-I agonist DHPG (50 μM). In DSI+ cell pairs in CA1, DHPG application is coupled with either spontaneous IN firing (A) or silence (B) by depolarizing or hyperpolarizing the presynaptic IN. DHPG was chased with group I mGluR antagonists (4 μM MPEP and 100 μM LY367385) to ensure washout. Each representative trace shows IN membrane potential above the paired PC current for indicated time points. Average traces taken before and after DHPG application are shown (overlaid) at the top left of each panel; individual traces taken during DHPG application are shown at the top right. (C and D) Cell pairs were classified as DSI+ or DSI−, and the presynaptic IN was either fired or held silent during a 10-min DHPG application: (DSI+, silent, open circles; DSI+, firing, filled circles; DSI−, firing, gray circles). (C) The two groups of DSI+ INs showed a similar transient depression in response to PC depolarization, unlike DSI− INs. (D) Coupling DHPG application with IN firing in DSI+ cell pairs (DSI+, firing) yielded a robust depression lasting at least 35 min after DHPG washout. In contrast, silencing the IN of DSI+ cell pairs during DHPG (DSI+, silent) produced significantly less LTD. The residual depression observed in DSI+, silent cell pairs was indistinguishable from that measured in DSI−, firing cell pairs, a group not expected to express eCB-LTD.