Abstract
For most adult vertebrates, glaucoma, trauma, and tumors close to retinal ganglion cells (RGCs) result in their neuron death and no possibility of vision reestablishment. For more distant traumas, RGCs survive, but their axons do not regenerate into the distal nerve stump due to regeneration-inhibiting factors and absence of regeneration-promoting factors. The annual clinical incidence of blindness in the United States is 1:28 (4%) for persons >40 years, with the total number of blind people approaching 1.6 million. Thus, failure of optic nerves to regenerate is a significant problem. However, following transection of the optic nerve of adult amphibians and fish, the RGCs survive and their axons regenerate through the distal optic nerve stump and reestablish appropriate functional retinotopic connections and fully functional vision. This is because they lack factors that inhibit axon regeneration and possess factors that promote regeneration. The axon regeneration in lower vertebrates has led to extensive studies by using them as models in studies that attempt to understand the mechanisms by which axon regeneration is promoted, so that these mechanisms might be applied to higher vertebrates for restoring vision. Although many techniques have been tested, their successes have varied greatly from the recovery of light and dark perceptions to partial restoration of the optomotor response, depth perception, and circadian photoentrainment, thus demonstrating the feasibility of reconstructing central circuitry for vision after optic nerve damage in mature mammals. Thus, further research is required to induce the restoration of vision in higher vertebrates. This paper examines the causes of vision loss and techniques that promote transected optic nerve axons to regenerate and reestablish functional vision, with a focus on approaches that may have clinical applicability.
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