Fig. 6

rCXCL2 protects long-distance axon projections targeting the brain in the retinal NMDA injury model. a Fluorescence images of anterograde CTB tracing of RGC axons in optic nerves from normal control eyes, and NMDA injection in the vehicle (PBS) or rCXCL2-treated eyes after 7 days. Scale bar, 100 μm. b The black-and-white images of a. c Quantification of CTB intensity in optic nerves normalized to the normal control group (100 a.u.). The results are shown as mean ± SEM, n = 4 to 6 nerves per group, *p < 0.05. d Schematic view of the location of ON cross-sections. e Scheme of the β-III Tubulin-positive axon counting in the cross-section. Squares represent counting fields. Scale bar, 30 μm. f Representative images of β-III Tubulin staining in cross-sections at 0.5–1.0 mm of ON. Scale bar, 20 μm. g The calculated density of β-III Tubulin–positive axons in cross-sections at 0.5–1.0 mm of ON. The results are presented as mean ± SEM, n = 5 to 6 samples per group, *p < 0.05. h Schematic illustration of anterograde CTB tracing of the LGN and SC. The right eye of mice was always as the normal control, and the left eye was given different treatment. i Fluorescence images of anterograde CTB tracing of RGC axons projecting to the LGN and SC from normal control eyes, and 7 days after NMDA injection in the vehicle (PBS) or rCXCL2-treated eyes. Scale bar, 200 μm. j Quantification of CTB intensity in the LGN and SC normalized to the normal control group (100 a.u.) after normalizing the right hemisphere to the left hemisphere. Data are presented as mean ± SEM, n = 4 brains per group, *p < 0.05