Fig. 2: Intravitreal administration of Nogo-A blocking antibody enhances visual recovery after retinal injury.

a To follow visual function changes following NMDA-induced injury (1), the optokinetic response was monitored before and after intravitreal injections (2). Control IgG (2μg/eye) or anti-Nogo-A IgG (11C7, 2 μg/eye) was delivered in the vitreous 2 days after NMDA injection. Electroretinograms were recorded in photopic conditions 6 weeks after NMDA injections (3, see Fig. S1). Retinal ganglion cell survival was assessed on retinal flat-mounts stained for RBPMS, the day following ERG recordings (4). At 0.5 nmol of NMDA, nine mice were examined for each antibody treatment (control IgG or 11C7). Six mice received control IgG and 11C7 after the injection of 2 nmol NMDA. b Immunofluorescent staining with RBPMS antibody revealed a ~30% reduction in the density of RGCs after injection of 0.5 nmol of NMDA and a ~70-% reduction following the administration of 2 nmol of NMDA relative to intact retinae. The level of cell death did not statistically vary between the two groups receiving either 11C7 or control IgG. c The optokinetic response of mice receiving 0.5 nmol of NMDA showed significant function deficits after control IgG treatment. Similar visual loss was obtained with 0.5 nmol NMDA alone, without antibody (data not shown). In contrast, blocking Nogo-A with 11C7 allowed much better recovery of optokinetic response sensitivity. The effect of 11C7 was not significant when injected after 2 nmol of NMDA. d The optokinetic response of individual animals revealed weak variability in groups injected with 0.5 nmol of NMDA compared with 2 nmol of NMDA. Statistics: c, ***P < 0.001, two-way ANOVA; d, ***P < 0.001, unpaired t-test. Scale bar = 100 μm.