Skip to main content
. 2016 Mar 15;24(5):877–889. doi: 10.1038/mt.2016.32

Figure 6.

Figure 6

BDNF prevents apoptotic cell death of FXN-deficient cerebellar neurons in vivo. Animals were co-transduced with concentrated lentivectors (shRNA-sc or shRNA-37) and HSV-1 amplicon vectors (HSV-LacZ or HSV-BDNF) by in vivo stereotaxic injection into the cerebellum. (a) Confocal images show representative staining of cells after immunohistochemistry for fractin (red) and the nucleus marker DAPI (blue), in the cerebellum of sham animals or treated with shRNA-sc or with shRNA-37 and HSV-LacZ or with shRNA-37 and HSV-BDNF. Cerebellar sections were from mice killed 4 days after injection. Yellow arrows indicate positive cell for fractin. Bar: 10 µm. (b) Quantification of fractin-positive cells in FXN-deficient cerebella indicated a significant decrease when BDNF was overexpressed compared with animals treated with HSV-LacZ. (c) Representative western-blot of PARP 1 and cleaved caspase-3 levels in cerebella of mice killed 4 days after injection. (d) Quantification of cleaved caspase-3 levels in FXN-deficient cerebella indicated a significant decrease when BDNF was overexpressed in comparison with animals treated with HSV-LacZ. (e) Quantification of cleaved PARP 1 levels in FXN-deficient cerebella indicated a significant decrease when BDNF was overexpressed compared with animals treated with HSV-LacZ. Data represent mean values ± SEM from three independent experiments, *P ≤ 0. 05, **P ≤ 0.005.