Fig. 5

Synaptic strength is more sensitivity to EGTA and downregulated by septin 5 in complex calyces. a Presynaptic compound action potential currents (pre-I_AP) and EPSCs (I_EPSC; axonal stimulation) were tested in control (black, simple calyx; red, complex calyx) and after EGTA injection (blue, 10 mM, 3–5 min loading). SD₁ (interval between peak₁ of pre-I_AP and EPSC onset) and SD₂ (interval between peak₂ of pre-I_AP and EPSC onset; dashed lines) are synaptic delays. b Bar graphs show EGTA effect on EPSC amplitudes (simple, control, 10.05 ± 0.64 nA, EGTA, 8.06 ± 0.55 nA, n = 8/7, t = 5.762, p = 0.0007, df = 7, paired t-test [p.t.t.]; complex, control, 14.44 ± 1.76 nA, EGTA, 8.77 ± 0.93 nA, n = 8/8, t = 5.558, p = 0.0009, df = 7, p.t.t.). The difference in EGTA effect on simple and complex calyces was quantified as EGTA/control (simple, 0.802 ± 0.032, n = 8/7, complex, 0.616 ± 0.042, n = 8/8, t = 3.552, p = 0.0032, df = 14, unpaired t-test [u.t.t.]). c EPSC amplitudes for all EGTA injected synapses were plotted against swelling number (black triangles, control; blue dots, EGTA) and fitted linearly (mean ± 95% confidence interval). d, Pre-I_AP and I_EPSC were tested in control (black, simple calyx; red, complex calyx) and after septin 5 antibody injection (blue, SP20, 1:1000, 3–5 min loading). e Bar graphs show SP20 effect on EPSC amplitudes 10–15 min after presynaptic pipette removal (simple, control, 12.53 ± 0.77 nA, SP20, 12.46 ± 0.70 nA, n = 6/4, t = 0.1137, p = 0.914, df = 5, p.t.t.; complex, control, 13.83 ± 0.76 nA, SP20, 18.29 ± 1.17 nA, n = 10/8, t = 6.808, p < 0.0001, df = 9, p.t.t.). The difference in SP20 effect on simple and complex calyces was quantified as SP20/control (simple, 1.002 ± 0.045, n = 6/4, complex, 1.323 ± 0.043, n = 10/8, t = 4.915, p = 0.0002, df = 14, u.t.t.). R demonstrates correlation strength. Bar graphs summarize mean ± SEM (**p < 0.01, ***p < 0.001). See Supplementary Figure 5