Fig. 6.

Degradation of axonal transport and visual acuity pauses in progression. (A) Coronal sections through superior colliculus (SC) following intravitreal injection of cholera toxin B (CTB; green) into control and microbead-injected eyes of C57 mice. Two weeks of elevated IOP induced deficits in anterogradely transported CTB (dotted lines). (Lower) Retinotopic maps reconstructed from serial sections of SC with optic disk gap indicated (circles). Density of signal from transported CTB ranges from 0% (blue) to 50% (green) to 100% (red). Medial (M) and rostral (R) orientations indicated. (Scale bar: 500 µm.) (B) Fraction of SC with intact anterograde transport (defined by ≥70% CTB signal) normalized to CTRL eye levels following 2 (n = 7) and 4 (n = 5) wk of elevated IOP. Remaining transport at 2 wk is significantly lower than control (*P = 0.018). Although 4-wk transport is also significantly lower than the corresponding control (^#P = 0.008), intact transport did not differ between 2 and 4 wk. (C) Difference in spatial frequency acuity in cycles per degree (c/deg) between control (n = 35) and microbead (n = 35) eyes increases significantly between ensuing measurements through 10 d (P < 0.001). Following a significant improvement at 2 wk (*P = 0.02), acuity did not decline past day 10 performance through nearly 4 wk (P ≥ 0.22). Mean postinjection IOP for CTRL eyes was 14.28 ± 1.3, and that for microbead eyes 18.5 ± 1.7 (P < 0.001). Data: mean ± SEM.