Retinal Physiology in Experimental Glaucoma

实验性青光眼的视网膜生理学

基本信息

项目摘要

DESCRIPTION (provided by applicant): Maximum preservation of visual function is the main goal of glaucoma research. A patient cares little about his or her intraocular pressure or optic disc topography so long as their sight is normal. It may thus seem surprising that virtually nothing in known about the effect of glaucoma on the physiological properties of retinal ganglion cells, the very cells that provide the brain with visual input and that are targeted by the disease. The objective of the research project in to fill this important gap in our understanding of glaucoma. The research project proposes to do so by recording in vivo the visually-evoked activity of single optic tract fibers in the rat model of pressure-induced glaucoma and putting directly to test the hypothesis that the functional characteristics of retinal ganglion cells change in chronically hypertensive eyes before the cells die. The specific aims are to quantitatively characterize: 1) the spatiotemporal response properties of ganglion cells in normal rats and 2) the spatiotemporal response properties of ganglion cells in rats with chronic ocular hypertension. One possible outcome of the research is that glaucoma has no ill effects on ganglion cell physiology. For all intensive purposes the cells behave normally up until the moment they receive the apoptotic signal to die. This would dampen the prospects of using non-invasive methods, like vision tests and electroretinograms, for glaucoma detection since cells would invariably have to die for these methods to detect the disease. The other possible outcome is that ocular hypertension alters the mean spike rate, receptive field size, or other response properties of surviving ganglion cells. The physiological effects might be confined to certain types of ganglion cell or shared by them all. This outcome would not only paint a more promising picture for early glaucoma detection but also suggest the kinds of vision test that would best reveal perceptual deficits, which would thereby help speed progress in the fight against the debilitating disease. Public Health: Glaucoma is an eye disease that kills the cells that provide visual input to the brain. The aim of this research is determine how glaucoma affects the neural messages of these cells while the cells are still alive. This information could be used to design novel vision tests that detect the disease at an early stage.
描述(由申请人提供):最大限度地保留视觉功能是青光眼研究的主要目标。只要视力正常,病人对眼压或视盘地形不太关心。因此,青光眼对视网膜神经节细胞生理特性的影响几乎一无所知,这似乎令人惊讶,而视网膜神经节细胞正是为大脑提供视觉输入的细胞,也是该病的目标细胞。该研究项目的目的是填补我们对青光眼认识的这一重要空白。本课题拟通过在体内记录压力性青光眼大鼠模型中单个视束纤维的视诱发活动,直接验证慢性高血压眼视网膜神经节细胞在细胞死亡前发生功能特征改变的假说。具体目的是定量表征:1)正常大鼠神经节细胞的时空反应特性;2)慢性高眼压大鼠神经节细胞的时空反应特性。

项目成果

期刊论文数量(0)
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CHRISTOPHER L PASSAGLIA其他文献

CHRISTOPHER L PASSAGLIA的其他文献

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{{ truncateString('CHRISTOPHER L PASSAGLIA', 18)}}的其他基金

Continuous measurement and control of intraocular pressure in normal and glaucomatous eyes
连续测量和控制正常眼和青光眼眼的眼压
  • 批准号:
    10330025
  • 财政年份:
    2016
  • 资助金额:
    $ 24.38万
  • 项目类别:
Continuous measurement and control of intraocular pressure in normal and glaucomatous eyes
连续测量和控制正常眼和青光眼眼的眼压
  • 批准号:
    10563159
  • 财政年份:
    2016
  • 资助金额:
    $ 24.38万
  • 项目类别:
Continuous Measurement and Control of Intraocular Pressure in Normal and Glaucomatous Eyes
正常眼和青光眼眼眼压的连续测量和控制
  • 批准号:
    9160449
  • 财政年份:
    2016
  • 资助金额:
    $ 24.38万
  • 项目类别:
Retinal Physiology in Experimental Glaucoma
实验性青光眼的视网膜生理学
  • 批准号:
    7483022
  • 财政年份:
    2006
  • 资助金额:
    $ 24.38万
  • 项目类别:
Retinal Physiology in Experimental Glaucoma
实验性青光眼的视网膜生理学
  • 批准号:
    7289790
  • 财政年份:
    2006
  • 资助金额:
    $ 24.38万
  • 项目类别:
Retinal Physiology in Experimental Glaucoma
实验性青光眼的视网膜生理学
  • 批准号:
    7678406
  • 财政年份:
    2006
  • 资助金额:
    $ 24.38万
  • 项目类别:
CORRELATED NEURONAL DISCHARGES IN THE RETINA
视网膜中相关的神经元放电
  • 批准号:
    6363114
  • 财政年份:
    2001
  • 资助金额:
    $ 24.38万
  • 项目类别:
CORRELATED NEURONAL DISCHARGES THE RETINA
视网膜相关神经元放电
  • 批准号:
    6164657
  • 财政年份:
    2000
  • 资助金额:
    $ 24.38万
  • 项目类别:
CORRELATED NEURONAL DISCHARGES AND THE RETINA
相关的神经元放电和视网膜
  • 批准号:
    2861431
  • 财政年份:
    1999
  • 资助金额:
    $ 24.38万
  • 项目类别:

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Mechanisms of NMDAR contribution to traumatic injury in retinal ganglion cells
NMDAR对视网膜神经节细胞创伤性损伤的作用机制
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    10570666
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视网膜色素细胞在年龄相关变性、功能障碍和损伤中的部分表观遗传重编程
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    10644270
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    2023
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Diversity Supplement: Advancing novel therapies for optic neuropathy with a nonhuman primate model
多样性补充:利用非人类灵长类动物模型推进视神经病变的新疗法
  • 批准号:
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机械敏感离子通道在青光眼中的作用
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    10572841
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Myopia and Glaucoma, Linked via Mechanotransduction Mechanisms Affecting the Ganglion Cell Complex
近视和青光眼通过影响神经节细胞复合体的机械传导机制联系起来
  • 批准号:
    10656793
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