Fig. 8
Generation of functional inhibitory synapses is impaired in Csf1r-cKO mice. a, b Representative traces of mIPSCs recorded in a control (a) or a Csf1r-cKO (b) PC in the presence of 1 μM TTX and 10 μM NBQX; Vh = −70 mV. Scale bars, 100 pA and 500 ms. c Cumulative fractions of amplitudes of mIPSCs in control (blue) and Csf1r-cKO (red) mice. Recordings were obtained from PCs in lobules IV–V at P10–P12. The incidence of mIPSCs with smaller amplitudes is significantly increased in Csf1r-cKO mice (p < 0.001, Kolmogorov–Smirnov test). Graphs consist of 8426 events from 10 control cells from three mice and 9847 events from 15 Csf1r-cKO cells from six mice. d, e Averaged amplitude (d) and frequency (e) of mIPSCs. Amplitude was significantly smaller (d, p = 0.006, Mann–Whitney U test) and frequency was significantly lower (e, p = 0.013) in Csf1r-cKO (red) than in control (blue) mice. Data were obtained from 10 cells from three control mice and 15 cells from six Csf1r-cKO mice. Data are presented as mean ± SEM. f–i Immunostaining for VGAT (f, h), and merged images for VGAT (red) and calbindin (green) (g, i) in a control (f, g) and a Csf1r-cKO mouse (h, i) at P11. Images were taken from lobules IV–V in the vermis. Scale bars, 20 μm. j Mean fluorescence intensity of VGAT staining in the granule cell layer (GCL), the PC layer (PCL), and the molecular layer (ML) in lobules IV–V of cerebellar vermis. Signal intensity of VGAT was significantly lower in Csf1r-cKO mice than in control mice in all layers (GCL: p = 0.001; PCL: p < 0.001; ML: p < 0.001, t test). Each data set was obtained from 15 images (256 μm × 256 μm) containing GCL, PCL, and ML from three control and three Csf1r-cKO mice at P10–P12. Scale bars, 30 μm. *p < 0.05; **p < 0.01; ***p < 0.001
