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Fig. 1 | Molecular Neurodegeneration

Fig. 1

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

Fig. 1

Ultrastructure of cross-sectioned axons in white matter tracts (WMTs). a Lower magnification of a coronal mouse brain section, stained with Luxol Fast blue (Sigma-Aldrich), showing the striatum. CC, corpus callosum; LV, lateral ventricle; WMTs shown as dark spots over the lightly stained striatal grey matter. Bar = 1 mm. b Cross section of a WMT in the dorsal striatum, consisting of myelinated axons. Image obtained by transmission electron microscope (TEM). Bar = 4 μm. c TEM images of coronal brain sections containing WMTs from A53T α-Syn and control mouse brains, at 4 months (healthy mice) or 12 months of age (symptomatic). Bar = 2 μm. d Bar graph showing the diameter (in μm) of cross-sectioned axons in WMTs. e. The number of axons per μm2 area of WMTs (axon density). Mean ± SE n = 4 brains, 5–8 WMTs per brain. f Intact myelin ultrastructure of a cross-sectioned axon in a WMT of 12 months old A53T α-Syn tg mouse brain. Bar = 200 nm. g A semi-thick A53T α-Syn mouse brain section (1 μm), stained with methylene blue (Sigma-Aldrich), showing cross-sectioned axons in a WMT. Bar = 20 μm. h Graph showing axon density in WMTs of Thy-1 hWT α-Syn and control mouse brains at 10–12 months of age. Determined in semi-thick sections (1 μm) stained with methylene blue. Mean ± SE of n = 4 brains, 8–10 WMTs per brain. i and j TEM images showing sagittal brain sections across the axons in corpus callosum of 12–14 months old A53T and age-matched control (C57BL/6JOlaHsd) mouse brains

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