The retina is an easily accessible part of the CNS with a well-defined cytological architecture. It allows for detailed study of the regulation of neurogenesis, determinants of cell fate specification, and signals for cell survival versus programmed cellular death during development. Within the retina, retinal ganglion cells (RGCs) are the only neurons connecting to the brain. Their axonal projection to the midbrain targets, the superior colliculus (SC), and the lateral geniculate nucleus (LGN) has been subject of a number of investigations, and led to the identification of molecular signals directing topographic information for precise wiring during development. Transcription factors, guidance molecules, extracellular matrix proteins, neurotrophic factors, and cell death-regulating factors of the Bcl-2 family and caspases, have all been reported to be involved in the processes of formation of a precise retino-collicular map, and regulation of developmental cell death.During adulthood, RGCs and their projection have to be maintained, since-to our current knowledge-they cannot be replaced following injury. On the other hand, insults of various kinds can be potentially hazardous to RGCs. Therefore, much work has been directed towards understanding of the molecular regulation of RGC degeneration following insults such as retinal ischaemia, axonal lesion, or in optic neuropathy. Experimental strategies are being devised towards protection of lesioned RGCs. Since following axonal lesion, these cells not only need to survive, but also have to reconnect in order to be functionally relevant, efforts are directed towards not only survival, but also axonal regeneration and proper rewiring of injured RGCs. This paper reviews the molecular determinants of RGC fate determination and the development of the retino-tectal projection. We summarize what is known (and hypothesized) on the determinants of RGC survival during normal adulthood, and the mechanisms of RGC degeneration in the injured retina. We also try to develop perspectives towards neuroprotection and regeneration of adult lesioned RGCs that may be applicable to lesioned CNS neurons in vertebrates in a broader sense.

中文翻译：

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视网膜神经节细胞发育，存活和再生的分子决定因素。

视网膜是具有明确定义的细胞学结构的中枢神经系统中易于访问的部分。它允许对神经发生的调节，细胞命运规格的决定因素以及发育过程中细胞存活与程序性细胞死亡的信号进行详细研究。在视网膜内，视网膜神经节细胞（RGC）是连接到大脑的唯一神经元。他们的轴突投射到中脑目标，上丘（SC）和外侧膝状核（LGN）已经受到了许多研究的关注，并导致了分子信号的识别，这些信号指导地形信息以在开发过程中进行精确布线。Bcl-2家族和胱天蛋白酶的转录因子，指导分子，细胞外基质蛋白，神经营养因子和细胞死亡调节因子，据报道所有这些都参与了精确的视网膜-胶状图的形成和发育细胞死亡的调节。成年期间，必须保持RGC及其预测，因为据我们目前的知识，它们不能被取代受伤后。另一方面，各种侮辱可能会对RGC造成潜在危害。因此，许多工作已经针对理解诸如视网膜缺血，轴突病变或视神经病变等损伤后RGC变性的分子调控。正在设计实验策略以保护受损的RGC。由于轴突病变后，这些细胞不仅需要存活，而且还必须重新连接才能与功能相关，因此，不仅要努力生存，而且还有轴突再生和受伤的RGC的正确布线。本文综述了RGC命运决定的分子决定因素以及视网膜-视网膜投射的发展。我们总结了正常成年期RGC存活的决定因素以及受损视网膜中RGC变性的机制的已知（并假设的）。我们还尝试发展对成年病变的RGC的神经保护和再生的观点，这些观点可能更广泛地适用于脊椎动物中病变的CNS神经元。以及视网膜损伤中RGC变性的机制。我们还尝试发展对成年病变的RGC的神经保护和再生的观点，这些观点可能更广泛地适用于脊椎动物中病变的CNS神经元。以及视网膜损伤中RGC变性的机制。我们还尝试发展对成年病变的RGC的神经保护和再生的观点，这些观点可能更广泛地适用于脊椎动物中病变的CNS神经元。