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. 2022 Jul 15;132(14):e158524. doi: 10.1172/JCI158524

Figure 5. Disruption of paranodal proteins following glial membrane targeting in vivo.

Figure 5

Neuronal and Glial mice were dosed i.p. with 50 mg/kg anti-GM1 Ab followed 16 hours later with 30 μL/g normal human serum (NHS) (injury, Inj) or NHS only (control, Con). The site of expected nodal protein immunostaining is indicated by arrowheads. (A) The presence of normal ankyrin B (AnkB) immunostaining at the distal paranode (black bars) was significantly reduced in injured Glial mice compared with all treatment groups in the presence of complement (green). (B) A pan-neurofascin (Nfasc) Ab was used to assess glial NF155 and axonal NF186 (magenta). Representative images show loss of NF155 staining at paranodal regions, indicated by dashed lines, and the preservation of NF186 when NoRs are decorated with anti-GM1 Ab (green) in Glial mice. (C) Normal Caspr1 (orange) immunostaining at the distal paranodes was significantly reduced in injured Glial mice compared with all other treatment groups. (D) There was a reduction in distal NoRs with normal Nav channel (orange) staining in injured Neuronal mice. Scale bar: 5 μm. Results are represented as the mean ± SEM. n = 4/genotype/treatment: 5–46 NoRs/mouse (median = 21, AnkB); 7–53 NoRs/mouse (median = 25, NFasc); 5–15 NoRs/mouse (median = 11, Caspr1); and 11–27 NoRs/mouse (median = 16, Nav) were analyzed. *P < 0.05, **P < 0.01, ***P < 0.001 for comparisons with the other treatment groups (A, C, and D) or compared with control (B) by 2-way ANOVA with Tukey’s post hoc test.