Stimulation of neural regeneration in the mouse retina

Stimulation of neural regeneration in the mouse retina
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DOI:
10.1073/pnas.0807453105
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发表时间:
2008-12-09
影响因子:
11.1
通讯作者:
Reh, Thomas A.
Reh, Thomas A.
中科院分区:
综合性期刊1区
文献类型:
--
作者:
Karl, Mike O.;Hayes, Susan;Reh, Thomas A.

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穆勒神经胶质细胞可以作为鱼类和鸟类视网膜损伤后新神经元的来源。体外哺乳动物视网膜再生的研究已经提供了一些证据表明,穆勒神经胶质细胞可以在视网膜损伤后增殖并产生新的视杆细胞;然而,体内发生这种情况的证据并不确凿。我们已经研究了Muller神经胶质细胞是否有潜力在小鼠视网膜中产生神经元,通过眼内注射NMDA消除神经节细胞和无长突细胞,并刺激Muller神经胶质细胞重新进入有丝分裂周期的治疗与特定的生长因子。增殖的Muller胶质细胞去分化,这些细胞的一个亚群分化为无长突细胞,如无长突细胞特异性标记物Calretinin、NeuN、Prox 1和GAD 67-GFP的表达所定义。这些结果首次表明,哺乳动物视网膜具有在体内再生内部视网膜神经元的潜力。
Muller glia can serve as a source of new neurons after retinal damage in both fish and birds. Investigations of regeneration in the mammalian retina in vitro have provided some evidence that Muller glia can proliferate after retinal damage and generate new rods; however, the evidence that this occurs in vivo is not conclusive. We have investigated whether Muller glia have the potential to generate neurons in the mouse retina in vivo by eliminating ganglion and amacrine cells with intraocular NMDA injections and stimulating Muller glial to re-enter the mitotic cycle by treatment with specific growth factors. The proliferating Muller glia dedifferentiate and a subset of these cells differentiated into amacrine cells, as defined by the expression of amacrine cell-specific markers Calretinin, NeuN, Prox1, and GAD67-GFP. These results show for the first time that the mammalian retina has the potential to regenerate inner retinal neurons in vivo.