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. Author manuscript; available in PMC: 2012 Jan 4.
Published in final edited form as: Neuron. 2007 Jun 21;54(6):949–959. doi: 10.1016/j.neuron.2007.06.002

Figure 2. Target cell-dependent short-term suppression is mediated by endocannabinoids.

Figure 2

Synaptically-evoked suppression of excitation (SSE; A, B) and depolarization-induced suppression of excitation (DSE; D, E) were examined at PF→GC synapses. Summary data of PC SSE (C) and DSE (F) are shown for comparison. Experiments were performed in control conditions (black traces and black symbols) and in the presence of the CB1R antagonist AM251 (2 µM, red traces and red symbols). Studies of SSE were performed using a K-based internal solution and PFs were stimulated in the ML. Studies examining DSE were performed with a Cs-based internal solution. (A) EPSCs recorded from a GC, evoked prior to (pre-burst) and 3 s following PF burst stimulation. Time course of EPSC amplitudes prior to and following burst stimulation is shown for synapses onto GCs (B; n = 5 cells in control, n = 5 cells in AM251) and PCs (C; n = 6 cells in control, n = 5 cells in AM251). (D–F) Cells were depolarized to 0 mV for 2 s. Representative recordings are shown for a GC (D) and the time course of synaptic strength prior to and following postsynaptic depolarization is shown for GCs (E; n = 15 cells in control, n = 7 cells in AM251) and PCs (F; n = 7 cells in control, n = 6 cells in AM251). Figures 2C and 2F reproduced from (Beierlein and Regehr, 2006) to allow comparison.

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