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首页> 美国政府科技报告 >Treatment of Retinal Injuries by Low-Energy Laser: Models of Neurodegeneration in Retinal Injuries and Treatment by Low Energy Laser
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Treatment of Retinal Injuries by Low-Energy Laser: Models of Neurodegeneration in Retinal Injuries and Treatment by Low Energy Laser

机译：低能量激光治疗视网膜损伤：视网膜损伤后神经退行性变的模型及低能量激光治疗

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摘要

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 to 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 op tic nerve. (1) 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. (2) 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. (3) Autoimmune neuroprotection is effective, at least in part, via local production of neurotrophic factors. 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. Immune neuroprotection is effective, at least in part, by local reactivation of the T cells so as to secrete neurotrophic factors.

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