Department of Ophthalmology, Visual and Anatomical Sciences, Wayne State University School of Medicine, Detroit, MI, USA.
Methods Mol Biol. 2025;2848:75-84. doi: 10.1007/978-1-0716-4087-6_5.
Zebrafish maintain a remarkable ability to regenerate their neural retina following rapid and extensive loss of retinal neurons. This is mediated by Müller glial cells (MG), which re-enter the cell cycle to produce amplifying progenitor cells that eventually differentiate into the lost retinal neurons. For example, exposing adult albino zebrafish to intense light destroys large numbers of rod and cone photoreceptors, which are then restored by MG-mediated regeneration. Here, we describe an updated method for performing these acute phototoxic lesions to adult zebrafish retinas. Next, we contrast this method to a chronic, low light lesion model that results in a more muted and sustained damage to photoreceptors and does not trigger a MG-mediated regeneration response. Thus, these two methods can be used to compare and contrast the genetic and morphological changes associated with acute and chronic methods of photoreceptor degeneration.
斑马鱼在视网膜神经元迅速大量丧失后，仍能保持出色的神经视网膜再生能力。这是由 Müller 胶质细胞（MG）介导的，MG 重新进入细胞周期，产生扩增前体细胞，最终分化为丢失的视网膜神经元。例如，将成年白化斑马鱼暴露在强光下会破坏大量的视杆和视锥光感受器，然后由 MG 介导的再生来恢复这些光感受器。在这里，我们描述了一种对成年斑马鱼视网膜进行急性光毒性损伤的更新方法。接下来，我们将这种方法与慢性低光损伤模型进行对比，慢性低光损伤模型对视锥细胞和视杆细胞造成的损伤更温和、更持久，并且不会引发 MG 介导的再生反应。因此，这两种方法可用于比较和对比与急性和慢性光感受器退化方法相关的遗传和形态变化。
