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Non-Visual Photopigments Effects of Constant Light-Emitting Diode Light Exposure on the Inner Retina of Wistar Rats

机译:恒定发光二极管曝光对Wistar大鼠内视网膜的非视觉色素的影响

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摘要

The retina is part of the central nervous system specially adapted to capture light photons and transmit this information to the brain through photosensitive retinal cells involved in visual and non-visual activities. However, excessive light exposure may accelerate genetic retinal diseases or induce photoreceptor cell (PRC) death, finally leading to retinal degeneration (RD). Light pollution (LP) caused by the characteristic use of artificial light in modern day life may accelerate degenerative diseases or promote RD and circadian desynchrony. We have developed a working model to study RD mechanisms in a low light environment using light-emitting diode (LED) sources, at constant or long exposure times under LP conditions. The mechanism of PRC death is still not fully understood. Our main goal is to study the biochemical mechanisms of RD. We have previously demonstrated that constant light (LL) exposure to white LED produces a significant reduction in the outer nuclear layer (ONL) by classical PRC death after 7 days of LL exposure. The PRCs showed TUNEL-positive labeling and a caspase-3-independent mechanism of cell death. Here, we investigate whether constant LED exposure affects the inner-retinal organization and structure, cell survival and the expression of photopigments; in particular we look into whether constant LED exposure causes the death of retinal ganglion cells (RGCs), of intrinsically photosensitive RGCs (ipRGCs), or of other inner-retinal cells. Wistar rats exposed to 200 lx of LED for 2 to 8 days (LL 2 and LL 8) were processed for histological and protein. The results show no differences in the number of nucleus or TUNEL positive RGCs nor inner structural damage in any of LL groups studied, indicating that LL exposure affects ONL but does not produce RGC death. However, the photopigments melanopsin (OPN4) and neuropsin (OPN5) expressed in the inner retina were seen to modify their localization and expression during LL exposure. Our findings suggest that constant light during several days produces retinal remodeling and ONL cell death as well as significant changes in opsin expression in the inner nuclear layer.
机译:视网膜是中枢神经系统的一部分,特别适合于捕获光子,并通过参与视觉和非视觉活动的感光性视网膜细胞将该信息传递到大脑。但是,过多的光线照射可能会加速遗传性视网膜疾病或诱发感光细胞(PRC)死亡,最终导致视网膜变性(RD)。现代生活中人造光的特征性使用造成的光污染(LP)可能会加速退化性疾病或促进RD和昼夜节律失调。我们已经开发了一种工作模型,以在LP条件下以恒定或较长的曝光时间使用发光二极管(LED)光源研究弱光环境下的RD机制。中华人民共和国死亡的机制仍不完全清楚。我们的主要目标是研究RD的生化机制。先前我们已经证明,恒定的光(LL)暴露于白色LED会由于LL暴露7天后经典的PRC死亡而显着减少外核层(ONL)。 PRCs显示出TUNEL阳性标记和不依赖caspase-3的细胞死亡机制。在这里,我们调查恒定的LED暴露是否会影响视网膜的内部组织和结构,细胞存活以及光色素的表达;特别是,我们要研究持续的LED暴露是否会导致视网膜神经节细胞(RGC),固有光敏性RGC(ipRGC)或其他视网膜内细胞死亡。 Wistar大鼠在200×lx的LED下暴露2-8天(LL 2和LL 8),进行组织学和蛋白质处理。结果显示,在所研究的任何LL组中,细胞核或TUNEL阳性RGC的数量无差异,也没有内部结构损伤,表明LL暴露影响ONL但不产生RGC死亡。然而,观察到在视网膜内层表达的光色素黑素(OPN4)和神经蛋白酶(OPN5)会改变它们的定位和表达。我们的发现表明,持续不断的光照在几天内会导致视网膜重塑和ONL细胞死亡,以及内核层中视蛋白表达的显着变化。

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