EVIDENCE OF BrdU- POSITIVE RETINAL NEURONS AFTER APPLICATION OF AN ALPHA7 NICOTINIC ACETYLCHOLINE RECEPTOR AGONIST

被引:15
作者
Webster, Mark K. [1 ]
Cooley-Themm, Cynthia A. [1 ]
Barnett, Joseph D. [1 ]
Bach, Harrison B. [1 ]
Vainner, Jessica M. [1 ]
Webster, Sarah E. [1 ]
Linn, Cindy L. [1 ]
机构
[1] Western Michigan Univ, Dept Biol Sci, Kalamazoo, MI 49008 USA
关键词
alpha7; nAChRs; Muller glia; retinal ganglion cells; BrdU; retina; Long Evans rat; OPTIC-NERVE DAMAGE; MULLER GLIA; INTRAOCULAR-PRESSURE; GANGLION-CELLS; RAT MODEL; REGENERATION; GLAUCOMA; NEUROPROTECTION; ACTIVATION; EXPRESSION;
D O I
10.1016/j.neuroscience.2017.01.029
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Irreversible vision loss due to disease or age is responsible for a reduced quality of life. The experiments in this study test the hypothesis that the alpha 7 nicotinic acetylcholine receptor agonist, PNU-282987, leads to the generation of retinal neurons in an adult mammalian retina in the absence of retinal injury or exogenous growth factors. Using antibodies against BrdU, retinal ganglion cells, progenitor cells and Muller glia, the results of this study demonstrate that multiple types of retinal cells and neurons are generated after eye drop application of PNU-282987 in adult Long Evans rats in a dose-dependent manner. The results of this study provide evidence that progenitor cells, derived from Muller glia after treatment with PNU-282987, differentiate and migrate to the photoreceptor and retinal ganglion cell layers. If retinas were treated with the alpha7 nAChR antagonist, methyllycaconitine, before agonist treatment, BrdU-positive cells were significantly reduced. As adult mammalian neurons do not typically regenerate or proliferate, these results have implications for reversing vision loss due to neurodegenerative disease or the aging process to improve the quality of life for millions of patients. (c) 2017 IBRO. Published by Elsevier Ltd. All rights reserved.
引用
收藏
页码:437 / 446
页数:10
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