Figure 5. GABA_B receptor inhibition promotes the development of synaptic resistance to depotentiation stimulation.

A, summary of experiments showing that in slices treated with GABA_B receptor antagonist SCH50911 (20 μm) the application of LFS at 10 min after two trains of 100 Hz HFS initially depressed fEPSPs that subsequently recovered to previously potentiated level (n = 8; •). B, summary of experiments showing that in contrast to control slices (n = 6; ○), a 5 min application of DCG-IV (3 μm) at 10 min after two trains of 100 Hz HFS failed to elicit a persistent depotentiation in SCH50911-treated slices (n = 7; •). C, summary of experiments showing that SCH50911 treatment did not significantly affect the induction of LFS-DEP of two trains of 100 Hz LTP when LFS was applied at 3 min after LTP induction (n = 6). D, summary of experiments showing that SCH50911 treatment had no effect on the induction of DCG-IV-DEP of two trains of 100 Hz LTP when DCG-IV was applied at 3 min after LTP induction (n = 6). E, summary of experiments showing that with 25 Hz/125 pulse stimulation of mossy fibre pathways, the fEPSP amplitude showed a higher potentiation in SCH50911-treated slices (n = 7; •) than in control slices (n = 6; ○). F, summary of experiments showing that in slices treated with the GABA_B receptor antagonist SCH50911 (20 μm), application of LFS at 10 min after 25 Hz/125 pulse stimulation did not produce a persistent depotentiation (n = 6; •). G, summary of experiments showing that treatment of slices with baclofen (0.2 μm) permitted persistent LFS-DEP of four trains of 100 Hz LTP (n = 5; •) but had no effect on the induction of LTP (n = 5; ○). H, summary of experiments showing that treatment of slices with baclofen also permitted persistent DCG-IV-DEP of four trains of 100 Hz LTP (n = 5).