Fig. 1

Enhanced SV docking of Fmr1KO synapses and lack of an effect of isoproterenol. Isoproterenol (100 µM, 10 min) increases SV docking in WT (a, c, d) but not in Fmr1KO (e, g, h) PF-PC synapses. Isoproterenol induces an increasing trend in the number of docked vesicles (0–10 nm) in WT (a) (n = 250/3 and 203/3 synapses/mice: P = 0.059) at the expense of SVs within 10–20 nm, which decreased in number (***P < 0.001). These changes are absent in Fmr1KO slices (e) (n = 238/4 and 224/4 synapses/mice, 0–10 nm: P = 0.997; 10–20 nm: P = 0.988). Note the increase in SV at 10–20 nm in Fmr1KO control as opposed to WT control slices (^##P < 0.01). c, d, g, h Electron microscopy of PF-PC synapses. (B,F) The effect of isoproterenol on the SV distribution: WT (0–5 nm: ***P < 0.001); Fmr1KO (0–5 nm: P > 0.05). Fmr1KO control vs WT control at 0–5 nm (^##P < 0.01). (i), Active Zone (AZ) length of WT (n = 250) and Fmr1 KO (n = 238) synapses (P > 0.05). The values represent the mean ± S.E.M. Scale bar in (c, d, g, h) 100 nm. Generalized Linear Mixed Models (GLMM) with genotype and treatment as fixed effects, and animal subject as a random effect. P-values for fixed effects and their interactions were obtained with type II Wald Chi-Square tests and post-hoc tests were adjusted with the Tukey HSD method (a, b, e, f) and unpaired student’s t test in (i). n is the number of synapses, many synapses were analyzed per slice and several slices per mice