Search results for "Ganglion Cells"

showing 10 items of 66 documents

Correlation of Crystallin Expression and RGC Susceptibility in Experimental Glaucoma Rats of Different Ages.

2018

Glaucoma is one of the leading causes of blindness worldwide with age being an important risk factor. However, the pathogenesis remains poorly understood. Aim of this study was to focus on age-dependent molecular changes in an experimental animal model of glaucoma.Intraocular pressure was elevated in Sprague-Dawley rats aged 3, 14, and 47 weeks for a period of 7 weeks by episcleral vein cauterization. Ganglion cell loss was monitored by an immunohistochemical staining of the Brain-specific homeobox/POU (Pit-1, Oct-2, Unc-86) domain protein 3A positive cells in retinal flat-mounts and spectral-domain optical coherence tomography measuring the retinal nerve fiber layer thickness. Molecular pr…

ProteomicsRetinal Ganglion CellsIntraocular pressureAgingGlaucomaCell CountBioinformaticsMass SpectrometryRetinaCorrelationPathogenesisRats Sprague-Dawley03 medical and health sciencesCellular and Molecular NeuroscienceTonometry Ocular0302 clinical medicineNerve FibersCrystallinMedicineAnimalsRisk factorIntraocular PressureBlindnessbusiness.industryGlaucomamedicine.diseaseCrystallinsSensory SystemsOphthalmologyDisease Models AnimalAgeing030221 ophthalmology & optometryFemalebusiness030217 neurology & neurosurgeryTomography Optical CoherenceCurrent eye research
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Biomarkers for glaucoma: from the lab to the clinic

2017

Glaucoma, a leading cause of irreversible blindness worldwide, is often not diagnosed until many years after disease onset. Early and objective diagnostic measures are yet missing. Besides the main risk factor, an elevated intraocular pressure (IOP), age, sex, and ethnicity are known to affect disease progression and severity. Furthermore, oxidative stress, elevated glutamate concentrations, and an autoimmune component are considered possible risk factors. We could identify several potential proteomic biomarkers in glaucoma and examine distinct changes in the glaucomatous human retina proteome. Using an experimental autoimmune glaucoma animal (EAG) model we could demonstrate an IOP-independ…

ProteomicsRetinal Ganglion CellsIntraocular pressuremedicine.medical_specialtygenetic structuresSwineGlaucomaAutoimmunitymedicine.disease_causeRetinal ganglionRetinaAutoimmunity03 medical and health sciences0302 clinical medicineOphthalmologyMedicineAnimalsHumansIntraocular PressureAutoantibodiesRetinabusiness.industryAutoantibodyGlaucomamedicine.diseaseeye diseasesCambridge Ophthalmological SymposiumOphthalmologyDisease Models Animalmedicine.anatomical_structureImmunoglobulin GImmunology030221 ophthalmology & optometryOptic nerveDisease ProgressionBiomarker (medicine)sense organsMicrogliabusiness030217 neurology & neurosurgeryBiomarkers
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Serum and antibodies of glaucoma patients lead to changes in the proteome, especially cell regulatory proteins, in retinal cells.

2012

PURPOSE: Previous studies show significantly specifically changed autoantibody reactions against retinal antigens in the serum of glaucoma and ocular hypertension (OHT) patients in comparison to healthy people. As pathogenesis of glaucoma still is unknown the aim of this study was to analyze if the serum and antibodies of glaucoma patients interact with neuroretinal cells. METHODS: R28 cells were incubated with serum of patients suffering from primary open angle glaucoma (POAG), normal tension glaucoma (NTG) or OHT, POAG serum after antibody removal and serum from healthy people for 48 h under a normal or an elevated pressure of 15000 Pa (112 mmHg). RGC5 cells were additionally incubated wi…

ProteomicsRetinal Ganglion CellsSerumProteomegenetic structuresOcular hypertensionGlaucomalcsh:MedicineAutoimmunityPathogenesischemistry.chemical_compoundMolecular Cell Biologylcsh:ScienceCellular Stress ResponsesMultidisciplinarySpectrometric Identification of ProteinsbiologyNeurodegenerative DiseasesBlood proteinsSignaling CascadesNeurologyMedicineRetinal DisordersElectrophoresis Polyacrylamide GelAntibodyGlaucoma Open-AngleRetinal NeuronsSignal TransductionResearch ArticleSpectrometry Mass Electrospray IonizationImmunologyImmunoglobulinsPeptide MappingAntibodiesStress Signaling CascadeCell LineAntigenmedicinePressureAnimalsHumansBiologylcsh:RAutoantibodyRetinalGlaucomamedicine.diseaseeye diseasesRatsOphthalmologychemistrySpectrometry Mass Matrix-Assisted Laser Desorption-IonizationImmunologybiology.proteinOcular HypertensionClinical Immunologylcsh:Qsense organsChromatography LiquidPLoS ONE
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Separate processing of “color” and “brightness” in goldfish

1991

Spectral sensitivity was measured under different adaptation levels using a behavioral training technique in which the fish had to discriminate between a dark test field and a test field illuminated with monochromatic light. Depending on which of the two test fields was used as training test field, two functions were obtained which differ (1) in absolute sensitivity and (2) in shape. When trained on the dark test field, the fish seems to discriminate on the basis of a "color" cue, but it uses a "brightness" cue when trained on the illuminated test field. This was concluded from measurements of wavelength discrimination. Under low levels of the adaptation light (1.5 and 0.2 lx instead of 20 …

Retinal Ganglion CellsBrightnessLightgenetic structuresField (physics)Color visionDark AdaptationAdaptation (eye)OpticsGoldfishPsychophysicsPsychophysicsAnimalsPhotoreceptor CellsVisual Pathwaysbusiness.industrySensory SystemsElectrophysiologyOphthalmologySpectral sensitivitySensory Thresholdssense organsMonochromatic colorPsychologybusinessSensitivity (electronics)Color PerceptionVision Research
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Images perceived after chromatic or achromatic contrast sensitivity losses.

2010

Purpose. We simulate how subjects with losses in chromatic and achromatic contrast sensitivity perceive colored images by using the spatiochromatic corresponding pair algorithm. Methods. This is a generalized version of the algorithm by Capilla et al. (J Opt Soc Am (A) 2004;21:176 –186) for simulating color perception of color deviant subjects, which incorporates a simple spatial vision model, consisting of a linear filtering stage, with a band-pass achromatic filter and two low-pass chromatic ones, for the red-green and blue-yellow mechanisms. These filters, except for the global scaling, are the subject’s contrast sensitivity functions measured along the cardinal directions of the color s…

Retinal Ganglion CellsBrightnessgenetic structuresColor visionmedia_common.quotation_subjectModels NeurologicalCorresponding pair algorithmColor spaceChromatic and achromatic CSFslaw.inventionContrast SensitivitylawImages simulationContrast (vision)HumansComputer visionChromatic scaleSensitivity (control systems)LightingÓpticaMathematicsmedia_commonbusiness.industryDiabetesColorfulnessGlaucomaOphthalmologyPattern Recognition VisualAchromatic lensArtificial intelligencebusinessColor PerceptionMathematicsOptometryOptometry and vision science : official publication of the American Academy of Optometry
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A new vicious cycle involving glutamate excitotoxicity, oxidative stress and mitochondrial dynamics

2011

Glutamate excitotoxicity leads to fragmented mitochondria in neurodegenerative diseases, mediated by nitric oxide and S-nitrosylation of dynamin-related protein 1, a mitochondrial outer membrane fission protein. Optic atrophy gene 1 (OPA1) is an inner membrane protein important for mitochondrial fusion. Autosomal dominant optic atrophy (ADOA), caused by mutations in OPA1, is a neurodegenerative disease affecting mainly retinal ganglion cells (RGCs). Here, we showed that OPA1 deficiency in an ADOA model influences N-methyl-D-aspartate (NMDA) receptor expression, which is involved in glutamate excitotoxicity and oxidative stress. Opa1enu/+mice show a slow progressive loss of RGCs, activation …

Retinal Ganglion CellsCancer ResearchReceptor expressionExcitotoxicityApoptosisNeurodegenerativeMitochondrionEyemedicine.disease_causeGTP PhosphohydrolasesMice0302 clinical medicineReceptorsoxidative stressPhosphorylationbcl-2-Associated X Protein0303 health sciencesbiologyGlutamate receptorMitochondriaUp-RegulationCell biologymitochondrial fusionAutosomal DominantOriginal Articlebcl-Associated Death ProteinMitochondrial fissionN-Methyl-D-AspartateBiotechnologymitochondrial fragmentationOncology and CarcinogenesisImmunologybcl-X ProteinSOD2Glutamic AcidReceptors N-Methyl-D-AspartateNMDA receptorsCell Line03 medical and health sciencesCellular and Molecular NeuroscienceBcl-2-associated X proteinOptic Atrophy Autosomal DominantmedicineAnimalsEye Disease and Disorders of Vision030304 developmental biologySuperoxide DismutaseNeurosciencesCell BiologyMolecular biologyeye diseasesOxidative StressOptic AtrophyMutationbiology.proteinOPA1 mutationBiochemistry and Cell Biologysense organsglutamate excitotoxicity030217 neurology & neurosurgeryCell Death & Disease
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Connecting temporal identity to mitosis: the regulation of Hunchback in Drosophila neuroblast lineages.

2006

Both in vertebrates and invertebrates, neural stem cells generate different cell types at different times during development. It has been suggested that this process depends on temporal identity transitions of neural progenitors, but the underlying mechanism has not been resolved, yet. Recently, Drosophila neuroblasts (NBs) have been shown to be an excellent model system to investigate this subject. Here, changes in temporal identity are regulated by sequential and transient expression of transcription factors in the NB, such as Hunchback (Hb) and Kruppel (Kr). The temporal expression profile is maintained in the progeny. Hb is expressed first and thus defines the earliest identity in a giv…

Retinal Ganglion CellsCell typeReceptors SteroidKruppel-Like Transcription FactorsDown-RegulationMitosisNerve Tissue ProteinsBiologyCell fate determinationKrüppelNeuroblastAnimalsDrosophila ProteinsNuclear export signalMolecular BiologyMitosisTranscription factorGeneticsNeuronsModels GeneticNuclear ProteinsCell DifferentiationCell BiologyNeural stem cellDNA-Binding ProteinsProtein BiosynthesisDrosophilaDevelopmental BiologyTranscription FactorsCell cycle (Georgetown, Tex.)
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PGC-1α signaling coordinates susceptibility to metabolic and oxidative injury in the inner retina.

2013

Retinal ganglion cells (RGCs), used as a common model of central nervous system injury, are particularly vulnerable to metabolic and oxidative damage. However, molecular mechanisms underlying this sensitivity have not been determined in vivo . PGC-1α (encoded by PPARGC1A ) regulates adaptive metabolism and oxidative stress responses in a tissue- and cell-specific manner. Aberrant PGC-1α signaling is implicated in neurodegeneration, but the mechanism underlying its role in central nervous system injury remains unclear. We provide evidence from a mouse model that PGC-1α expression and activity are induced in adult retina in response to metabolic and oxidative challenge. Deletion of Ppargc1a d…

Retinal Ganglion CellsCentral nervous systemOxidative phosphorylationBiologymedicine.disease_causeRetinal ganglionPathology and Forensic MedicineMicemedicineIn Situ Nick-End LabelingAnimalsHumansIn Situ HybridizationMice KnockoutRetinaReverse Transcriptase Polymerase Chain ReactionNeurodegenerationAnatomyTFAMmedicine.diseaseImmunohistochemistryPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaCell biologyOxidative Stressmedicine.anatomical_structureAstrocytessense organsOxidative stressAstrocyteSignal TransductionTranscription FactorsThe American journal of pathology
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Metabolomic changes in the rat retina after optic nerve crush.

2013

Purpose To identify metabolic pathways and metabolites affected by optic nerve crush that can act as predictors of the disease or therapeutic targets. Methods The left optic nerve of adult rats was intraorbitally crushed and retinas were dissected 24 hours or 14 days after the lesion (n = 10 per group). Metabolic profiling analysis was carried out by Metabolon, Inc. A total of 195 metabolites were unambiguously detected. Data were normalized and the regulated metabolites were identified after comparing the different conditions. Metabolite concentration changes were analyzed using single and multivariate statistical analysis to detect discriminatory metabolites. Functional clustering and met…

Retinal Ganglion CellsNerve CrushMetaboliteProtein Array AnalysisApoptosisPharmacologymedicine.disease_causeGas Chromatography-Mass SpectrometryRetinaLesionRats Sprague-Dawleychemistry.chemical_compoundMetabolomicsTandem Mass SpectrometrymedicineAnimalsMetabolomicsAmino AcidsChemistryLipid metabolismAxotomyOptic NerveLipid MetabolismAxonsRatsMetabolic pathwayOxidative StressOptic nerveCarbohydrate MetabolismFemaleMetabolonmedicine.symptomOxidative stressChromatography LiquidSignal TransductionInvestigative ophthalmologyvisual science
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Preclinical Retinal Neurodegeneration in a Model of Multiple Sclerosis

2012

Neurodegeneration plays a major role in multiple sclerosis (MS), in which it is thought to be the main determinant of permanent disability. However, the relationship between the immune response and the onset of neurodegeneration is still a matter of debate. Moreover, recent findings in MS patients raised the question of whether primary neurodegenerative changes can occur in the retina independent of optic nerve inflammation. Using a rat model of MS that frequently leads to optic neuritis, we have investigated the interconnection between neurodegenerative and inflammatory changes in the retina and the optic nerves with special focus on preclinical disease stages. We report that, before manif…

Retinal Ganglion CellsPathologyTime FactorsStilbamidinesgenetic structuresJournal ClubFreund's Adjuvantchemistry.chemical_compoundBlood-Retinal BarrierStudent’s SectionCell DeathMicrogliabiologyGeneral NeuroscienceRetinal DegenerationNeurodegenerationArticlesmedicine.anatomical_structureSpinal CordRetinal ganglion cellOptic nerveFemaleMicrogliaMyelin Proteinsmedicine.medical_specialtyMultiple SclerosisEnzyme-Linked Immunosorbent AssayRetinaMyelin oligodendrocyte glycoproteinMicroscopy Electron TransmissionAntigens CDOccludinGlial Fibrillary Acidic ProteinIn Situ Nick-End LabelingmedicineAnimalsOptic neuritisAquaporin 4Retinabusiness.industryMacrophagesMultiple sclerosisMembrane ProteinsRetinalOptic Nervemedicine.diseaseeye diseasesRatsDisease Models Animalchemistrybiology.proteinMyelin-Oligodendrocyte Glycoproteinsense organsbusinessNeuroscienceThe Journal of Neuroscience
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