Article Figures & Data
Figures
- Fig. 1.
Concentration-dependent depression of EPSP byl-CCG. A, Application of l-CCG for 10 min resulted in an initial depression of EPSP, which was followed, upon washout of the l-CCG, by LTD.B, Concentration-dependent effects of l-CCG on the initial depression and LTD.
- Fig. 2.
Blockade of l-CCG-induced LTD by mGluR II antagonists. A, Application ofl-CCG (10 μm) in the presence of MCCG (100 μm) failed to cause initial depression and LTD.Inset shows superimposed traces taken at the time points indicated. B, Application of EGLU (10 μm) did not affect the EPSP significantly but blocked the effect of l-CCG (10 μm). Insetshows the traces taken at the time points indicated.
- Fig. 3.
LTD induced by l-CCG is independent of NMDA receptor activation and is accompanied by an increase in PPF.A, Application of l-CCG (10 μm) in the presence of d-APV (50 μm) induced LTD that was not significantly different from control LTD. B, EPSPs evoked by paired stimuli in control and 60 min after the washout of l-CCG (10 μm). The control EPSP evoked by the first stimulus is scaled to that recorded 60 min after LTD induction. It is clear that there is a greater PPF after l-CCG LTD.
- Fig. 4.
l-CCG-induced LTD and LFS-induced LTD are not mutually occluded. A, One application of 10 μm L-CCG for 15 min was given to saturate LTD. Sixty minutes after washout of l-CCG, 1 Hz stimulation (900 pulses, 15 min) was delivered. LFS produced a further depression.B, An example of experiments showing that, after LTD was induced to a maximal level by three periods of LFS, subsequent application of l-CCG (10 μm) induced a further LTD.
- Fig. 5.
Induction of l-CCG LTD is dependent on presynaptic activity. Summary of eight experiments showing thatl-CCG LTD was blocked when synaptic stimulation was stopped both during the application of l-CCG (10 μm) and 10 min after the washout.
- Fig. 6.
Presynaptic but not postsynaptic Ca2+ increase is required for l-CCG LTD.A, Summary of eight experiments showing that the membrane-permeable Ca2+ chelator BAPTA-AM (100 μm) suppressed synaptic transmission and blockedl-CCG LTD. B, Superimposedtraces taken immediately (1 min) and 30 min after the impalement of cell with a BAPTA-containing electrode to show the block of afterhyperpolarization. Electrode was filled with BAPTA (50 mm) as described in Materials and Methods.C, LFS LTD but not l-CCG LTD was blocked by intracellular BAPTA.
- Fig. 7.
l-CCG LTD can be potentiated by Iso.A, Application of l-CCG (10 μm) induced an LTD. Twenty minutes after LTD stabilized, Iso (15 μm) was applied, which increased the synaptic strength back to the original level. B, Parallel experiments in which l-CCG and Iso were applied in the reverse order. Application of Iso (15 μm) induced an LTP.l-CCG (10 μm) application 20 min after the washout of Iso caused a complete reversal of LTP.
- Fig. 8.
l-CCG LTD is blocked by adenylyl cyclase and PKA inhibitors. A, Slices were incubated for at least 1 hr in 1 μm KT 5720 or 20 min in 50 μm SQ 22536 before being transferred to the recording chamber in which the same concentration of drug was maintained.l-CCG LTD normally observed in control slices was blocked in the KT 5720- or SQ 22536-treated slices. Inset shows the representative traces taken before and 60 min after the washout of l-CCG. Calibration: 10 mV, 40 msec.B, Block of l-CCG-induced initial depression by PMA. Slices were incubated for at least 1 hr in KT 5720 (1 μm) plus PMA (1 μm). Insetshows the representative traces taken before and 60 min after the washout of l-CCG. Calibration: 10 mV, 40 msec.
- Fig. 9.
Glutamate release by brief titanic stimulation activates presynaptic mGluR II and induces LTD. In the presence ofd-APV (50 μm) and the glutamate uptake inhibitor trans-PDC (100 μm), brief titanic stimulation (100 Hz, 1 sec) evoked an LTD that was completely blocked by MCCG (100 μm). Inset shows the representative traces taken before and 60 min after the stimulation. Calibration: 10 mV, 40 msec.
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