Fig. 5.

SAG protects against neurotoxic effects of prednisolone. (A) Scheme for administration of vehicle, prednisolone, or prednisolone + SAG according to “daily (P0-P7)” or “acute (P7 only)” schedule and histological analysis at P7 or P21. (B to F) Immunocytochemistry of the mitotic marker pH3, apoptosis marker cleaved caspase 3 (Casp3), CGNP markers Zic1 and Pax6, and Purkinje cell marker calbindin (Calb) at P7 and P21. (C) At P7, daily SAG treatment prevented the significant antiproliferative (prednisolone versus prednisolone + SAG: P < 0.02, ANOVA with Tukey’s post hoc, n = 3) and (E) acute SAG treatment proapoptotic (prednisolone versus prednisolone + SAG: P < 0.003, ANOVA with Tukey’s post hoc, n = 3) effects of prednisolone on neonatal CGNPs of the EGL. The prednisolone group is significantly different from all other groups (vehicle, prednisolone + SAG, and SAG). Only the P values of the Tukey’s post hoc test between the prednisolone and the prednisolone + SAG groups are given. (F and G) Significant reduction in the volume of the IGL at P21 induced by prednisolone treatment (P < 0.02, ANOVA with Tukey’s post hoc, n = 3), which was prevented by SAG. Images of lobe VII of the cerebellum shown in (F) are representative of the results in all lobes of the cerebellum. Asterisks indicate significant changes with the Tukey’s post hoc test. Scale bars, 100 μm [(B) and (D)] and 300 μm (F).