CELLULAR MECHANISMS OF ACQUIRED COLOR VISION LOSS

获得性色觉丧失的细胞机制

基本信息

  • 批准号:
    3266086
  • 负责人:
  • 金额:
    $ 2.78万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    1990
  • 资助国家:
    美国
  • 起止时间:
    1990-08-01 至 1993-01-31
  • 项目状态:
    已结题

项目摘要

This application's long-term objectives are to investigate the histochemical differences between rods and cones and, exploiting these differences, to specify the degenerative changes that occur in human retinal photoreceptor cells with aging and disease. Previous studies revealing histochemical and morphological differences between the blue-sensitive cones and the red- and green sensitive cones will be expanded. Further documentation will be obtained that a sub-population of cones, identified by its absence of carbonic anhydrase (CA) enzymatic activity, is the blue-sensitive cones. Specifically, an attempt will be made to correlate immunocytochemistry for CA with enzyme histochemistry in the human retina. Existing antibodies to putative red/green cones and to blue cones will be compared to CA distribution. Blue cones will also be identified by exposure to vital dyes and to strong spectral lights. The labeled or damaged cones will be compared to CA distribution. Morphological quantitation of the normal anatomical characteristics of blue cones compared to red and green cones will be performed at both the light (LM) and electron microscopic (EM) level. Ultrastructural localization of CA will be employed for the EM studies. The pathogenesis of acquired dyschromatopsia in retinal disease will be studied by examining changes in the morphology and prevalence of the blue cone population versus the red/green cone population in several disorders such as retinal detachment, diabetic retinopathy and glaucoma. Surgical specimens as well as an animal model will be utilized for retinal detachment. Donated eyes with representative stages of diabetic retinopathy will be examined. Glaucoma will be studied with human donor material and an animal model of ocular hypertension. Knowledge gained of the time course of degenerative changes, reversibility of damage and comparative susceptibilities of the four types of photoreceptors may influence accepted approaches to treatment.
该应用程序的长期目标是调查 视杆细胞和视锥细胞之间的组织化学差异, 差异,以说明发生在人类中的退行性变化 视网膜感光细胞的老化和疾病。 先前的研究揭示了组织化学和形态学差异 在对蓝色敏感的视锥细胞和对红色和绿色敏感的视锥细胞之间 将扩大。将获得进一步的文件,证明 球果的亚群,通过其碳酸酐酶的缺乏来鉴定 (CA)酶活性,是蓝色敏感锥。具体来说, 将尝试将CA的免疫细胞化学与酶 人类视网膜的组织化学现有的抗体, 红色/绿色视锥和蓝色视锥将与CA分布进行比较。蓝色 视锥细胞也将通过暴露于活体染料和强 光谱光将标记或损坏的视锥细胞与CA进行比较 分布正常解剖结构的形态学定量 与红色和绿色视锥细胞相比,蓝色视锥细胞的特征将 在光(LM)和电子显微镜(EM)水平上进行。 CA的超微结构定位将用于EM研究。 视网膜疾病中获得性色觉障碍的发病机制将是 研究通过检查形态学的变化和流行的蓝色 在几种疾病中视锥细胞群与红/绿色视锥细胞群 例如视网膜脱离、糖尿病视网膜病变和青光眼。手术 标本以及动物模型将用于视网膜 支队具有糖尿病视网膜病变代表性阶段的供体眼睛 将被审查。青光眼将用人类供体材料和一种 高眼压动物模型。时间进程的知识 退行性变化、损伤的可逆性和比较 四种类型的光感受器的敏感性可能会影响接受 治疗方法。

项目成果

期刊论文数量(0)
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T MICHAEL NORK其他文献

T MICHAEL NORK的其他文献

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{{ truncateString('T MICHAEL NORK', 18)}}的其他基金

Large Animal Core
大型动物核心
  • 批准号:
    10668164
  • 财政年份:
    2023
  • 资助金额:
    $ 2.78万
  • 项目类别:
The Role of Outer Retinal Injury in Glaucoma
外视网膜损伤在青光眼中的作用
  • 批准号:
    6726084
  • 财政年份:
    2002
  • 资助金额:
    $ 2.78万
  • 项目类别:
The Role of Outer Retinal Injury in Glaucoma
外视网膜损伤在青光眼中的作用
  • 批准号:
    6623130
  • 财政年份:
    2002
  • 资助金额:
    $ 2.78万
  • 项目类别:
The Role of Outer Retinal Injury in Glaucoma
外视网膜损伤在青光眼中的作用
  • 批准号:
    6463315
  • 财政年份:
    2002
  • 资助金额:
    $ 2.78万
  • 项目类别:
CELLULAR MECHANISMS OF ACQUIRE COLOR VISION LOSS
获得性色觉丧失的细胞机制
  • 批准号:
    3266088
  • 财政年份:
    1993
  • 资助金额:
    $ 2.78万
  • 项目类别:
CELLULAR MECHANISMS OF ACQUIRED COLOR VISION LOSS
获得性色觉丧失的细胞机制
  • 批准号:
    3266085
  • 财政年份:
    1990
  • 资助金额:
    $ 2.78万
  • 项目类别:
CELLULAR MECHANISMS OF ACQUIRED COLOR VISION LOSS
获得性色觉丧失的细胞机制
  • 批准号:
    3266084
  • 财政年份:
    1990
  • 资助金额:
    $ 2.78万
  • 项目类别:
CELLULAR MECHANISMS OF ACQUIRED COLOR VISION LOSS
获得性色觉丧失的细胞机制
  • 批准号:
    2162448
  • 财政年份:
    1990
  • 资助金额:
    $ 2.78万
  • 项目类别:
CELLULAR MECHANISMS OF ACQUIRED COLOR VISION LOSS
获得性色觉丧失的细胞机制
  • 批准号:
    3266087
  • 财政年份:
    1990
  • 资助金额:
    $ 2.78万
  • 项目类别:

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