Retinal degeneration in the nervous mutant mouse.: IV.: Inner retinal changes

被引:11
作者
Ren, JC
Stubbs, EB
Matthes, MT
Yasumura, D
Naash, MI
Lavail, MM
Peachey, NS
机构
[1] Loyola Univ, Stritch Sch Med, Program Neurosci, Maywood, IL 60153 USA
[2] Loyola Univ, Stritch Sch Med, Dept Neurol, Maywood, IL 60153 USA
[3] Edward Hines Jr VA Hosp, Res Serv 151, Hines, IL 60141 USA
[4] Univ Calif San Francisco, Beckman Vis Ctr, San Francisco, CA 94143 USA
[5] Univ Illinois, Coll Med, Dept Ophthalmol & Visual Sci, Chicago, IL 60612 USA
[6] Loyola Univ, Stritch Sch Med, Dept Ophthalmol, Maywood, IL 60153 USA
关键词
amacrine cell; apoptosis; degeneration; nervous mutant mouse; photoreceptor; retina;
D O I
10.1006/exer.2000.0961
中图分类号
R77 [眼科学];
学科分类号
100212 ;
摘要
We have recently noted that the inner nuclear layer (INL) and the inner plexiform layer (IPL) were significantly thinner in mice homozygous for the nervous defect (nr/nr) than in control (nr/+ or +/+) littermates. Here, we have carried out a series of anatomical studies to further understand these inner retinal changes. At postnatal day (P) 13. there was no difference in the inner retina between nervous and control mice, while a significant difference was observed at P30. Similar changes were not seen in other mouse models of photoreceptor degeneration. There was a significant reduction in the density of cells in the INL that were stained by antibodies against the inhibitory neurotransmitters GABA and glycine. These results indicate that the nervous defect causes a degeneration of one or more sub-types of amacrine cells, in addition to the loss of cerebellar Purkinje cells and retinal photoreceptors that is known to occur in these mutant animals. Finally, evidence is provided that photoreceptors die by an apoptotic pathway in nervous mice. (C) 2001 Academic Press.
引用
收藏
页码:243 / 252
页数:10
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