Light Induced Retinopathy In Juvenile Rats

Background and Purpose:The retina is the major organ to capture light and produce vision. It consists of various kinds of cells, which construct the outer retina and the inner retina. The retina is rich in unsaturated fatty acid, especially DHA, which makes the retina very sensitive to oxidative stress. In addition, since there is no vascularzition in the outer retina, the exchange of oxigen and nutrients can only be conducted through the arachnoid membrane so that the mtebolism of the retina is undermined. All these features of the retina make it vulnerable to bright light.Bright light exposure causes retina to produce more free radicals, the accumulation of which will induce photoreceptor cell death, and consiquantly lead to retinal degeneration both in function and structure. The activation of the cells in the retina is becoming less and less during the process of retinal maturation, which featuring the decrease of self-adaption and plasiticity. Some research showed that juvenile rats have remarkablly resistance to birght light exposure compared to adult rats.Juvenile rats can be made an effective model to study the maturation of the primary visual pathway which takes place in the human uterus. Further understanding the process of juvenile light induced retinopathy, as well its protective mechanism, will provide us a method to study certain degenerative diseases in human retina.Method:Juvenile SD rats were exposed to 10000 lux bight light from P14 to P28, and then were moved to normal enviroment. From P30 to P60, at 5 days interval, they were performed flash electroretinogram recording, flash visual evoke potencial recording, and also multi-focal electroretinogram recording. Then their retina were harvested for histology observation and CNTF quantification.Results:Bright light exposure caused significant reduction in retinal function. While this reduction partially recovered from P30 to P40, and then continued to decrease to the P30 value. The degeneration of the retinal structure was also observed, especially in the outer neuclear layer. The regrowth of outer segments were observed right after light exposure. This process lasted for about 10 days. The retinal thickness appeared a hemiretinosphere disparity. The supiroir retina was more damaged than the infirior retina. In addtion, CNTF was more up-regulated in the supirior retina.Conclusion:Light damage in juvenile rats is a progressively developed degeneration, with an acute phase and an chronic phase. A specific area of the supirior retina is more vulnerable to light damage, which leads to the up-regulation of CNTF. Therefore, the severity of photoreceptor apoptosis could be one of the factors for regulating the secretion of neurogrowth factors.