Figure 3. Ras/MAPK mediates the ISI-dependent inhibition in synaptic plasticity. A–D, Quantification of new synaptic boutons 40 min after stimulation conditions: Control nonstimulated (NS) compared with spaced (S) and pseudo-massed stimulation (PM) in control genotype and Ras.N17 genotype (A), Ras.RNAi (B), Ras.WT genotype (C), and rl.RNAi genotype (D). n = 9 NMJ from 5 animals. A, Control genotype: NS versus S, p = 0.0017; Ras.N17 genotype: NS versus S, p = 0.0205 and NS versus PM, p = 0.0017; PM stimulation: control genotype versus Ras.N17, p = 0.0462. B, Control genotype: NS versus S, p = 0.0005; Ras.RNAi genotype: NS versus S, p = 0.0009; and NS versus PM p = 0.02. C, Control genotype: NS versus S, p = 0.0017. D, Control genotype: NS versus S, p = 0.0017; rl.RNAi genotype: NS versus S, p = 0.003; and NS versus PM, p = 0.0365, Kruskal–Wallis test followed by Dunn's multiple-comparisons test. For A–C, a single test was made including all the data. E, Quantification of new synaptic boutons 40 min after stimulation conditions: Control NS compared with massed stimulation (M16′) in control genotype and Ras.N17, Ras.RNAi, Ras.WT, and rl.RNAi genotypes. n = 9 NMJs from 5 animals. Scatter dot plot showing median (gray line) with interquartile range. *Significant difference NS versus M16′, control genotype, p < 0.0001; Ras.N17, p = 0.0071; Ras.RNAi, p = 0.0346; Ras.WT, p = 0.0136; and rl.RNAi, p = 0.0351, Kruskal–Wallis test followed by Dunn's multiple-comparisons test.