Figure 5.

Syndecan-1–null axons are impaired in their ability to reinnervate the cornea after trephine injury. (A) Corneas from WT and SDC1-null mice were obtained at the following times after trephine injury: 1, 2, 3, 4, 7, 14, 28, and 42 days. Axons were visualized using an antibody against βIII tubulin. Representative images obtained 1, 28, and 42 days after trephine injury are shown. Both genotypes appear to lose similar numbers of ICNs after trephine injury at 1 day. Syndecan-1–null corneas continue to improve between 28 and 42 days; WT corneas appear similar to controls at 28 days. (B) Images of corneas stained for ICNs were used to quantify the axon density using Sholl analysis. Data are normalized relative to 8-week unwounded controls for each genotype with the exception of the 42-day injured corneas, which were normalized against genotype and age-matched controls to compensate for the loss of axon density with aging. Asterisks within bars indicate significant differences in axon density relative to unwounded controls. In the corneal center, normalized WT ICN density is restored to control levels at 3 days; SDC1-null ICN density is restored to control levels by 7 days but reduces again at 28 days before increasing at 42 days. (C) Axon thickness was assessed at the center and periphery at 3, 14, 28, and 42 days after trephination in WT and SDC1-null corneas. Data have been normalized relative to unwounded mice. Normalized axon thickness is reduced in SDC1-null corneas compared with controls at 3, 14, 28, and 42 days in the corneal center and periphery. It is reduced compared with WT in the center at 14 and 28 days and in the periphery at 3, 14, and 28 days. Scale bar in (A): 300 μm.