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The vertebrate visual system is a valuable model for examining recovery after injury to the central nervous system (CNS). It is a relatively "simple" part of the CNS having one major class of projection neuron, the retinal ganglion cells (RGCs), which make topographic connections within well defined visual nuclei, thus recreating visual space within the brain. Topographic maps can be readily assessed electrophysiologically and anatomically and are a critical template for useful visually guided behaviour which can be examined behaviourally. Furthermore, the optic nerve is accessible, an extra-foramenal crush injury severing all RGC axons but leaving the meningeal sheath intact as a conduit for regeneration and preventing gross axonal mis-routing. The procedure also leaves the blood supply to the eye patent, avoiding ischaemic-induced RGC death. [ABSTRACT FROM AUTHOR]

Retinal neovascularization is a feature shared by many disease processes including diabetic retinopathy, retinopathy of prematurity, branch retinal vein occlusion and central retinal vein occlusion, which are collectively referred to as ischemic retinopathy (Campochiaro, 2000). Retinal neovascularization is the most common cause of blindness in young diabetic patients. Investigations of the pathogenic mechanisms and therapeutic interventions for retinal neovascularization require reproducible and clinically related animal models. Currently, all diabetic models exhibit only early retinal vasculopathy after 1 or 2 years of the disease (Kondo and Kahn, 2004). The lack of retinal neovascularization in diabetic models is probably due to the natural short life span of rodents (2-3 years). In humans, DR is detected only after at least 3 years of diabetes (Dorchy et al., 2002). As angiogenesis is tightly controlled by the relative balance of stimulators and inhibitors, a shift in their balance, such as increased expression of vascular endothelial growth factor (VEGF) or decreased production of pigment epithelium-derived factor, would initiate angiogenesis (Okamoto et al., 1997; Ruberte et al., 2004; Renno et al., 2002). It is clear from literature that ischemia-induced upregulation of VEGF is a potent mediator of retinal neovascularization (Campochiaro, 2000; Miller, 1997). Animal models of retinal neovascularization have been established by oxygen-induced retinal ischemia, photodynamically-induced retinal branch vein occlusion and intravitreal implantation of VEGF sustained-release pellets (Campochiaro, 2000; Saito et al., 1997; Ozaki et al., 1997; Tolentino et al., 2002). However, retinal neovascularization in these animal models is either transient or occurs with a delayed onset. [ABSTRACT FROM AUTHOR]

Retinal neovascularisation is a major clinical complication of diabetic retinopathy that takes place late in the disease process and constitutes the most damaging phase resulting in loss of vision (Klein et al., 1984). Neovascularisation is defined as the growth of new blood vessels which, in a disease process such as diabetic retinopathy, occurs in abnormal retinal locations. Long term consequences of retinal neovascularisation include the formation of epiretinal membranes and retinal detachment (Smith et al., 1999). In addition, new blood vessels lack a patent blood retinal barrier and exhibit leukostasis presumably resulting in cytotoxic damage (Ishida et al., 2003; Qaum et al., 2001). [ABSTRACT FROM AUTHOR]