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Fig. 5 | Molecular Neurodegeneration

Fig. 5

From: A role for α-Synuclein in axon growth and its implications in corticostriatal glutamatergic plasticity in Parkinson’s disease

Fig. 5

Differences in WMTs between α-Syn transgenic and control mouse brains. a Paraffin embedded coronal brain section (6 μm) from A53T α-Syn tg mouse, immunoreacted with anti NF-200 (green) and anti PI4,5P2 (red) antibodies. Showing a WMT and the localization of the immunoreactivity to axon membrane. b Graph showing the immunoreactive signal ratio obtained for PI4,5P2 and NF-200 within WMTs (per area) for A53T α-Syn or Thy-1 hWT α-Syn tg mouse models, presented as percent of age- and genotype- matched control mice set at 100% (represinted by a vertical line). Mean ± SE, n = 4 brains, *, p < 0.05, one-way ANOVA. c Paraffin embedded coronal brain sections (6 μm) of A53T α-Syn and control (α-Syn−/−, C57BL/6JOlaHsd) mouse brains at 12 months of age, containing the dorsal striatum, immunoreacted either with antibodies against axonal markers SMI-32, SMI-31 and NF200 or anti APP antibody, a marker for axonal damage. Bar =50 μm. d Quantification of the immunoreactivity obtained as in (c) in WMTs of A53T α-Syn tg and control (α-Syn−/−, C57BL/6JOlaHsd) mouse brains, at 2, 8 and 12–14 months of age. Vertical line represents age-matched control mice, set at 100% for each of the tested antibodies. Mean ± SE; n = 5 mouse brain. *, P < 0.05, one-way ANOVA. e Consecutive brain sections (as in c and d) co-immunoreacted with syn303 anti α-Syn and anti SMI-32 antibodies. Bar = 20 μM

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