Fig. 3.

PKA and MAPK mediate the protein synthesis-dependent component of L-LTP. A, PKA inhibitor blocks L-LTP. In the presence of KT5720 (1 μm) LTP induced by five trains of tetanus (100 Hz, 1 sec at 3 min interval) was depressed shortly after tetanus and decayed to the baseline in 60–90 min (filled circles; n = 6). KT5720 (1 μm) has no effect on the baseline synaptic response (filled triangles; n= 5). B, Forskolin-induced synaptic potentiation is blocked by anisomycin. A brief application of forskolin (50 μm) induced a large potentiation (open circles; n = 6). Anisomycin (20 μm) was perfused 30–60 min before the application of forskolin and then perfused for 2 hr. Forskolin failed to induce any significant potentiation in the presence of anisomycin (open squares; n = 6). Representative field potentials before and 3 hr after forskolin application in forskolin alone (left) and forskolin with anisomycin (right) are shown at the topof this panel. Calibration: 5 msec, 0.5 mV. C, MAPK inhibitor blocks L-LTP. PD98059 (20 μm) was applied 30–60 min before tetanus and perfused for 2 hr. L-LTP was significantly depressed in the slices that were treated with PD98059 (open circles; n = 6) as compared with the control experiments (filled circles;n = 6). The application of 0.1% DMSO had no effect on amygdala L-LTP (filled triangles;n = 4). D, Forskolin-induced synaptic potentiation was depressed by a MAPK inhibitor. PD98059 (50 μm) was applied 30–60 min before the application of forskolin and perfused for 90 min. Forskolin induced only a weak synaptic potential in the presence of PD98059 (n = 6). The application of PD98059 (50 μm) had no effect on the baseline synaptic response (n = 5).