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. 2022 Jul 1;11:e78055. doi: 10.7554/eLife.78055

Figure 5. Decreased soluble α-synuclein (αSyn) at the axon terminals as pathology develops.

Figure 5.

(A1–B3) Representative confocal images showing αSyn immunoreactivity within vesicular glutamate transporter 1 (vGluT1+) puncta in the basolateral amygdala (BLA) using SYN1 antibody from control (A1–A3) and PFFs-injected mice (B1–B3).(C) Summarized graph showing a reduced αSyn immunoreactivity per vGluT1 immunoreactive puncta in PFFs-injected mice relative to controls (control=1049 ± 50; preformed fibrils (PFFs)= 617 ± 18, n=100 puncta/group, p<0.0001, MWU). (D) Summarized graph showing a reduced percentage of vGluT1 immunoreactive puncta associated with detectable αSyn immunoreactivity in PFFs-injected mice relative to controls (controls=85 ± 5.2%; PFF=26 ± 1.7%, n=6 slices/group, p=0.002, MWU). (E1–F3) Representative confocal images showing αSyn immunoreactivity within vGluT1+ puncta in the BLA using SYN9027 antibody from control (E1–E3) and PFFs-injected mice (F1–F3). (G) Summarized graph showing a reduced αSyn immunoreactivity per vGluT1 immunoreactive puncta in PFFs-injected mice relative to controls (control=954 ± 29; PFFs=633 ± 27, n=241 puncta/group, p<0.0001, MWU). (D) Summarized graph showing a reduced percentage of vGluT1 immunoreactive puncta associated with detectable αSyn immunoreactivity in PFFs-injected mice relative to controls (controls=87 ± 1.5%, n=12 slices; PFF=74 ± 1.6%, n=11 slices, p<0.0001, MWU).

Figure 5—source data 1. Source data for plots in Figure 5.