Barrier tightness is maintained in EAE-affected NG2KO mice.

a-d Representative confocal images from mice injected with FITC-Dextran 70 kDa for BBB permeability assessment, then immunolabelled for PDGFRα to show vessel/OPC association. a, b The exogenous tracer stains the vessel lumen in BBB cerebrocortical microvessels of both naïve WT and naïve NG2KO mice: note in (a) a transversely cut microvessel with FITC-dextran in the vessel lumen (arrow) and in (b) a minimal leakage around a small venule (arrows). c, d The deep cerebral cortex microvessels (at the boundary with the subcortical white matter) of EAE-affected WT mice appear permeable to the exogenous tracer that forms a fluorescent halo in the surrounding neuropil (c), while little signs of increased permeability are shown by cortex microvessels in EAE-affected NG2KO mice (d). E The bar chart shows the percentage of JV OPCs associated with leaky microvessels, a value that is significantly increased in EAE-affected WT mice (20 dpi) compared with naïve WT mice. No significant differences are observed between naïve NG2KO and EAE NG2KO mice (mean ± SD; n = 5;*p .05). FITC-dextran injected EAE WT mice (20 dpi clinical score range: 1.5–2.5, mean number of counted JV OPCs contacting leaky vessel: 14 per mouse), FITC-dextran injected EAE NG2KO (20 dpi clinical score range: 1.5–2.5, mean number of counted JV OPCs contacting leaky vessel: 5 per mouse). Nuclear counterstaining with TO-PRO-3. Scale bars, 50 μm.