Fig. 1

Impairment of CF synapse elimination in BDNF-PC-KO mice after P16. a Representative traces of CF-EPSCs recorded in a PC from a control (left, P21) and a BDNF-PC-KO (right, P21) mouse. Holding potential was −10 mV. Single traces recorded at different stimulus intensities were superimposed. Scale bars, 10 ms and 1 nA. b Frequency distribution histogram for the number of CFs innervating each PC in control (open columns, n = 80 PCs from 10 mice) and BDNF-PC-KO (filled columns, n = 81 PCs from 12 mice) mice during P21–P50 (P = 0.0055, Mann–Whitney U-test). **P < 0.01. c–h Representative traces of CF-EPSCs (c, e, g) and frequency distribution histograms for the number of CFs innervating each PC (d, f, h) for control (open columns) and BDNF-PC-KO (filled columns) PCs during P10–P12 (c, d), P13–P15 (e, f), and P16–P20 (g, h). CF-EPSCs were recorded in cerebellar slices from a mouse at P11 (c), P14 (e), or P17 (g). Holding potential was −10 mV. Single traces recorded at different stimulus intensities were superimposed. Scale bars, 10 ms and 1 nA. Sample sizes for frequency distribution histograms were 37 PCs from 5 control mice and 45 PCs from 5 BDNF-PC-KO mice for P10–P12 (P = 0.788, Mann–Whitney U-test) (d), 72 PCs from 6 control mice and 67 PCs from 6 BDNF-PC-KO mice for P13–P15 (P = 0.553, Mann–Whitney U-test) (f) and 34 PCs from 5 control mice and 42 PCs from 6 BDNF-PC-KO mice for P16–P20 (P = 0.037, Mann–Whitney U-test) (h). *P < 0.05, ns indicates no significant difference between the groups