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. Author manuscript; available in PMC: 2010 Dec 10.
Published in final edited form as: Neuron. 2009 Dec 10;64(5):617–623. doi: 10.1016/j.neuron.2009.11.021

Figure 1. SOCS3 deletion promotes RGC axon regeneration.

Figure 1

(A–E) Confocal images of optic nerves showing CTB-labeled axons around the lesion sites at 14 days (A and B), 1 day (C), 3 day (D), 7 days (E) post crush injury (dpc) from SOCS3f/f mice injected with AAV-GFP (A) or AAV-Cre (B–E). *: crush site. Scale bar: 100 µm.

(F) Quantification of regenerating axons at different distances distal to the lesion sites at 14 days after crush injury. At least 5 different sections (every 4th section) from each animal were quantified. At 14 dpc, there were significant differences between control and SOCS3-deleted mice groups (ANOVA with Bonferroni’s post-test, p < 0.05 for each distance, 8 animals in each group).

(G) Fluorescent photomicrographs of retinal whole-mounts showing surviving TUJ1+ RGCs at 14 days after injury. Scale bar: 50 µm.

(H) Quantification of RGC survival at 14 dpc, expressed as a percentage of the total number of TUJ1+ RGCs in the contralateral (intact) retina. (n = 8 for each group). For each retina, 15–20 fields were chosen from different parts of the retina. The total viable RGC number was obtained by multiplying the average number per field of TUJ1+ cells in the ganglion cell layer by the retinal area. *: p < 0.01, Dunnett’s test.