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. 2021 Oct 6;16(10):e0252635. doi: 10.1371/journal.pone.0252635

Fig 3. Inter-neuronal spreading of a-syn aggregate pathology from the DG to the CA1 region occurs independently of PLK2 inhibition.

Fig 3

a) Segmentation of DG and CA1 regions in organotypic hippocampal slices labelled with DAPI, shown in gray scale. The DG is bounded manually by a box, and the CA1 regions is afterwards defined by extrapolation of one side of the DG box and a diagonal line through the box. Scale bar = 200 μm. b) Immunostaining of S129A PFF-injected OHSCs showing aggregated α-syn at the CA1 region 7 dpi detected by both MJF-14 and pS129. PLK2i-treatment reduces the nuclear pS129-signal at CA1 that overlaps with DAPI (arrowheads) but has no influence on the PFF-induced aggregate-specific pS129-signal that overlaps with MJF-14-signal (arrows). Scale bars = 50 μm. c-d) Quantification of α-syn aggregate area (MJF-14 area normalized to tissue area) at the DG (c) and CA1 region (d) shows no significant effects on aggregation at either region following PLK2i treatment. P-values 0.1502 (c) and 0.1048 (d) using an unpaired Welch’s T test. e) Aggregate levels at the CA1 region were normalized to aggregate levels in DG of the same slice to address the relative spreading of S129A PFF-induced α-syn aggregates, based on MJF-14 staining. PLK2i treatment did not affect relative spreading of MJF14-positive pathology (p-value = 0.829 using an unpaired Welch’s T test). Bars represent mean ± SD of 5–6 slices per group. Images are representative of three independent experiments.