Abstract
BackgroundResearch into retinal ganglion cell (RGC) degeneration and neuroprotection after optic nerve injury has received considerable attention and the establishment of simple and effective animal models is of critical importance for future progress.Methodology/Principal FindingsIn the present study, the optic nerves of Wistar rats were semi-transected selectively with a novel optic nerve quantitative amputator. The variation in RGC density was observed with retro-labeled fluorogold at different time points after nerve injury. The densities of surviving RGCs in the experimental eyes at different time points were 1113.69±188.83 RGC/mm2 (the survival rate was 63.81% compared with the contralateral eye of the same animal) 1 week post surgery; 748.22±134.75 /mm2 (46.16% survival rate) 2 weeks post surgery; 505.03±118.67 /mm2 (30.52% survival rate) 4 weeks post surgery; 436.86±76.36 /mm2 (24.01% survival rate) 8 weeks post surgery; and 378.20±66.74 /mm2 (20.30% survival rate) 12 weeks post surgery. Simultaneously, we also measured the axonal distribution of optic nerve fibers; the latency and amplitude of pattern visual evoke potentials (P-VEP); and the variation in pupil diameter response to pupillary light reflex. All of these observations and profiles were consistent with post injury variation characteristics of the optic nerve. These results indicate that we effectively simulated the pathological process of primary and secondary injury after optic nerve injury.Conclusions/SignificanceThe present quantitative transection optic nerve injury model has increased reproducibility, effectiveness and uniformity. This model is an ideal animal model to provide a foundation for researching new treatments for nerve repair after optic nerve and/or central nerve injury.
Highlights
The optic nerve, which consists of retinal ganglion cell (RGC) axons, is part of the central nervous system (CNS) [1]
The results showed that the mean density of RGCs in the control eyes was 1741.236104.33 cells/mm2 for all the control groups (n = 30)
The mean rate of RGC apoptosis is highest in week 1, with 627.54 cells/mm2 per week undergoing apoptosis, following which it slowly decreased as follows: between weeks 1 and 2, the rate was 365.47 cells/mm2 per week; from weeks 2 to 4, the rate was 121.60 cells/mm2 per week; from weeks 4 to 8, the rate was 17.04 cells/mm2 per week; and from weeks 8 to 12, the rate was 14.66 cells/mm2 per week (Figure 2,3)
Summary
The optic nerve, which consists of retinal ganglion cell (RGC) axons, is part of the central nervous system (CNS) [1]. Establishing an effective animal model of optic nerve injury is important to better understand the mechanisms behind RGC degeneration and neuroprotection, and further explore new drug targets and treatment options, such as cell transplantation, for optic nerve functional recovery and regeneration [7,8]. Incomplete models are difficult to ensure uniformity in the degree of optic nerve injury and quantify accurately [15] They are not suitable for topical drug administration during treatment. The features of the complete injury model ensure fewer experimental errors It is a sufficient model for examining nerve degeneration and apoptosis after injury. Research into retinal ganglion cell (RGC) degeneration and neuroprotection after optic nerve injury has received considerable attention and the establishment of simple and effective animal models is of critical importance for future progress
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