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Fig. 3 | Molecular Neurodegeneration

Fig. 3

From: α-Synuclein accumulation and GBA deficiency due to L444P GBA mutation contributes to MPTP-induced parkinsonism

Fig. 3

Effect of α-synuclein on susceptibility of GBA+/L444P mice to MPTP-induced PD-like symptoms. a Representative photomicrographs from coronal mesencephalon sections containing TH-positive neurons in littermate WT control, GBA+/L444P, SNCA−/−, and SNCA−/-GBA+/L444P mice treated with saline or MPTP, respectively (scale bar, 500 μm). b Stereology counts of TH, and c Nissl-positive neurons in the SNpc region. Unbiased stereologic counting was performed for the SNpc region. d Representative photomicrograph of striatal sections stained for TH immunoreactivity with low (scale bar, 100 μm) and high magnification (scale bar, 50 μm). e Quantification of dopaminergic fiber densities in the striatum using Image J software (NIH). a-e Error bars represent the mean ± S.E.M (n = four mice per group). f Pole test was conducted on the sixth day post MPTP injection. g Grip strength test was conducted on the sixth day post MPTP injection. Behavioral abnormalities and susceptibility in pole test and grip strength test induced by MPTP injection were ameliorated in SNCA−/− and SNCA−/-GBA+/L444P mice. Maximum time to climb down the pole was limited to 60 s. f, g Error bars represent means ± S.E.M (n = six or seven 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. MPTP-treated WT group, or MPTP-treated WT and GBA+/L444P group. n.s: not significant

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