Fig. 5

Injury site-targeted complement inhibition prevents the formation of visual deficits in the ipsilateral eye after controlled cortical impact. A Treatment paradigm. CR2-Crry (16 mg/kg) or saline was administered via i.v. tail vein injection one hour after CCI. Behavioral testing was performed at the timepoints indicated. CCI controlled cortical impact. OKR optokinetic response. OCT optical coherence tomography. B Acute inhibition of complement activation preserved visual function in the ipsilateral eye, as measured by the optomotor response. C Animals almost always step away from the cliff when it is in their ipsilateral field of vision. D Both vehicle and CR2-Crry-treated animals step toward the cliff or safe sides with equal frequency when the cliff is in their contralateral field of vision. E Acute inhibition of complement activation significantly reduced time to find the escape hole in the Barnes maze relative to vehicle on the fifth training day and retention day. The results of a two-way ANOVA with repeated measures comparing the training curve for each experimental group is shown to the right of the first graph, and the results of a one-way ANOVA for each day above the corresponding day. B–E one-way ANOVA with Tukey correction for multiple comparisons. E two-way ANOVA with repeated measures with Tukey’s correction for multiple comparisons *p < 0.05, **p < 0.01, ***p < 0.001. Error bars = mean ± s.e.m