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Figure 2 | Acta Neuropathologica Communications

Figure 2

From: PGC-1α activity in nigral dopamine neurons determines vulnerability to α-synuclein

Figure 2

PGC-1α reduces the number of mitochondria and rescues the abnormal mitochondrial phenotype observed in the SNpc of PGC1α-KO mice. (a) Electron micrographs of neuronal soma in the SNpc of 10 month-old PGC1α-KO mice, PGC1α-KO mice injected with a vector encoding PGC-1α (PGC1α Inj) and WT mice. Note the presence of lipofuscin granules (black arrowheads) and giant mitochondria with disorganized cristae (black arrows). Nu indicates the neuronal nucleus (Nu). (b) Mitochondria are outlined with black lines. Neuronal nuclei and membranes are outlined with a grey line to indicate the limits of the neuronal cytosol. Note the increase in the density of mitochondrial clusters in PGC1α-KO mice. Scale bar: 1 μm. (c) Quantification of mitochondrial density reveals a significant increase in PGC1α-KO mice compared to the other groups. (d) Average area of mitochondria. Note the increased size in PGC1α-KO mice, compared to PGC1α Inj and WT mice. (e) Box and whisker plots showing the distribution of mitochondrial size in the SNpc of PGC1α-KO, PGC1α Inj and WT mice. The thick line represents the median and the box indicates the 10th and the 90th percentiles. Whiskers show the extreme values for each group. Note the presence of abnormal, enlarged mitochondria in PGC1α-KO mice. (f) Nearest neighbor analysis of mitochondrial distribution in the neuronal cytosol, demonstrating reduced clustering in PGC1α Inj mice. (g) Density of lipofuscin granules, which is significantly increased in the PGC1α Inj group. Statistical analysis: one-way ANOVA with Newman-Keuls post-hoc test; (C,F,G): WT: n = 79 neurons; PGC1α-KO: n = 89 neurons; PGC1α Inj: n = 113 neurons. (D,E): WT: n = 2729 mitochondria; PGC1α-KO: n = 3527; PGC1α Inj: n = 2544; **p < 0.01, ***p < 0.001. Micrographs were obtained from 3 animals in each group.

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