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This dissertation, "Neuroprotection of Low Energy Laser on Retinal Ganglion Cells Survival After Optic Nerve Injury" by 林瑋源, Wai-yuan, Leon, Lam, was obtained from The University of Hong Kong (Pokfulam, Hong Kong) and is being sold pursuant to Creative Commons: Attribution 3.0 Hong Kong License. The content of this dissertation has not been altered in any way. We have altered the formatting in order to facilitate the ease of printing and reading of the dissertation. All rights not granted by the above license are retained by the author. DOI: 10.5353/th_b3122286 Subjects: Retinal ganglion cells Optic nerve - Wounds and injuries Optic nerve - Laser surgery
We have demonstrated in previous studies that low energy laser reduces injury-induced deficits caused by acute partial injury of the rat optic nerve. The results of in-depth analysis suggest that the laser effect in this model is of a neuroprotective nature. We have devoted the time lapsed since approval of funding of the present study to characterization of the optic nerve partial lesion model, in an attempt to determine whether the progressive degeneration which occurs subsequently to the primary insult and continues in the absence of any external insult, is of a self-perpetuating nature, and whether such progressive degeneration follows any topographical pattern and whether any such pattern might be a reflection of the severity of the primary injury itself. By clarify the above points, we may turn our model into an ideal model for studying the neuroprotection of the optic nerve and retinal ganglion cells from injurious conditions.
Many retinal and optic nerve disorders have no effective therapy, or are treated incompletely and with considerable side effects. Recent advances have suggested the significant benefits associated with neuroprotection - that is, when treatment strategies are directed to photoreceptors, retinal ganglion cells, or other neural targets. Enter Ocular N
Background and Purpose: Injury to the central nervous system (CNS) in general, and to the visual system (retina or optic nerve) in particular, has a final outcome which is far more severe than the initial damage. If neighboring neurons that escaped the initial insult are to be rescued from eventual degeneration, ways must be found protect them. Adequate neuroprotection presupposes a basic understanding of the way in which the damage spreads, the nature of the mediators of toxicity, the most efficient means of neutralizing these harmful agents or their effects, and ways of making the neural tissue more resistant to the toxicity mediators. Methods: Our choice of model for studying mediators of toxicity and methods of neuroprotection is a partial crush injury of the rat optic nerve. Results: Partial injury of the rat optic nerve leads to a gradual spread of damage from the injured neurons, commencing in either the axons or the cell bodies of adjacent neurons that escaped initial injury. The continuing degeneration is associated with an increase in extracellular glutamate and nitric oxide, and possibly also an increased susceptibility of the spared neurons to the toxicity. We have provided evidence that the immune response, in the form of autoimmune T cells directed against the CNS self antigen myelin basic protein, if suitably boosted, is beneficial in reducing the spread of damage. Conclusion: Partial lesion of the optic nerve results in a self perpetuating and self limiting spread of neuronal damage, which is mediated in part by a toxic increase in physiological compounds, in combination with an increased susceptibility of the affected neurons. Autoimmunity, if suitably controlled, may-be a benign response adapted for the protection and maintenance of the damaged tissue.
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