2004 Fiscal Year Final Research Report Summary
The quantitative analyses of electroretinogram and histology for retinal degeneration using transgenic mice
| Project/Area Number |
14571676
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Ophthalmology
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| Research Institution | Kyushu University |
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Principal Investigator |
GOTO Yoshinobu Kyushu University, Faculty of Medicine, Assistant Professor, 大学院・医学研究院, 講師 (30336028)
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| Co-Investigator(Kenkyū-buntansha) |
TOBIMATSU Shozo Kyushu University, Faculty of Medicine, Professor, 大学院・医学研究院, 教授 (40164008)
SAKAMOTO Taiji Kagoshima University, Faculty of Medicine, Professor, 医学部, 教授 (10235179)
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| Project Period (FY) |
2002 – 2004
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| Keywords | retinal degeneration / transgenic models / electroretinogram / rods / cones / function of inner layer of retina / dark reared / gene therapy |
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| Research Abstract |
The electrophysiological dysfunction of retina in retinitis pigmentosa should be caused by the retinal cells degeneration. The purposes of this project were to clarify the mechanism of this dysfunction and to advocate the new treatment in retinitis pigmentosa using the transgenic mouse and rat models. To address these issue, we quantitatively analyzed the electroretinograms and the histopathological changes of retina to evaluate the functional changes of rods, cones and inner cell layer in each transgenic mouse. We also compared the retinal functions between cyclic-light-reared and dark-reared mice to evaluate the retinal damages by the light. In addition, we transplanted the growth factor gene in subretina using the viral vector, and analyzed the protecting effects from the retinal degeneration. Our results were summarized as follows ; 1)the functions of ON- and OFF- bipolar cells in CMYC mouse were kept until 1 month, but disappeared at 6 month, 2)the dysfunctions of inner layer of r
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etina in each transgenic animal were started at earlier than the histological changes, 3)the dark-reared for 3 months was slowed the retinal degeneration in CMYC mouse, 4)the protecting effects for retinal functions by gene transplantation was observed in res rats (Ikeda et al.,2003;Miyazaki et al.,2003), and 5) there was not statistically significant the protecting effects for retinal functions by gene transplantation in dark-reared CMYC mouse. Overall, our findings suggest that the functional changes of rods, cones, and inner layers of retina were caused by the retinal cell degenerations. According to the new treatment, at present, the decrement of the light should be the first choice to protect the remaining functions of retina in retinal degeneration disease. In addition, the gene therapy should become a good treatment for this disease in near future, however we must improve the more practical methods of the vector transplantation to the retina. Finally, we could get the beneficial results at this project for the mechanism of functional decrements of retina and the treatment for the retinal degeneration in retinitis pigmentosa. Less
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