Fig. 4
Deficiency of α-synuclein leads to decreased susceptibility of GBA+/L444P mice to MPTP-induced mitochondrial defects. a, b Relative quantity of mitochondrial DNA (mtDNA) in the ventral midbrain was measured using two different mtDNA markers (CYTB and COX) normalized to GAPDH. c Representative immunofluorescent images of TH (green), SDHA (red), and DAPI (blue). White dot line is shown in TH neurons. d Intensities of SDHA positive signals in the SNpc of mice treated with saline or MPTP were quantified and shown as a graph. e Immunoblots of SDHA, PDH, VDAC, TH, α-synuclein, and GBA. VMB lysates were immunoblotted with anti-SDHA, anti-PDH, anti-VDAC, anti-TH, anti-α-synuclein, and anti-GBA antibodies. f SDHA, g PDH, h VDAC, i TH, j α-synuclein, and k GBA expression levels were normalized against β-actin. a-k Error bars represent the mean ± S.E.M (n = three mice per group). Two-way ANOVA was used for statistical analysis followed by post-hoc Bonferroni test for multiple group comparison. *P < 0.05, **P < 0.01, ***P < 0.001 vs. saline-treated WT or saline-treated GBA+/L444P or MPTP-treated WT group. n.s: not significant