Optic nerve injury models in the rat

Abstract

AbstractGlaucoma is a degenerative disorder of the optic nerve which can be secondary to many diseases and the pathology occurs at the optic nerve head (ONH). It is important to know the effects of cell types, cell interactions, the trophic factors, receptors, channels, and matrix molecules in glaucoma. Research on the optic nerve in rats, mice, and nonhuman primates are necessary not just neurons in retina and optic nerve but also in central nervous system.Experimentally‐induced animal models help in understanding how retinal ganglion cells (RGC) die and how ON take place in this process. Special care must be taken to select controls and to use adequate number of animals. Experiments should be performed to understand the mechanism of pressure‐induced optic nerve damage and protect the optic nerve in glaucoma. An effective model should allow for the obstruction of aqueous humor outflow in order to raise IOP and for monitoring of intraocular pressure. Raised intraocular pressure, altered ocular perfusion, loss of auto regulation, alteration of vascular structure and characteristics of the blood‐brain barrier at the optic disc are alsopossible candidates in the pathogenesis of glaucoma. Animal studies indicate a response inoxidative metabolism to varied IOP and mean arterial blood pressure, and that low blood pressure leads to loss of autoregulation and ischemia of the optic nerve head.A number of techniques for increasing the intraocular pressure in rat are available. One of them involves sclerosing the trabecular meshwork using hypertonic saline. By cannulating theveins and injecting the corrosive saline retrogradely into the canal of Schlemm, it is possible to scar and close up the trabecular meshwork. Intraocular pressure elevates in approximately a week and lesions begin to develop. The lesions seen in the rat optic nerve following this procedure includes a decrease in axon density and an increase in vesicular bodies and vacuoles that is most prominent in the superior region of the optic nerve.We also carried out different models of rat studies either by damaging the ON mechanically or by ischemia to show the histological alterations in the ONH and retina. We also investigated the effects of oxidative stress and apoptosis on these alterations. Understanding the mechanism of nerve damage in these different models may provide new insights into the pathogenesis of human glaucoma.