Fig. 7.

Cerebellar granule neurons of Npc1^−/− mice exit the cell cycle earlier than those of wild-type mice. Cerebellar sections of PN11 Npc1^+/+ and Npc1^−/− mice, either untreated or treated with a single injection of HPBCD at PN7 (3–4 mice/group; 3–4 sections/mouse) were immunostained with anti-p27Kip1 antibodies (brown). Nuclei were stained with methyl green. A representative field of fissure between lobules II and III is shown. Note the presence of scattered p27Kip1-positive GNs along the entire EGL of Npc1^−/−. Low and high magnification of the same fields is shown in the right and left panels, respectively. The HPBCD treatment partially re-established the p27Kip1 expression pattern in Npc1^−/− mice. Numbers (mean ± SEM) of p27Kip-positive GNs/100 μm² were: Npc1^+/+, 17.20 ± 0.81; Npc1^−/−, 21.8 ± 0.79; HPBCD-treated Npc1^−/−, 19.20 ± 0.95 (Npc1^+/+ vs Npc1^−/−, p = 0.03; HPBCD-treated Npc1^−/− vs Npc1^+/+, p = 0.15; HPBCD-treated Npc1^−/− vs Npc1^−/−, p = 0.09). oEGL: outer External Granule Layer; iEGL: inner External Granule Layer. Scale bars indicate 50 μm (left) and 25 μm (right).