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. Author manuscript; available in PMC: 2022 Aug 5.
Published in final edited form as: Cell. 2021 Jul 22;184(16):4299–4314.e12. doi: 10.1016/j.cell.2021.06.031

Figure 3. Reactivation of CaMKII provides post-injury and long-term RGC protection after excitotoxic or axonal injuries.

Figure 3.

(A-B) Confocal images of retinal whole-mounts showing surviving RGCs labeled by Tuj1 immunoreactivity at 2 weeks after optic nerve crush in control (AAV-EBFP) or AAV-CaMKIIα T286D post-injury treatment. Scale bar, 40 µm.

(C) Quantification of RGC survival 2 weeks after optic nerve crush, expressed as numbers of RGCs (left Y-axis), and percentages of RGCs relative to those in the uninjured retina (right Y-axis). Data are presented as mean ± s.d., n=5 retinas per group. Unpaired t-test, *P<0.0001.

(D-G) Confocal images of retinal whole-mounts showing surviving RGCs labeled by Tuj1 immunoreactivity at 2 months and 12 months post NMDA injection in control (AAV-EBFP) and AAV-CaMKIIα T286D treated eyes. Scale bar, 40 µm.

(H) Quantification of RGC survival 2 months and 12 months post NMDA injection. Data are presented as mean ± s.d., n=4 retinas per group. One-way ANOVA with Tukey’s multiple comparisons test, F:1370, R2:0.9971, *P<0.0001.

(I-N) Confocal images of retinal whole-mounts showing surviving RGCs labeled by Tuj1 immunoreactivity at 1 month, 2 months, and 6 months post optic nerve crush in control (AAV-EBFP) or AAV-CaMKIIα T286D treated eyes. Scale bar, 40 µm.

(O) Quantification of RGC survival 1 month, 2 months and 6 months post optic nerve injury. Data are presented as mean ± s.d., n=4 retinas per group. One-way ANOVA with Tukey’s multiple comparisons test, F:523.2, R2:0.9932, *P<0.0001.