Retinal Physiology in Experimental Glaucoma
Retinal Physiology in Experimental Glaucoma
批准号:
7678406
负责人:
CHRISTOPHER L PASSAGLIA
金额:
$23.67万
依托单位国家:
美国
项目类别:
财政年份:
2006
资助国家:
美国
项目状态:
已结题
起止时间:
2006-09-30 至 2011-08-31
关键词:
AffectAnimalsApoptoticAttentionBiological PreservationBlindnessBrainCell CountCell DeathCell physiologyCellsCessation of lifeCharacteristicsChronicClinicClinicalComplementDetectionDeveloped CountriesDeveloping CountriesDiagnosisDiseaseEarly DiagnosisElectroretinographyExperimental ModelsEyeEye diseasesFiberFortuneGlaucomaGoalsIndividualInjuryKnowledgeLeftMammalsMeasurementMeasuresMedicineMethodsModelingNoiseOcular HypertensionOptic DiskOptic tract structureOutcomeOutcomes ResearchPaintPatient CarePhysiologic Intraocular PressurePhysiologicalPhysiologyPopulationPropertyPsychophysiologyPublic HealthRattusResearchResearch PersonnelResearch Project GrantsRestRetinaRetinalRetinal DiseasesRetinal Ganglion CellsSignal TransductionSpeedStagingSumTestingTimeVisionVision TestsVisualVisual FieldsVisual impairmentWorkcell behaviorcell killingcell typedesigndriving forcefight againstganglion cellimprovedin vivokillingsnovelpressureprogramsreceptive fieldrelating to nervous systemresponseretinal damagespatiotemporalstatistics
中文摘要
描述(由申请人提供):最大限度地保护视觉功能是青光眼研究的主要目标。只要视力正常,患者就不太关心他或她的眼内压或视盘地形。因此,似乎令人惊讶的是,几乎没有人知道青光眼对视网膜神经节细胞的生理特性的影响,这些细胞为大脑提供视觉输入,并且是疾病的目标。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。该研究项目建议通过在压力诱导的青光眼大鼠模型中记录体内单个视神经束纤维的视觉诱发活动,并直接测试视网膜神经节细胞在细胞死亡前的功能特性在慢性高血压眼中发生变化的假设。具体目的是定量表征:1)正常大鼠神经节细胞的时空响应特性和2)慢性高眼压大鼠神经节细胞的时空响应特性。
这项研究的一个可能结果是青光眼对神经节细胞的生理学没有不良影响。对于所有密集的目的,细胞行为正常,直到它们收到凋亡信号死亡的那一刻。这将抑制使用非侵入性方法(如视力测试和视网膜电图)进行青光眼检测的前景,因为这些方法检测疾病总是需要细胞死亡。另一个可能的结果是高眼压改变了存活神经节细胞的平均峰电位率、感受野大小或其他反应特性。生理效应可能仅限于某些类型的神经节细胞或由所有神经节细胞共享。这一结果不仅为早期青光眼检测描绘了一幅更有希望的图景,而且还提出了最能揭示感知缺陷的视力测试类型,从而有助于加速与这种使人衰弱的疾病作斗争的进展。
公共卫生:青光眼是一种眼部疾病,它会杀死向大脑提供视觉输入的细胞。这项研究的目的是确定青光眼如何影响这些细胞的神经信息,而这些细胞仍然活着。这些信息可以用来设计新的视力测试,在早期阶段检测疾病。
英文摘要
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.
期刊论文(3)
专著(0)
科研奖励(0)
会议论文
Single-unit in vivo recordings from the optic chiasm of rat.
大鼠视交叉的单单位体内记录。
DOI:
10.3791/1887
发表时间:
2010
期刊:
Journal of visualized experiments : JoVE
影响因子:
--
作者:
[Freeman,DanielK, Heine,WalterF, Passaglia,ChristopherL]
通讯作者:
Passaglia,ChristopherL
Continuous measurement and control of intraocular pressure in normal and glaucomatous eyes
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批准号:10330025
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项目类别:
-
资助金额:$34.67万
-
财政年份:2016
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负责人:CHRISTOPHER L PASSAGLIA
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依托单位:
Continuous measurement and control of intraocular pressure in normal and glaucomatous eyes
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批准号:10563159
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项目类别:
-
资助金额:$35.65万
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财政年份:2016
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负责人:CHRISTOPHER L PASSAGLIA
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依托单位:
Continuous Measurement and Control of Intraocular Pressure in Normal and Glaucomatous Eyes
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批准号:9160449
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项目类别:
-
资助金额:$35.81万
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财政年份:2016
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负责人:CHRISTOPHER L PASSAGLIA
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依托单位:
Retinal Physiology in Experimental Glaucoma
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批准号:7483022
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项目类别:
-
资助金额:$23.19万
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财政年份:2006
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负责人:CHRISTOPHER L PASSAGLIA
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依托单位:
Retinal Physiology in Experimental Glaucoma
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批准号:7289790
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项目类别:
-
资助金额:$23.67万
-
财政年份:2006
-
负责人:CHRISTOPHER L PASSAGLIA
-
依托单位:
Retinal Physiology in Experimental Glaucoma
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批准号:7145349
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项目类别:
-
资助金额:$24.38万
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财政年份:2006
-
负责人:CHRISTOPHER L PASSAGLIA
-
依托单位:
CORRELATED NEURONAL DISCHARGES IN THE RETINA
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批准号:6363114
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项目类别:
-
资助金额:$4.2万
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财政年份:2001
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负责人:CHRISTOPHER L PASSAGLIA
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依托单位:
CORRELATED NEURONAL DISCHARGES THE RETINA
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批准号:6164657
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项目类别:
-
资助金额:$3.75万
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财政年份:2000
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负责人:CHRISTOPHER L PASSAGLIA
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依托单位:
CORRELATED NEURONAL DISCHARGES AND THE RETINA
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批准号:2861431
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项目类别:
-
资助金额:$3.17万
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财政年份:1999
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负责人:CHRISTOPHER L PASSAGLIA
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依托单位:
海外基金