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1

Ugarte, Marta. "Influence of zinc on the normal retina and the retina given an insult of ischaemia : in vitro and in vivo studies." Thesis, University of Oxford, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.325776.

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2

Rheey, Jinguen. "Otx2 promotes survival of injured adult retinal ganglion cells non cell-autonomously and regulates development of inner retinal cells in post-natal mouse cell autonomously." Paris 6, 2011. http://www.theses.fr/2011PA066176.

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3

Bec, Jean-Michel. "Etude de la stimulation laser de neurones pour des applications de prothèses visuelles." Thesis, Montpellier 2, 2010. http://www.theses.fr/2010MON20029/document.

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Ce travail se situe dans le cadre d'un projet pluridisciplinaire visant à développer une prothèse visuelle. La technique la plus utilisée actuellement dans de nombreux types de neuroprothèses est basée sur l'excitation par voie électrique via des électrdes. Les inconvénients d'une telle technique (très invasive, de faible résolution spatiale et par contact) pourraient être surmontés en utilisant une stimulation par laser infra-rouge. Nous présentons dans un premier temps les caractéristiques des trois diodes lasers fibrés émettant à 1875 nm, 1535 nm et 1470 nm pour des gammes de puissances optiques de quelques centaines de mW qui ont été utilisés et intégrés à deux dispositifs de mesures permettant l'observations de variations d'échanges ioniques transmembranaires (imagerie de fluorescence des ions calciums et mesure électrophysiologique par la technique de patch clamp). Nous montrons ensuite que des réponses biologiques ont été obtenues par les trois lasers, non seulement sur des cellules ganglionnaires de la rétine et du vestibule de culture mais aussi sur des tranches de rétine. L'influence des paramètres clés comme la longueur d'onde, la durée de stimulation, les seuils d'énergie a été étudié, et a permis d'établir que les seuils d'énergie de stimulation dépendent de la valeur du coefficient d'absorption de l'eau qui varie suivant la longueur d'onde utilisée. Enfin, une étude est consacrée pour expliquer les mécanismes physiques et biologiques apparaissant au cours de l'interaction du laser avec le neurone au niveau cellulaire. Des simulations numériques quantifiant l'élévation de température associées à des tests pharmacologiques cherchant à déterminer la nature des canaux ioniques spécifiques mis en jeu suggèrent la prédominance d'un effet thermique
This work is part of a pluridisciplinary project, aiming at developing a visual prosthesis. The most used technique for this kind of neuroprosthesis is based on the electrical stimulation of nerves by electrodes. Drawbacks of such a technique (very intrusive, low spatial resolution and physical contact) could be overcome by the use of an infra red laser based stimulation. We present first the three fibre pigtailed laser diode characteristics emitting few hundred of mW at 1875 nm, 1535 nm and 1470 nm. These lasers have been integrated on two measurement devices (a fluorescence microscope and a microscope using patch clamp recording), for the observation of ionic membrane exchanges. Our results show that action potentials have been obtained by laser stimulation from the three lasers, both on retinal or vestibular ganglion cells from mass cultures and on retinal slices. The effect of key parameters as the wavelength, the stimulation time, the energy thresholds has been studied and show that the energy thresholds clearly depend on the absorption coefficient of water which varies with the wavelength. Finally, we present the results of a preliminary study aiming at determining the biophysical interaction mechanisms at cell level. Numerical simulations giving the local increase of temperature and tests of specific blocking molecules in order to know the exact nature of the ionic channels involved suggest a predominant thermal mechanism
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4

Stanke, Jennifer J. "Beyond Neuronal Replacement: Embryonic Retinal Cells Protect Mature Retinal Neurons." The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1250820277.

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5

Icha, Jaroslav. "Ganglion cell translocation across the retina and its importance for retinal lamination." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2017. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-218914.

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Correct layering (lamination) of neurons in the central nervous system (CNS) is critical for the tissue functionality. Neuronal lamination is established during development, when the majority of neurons have to move from their birthplace to the appropriate layer, where they function. Therefore, to grasp the logic of CNS development, it is essential to understand the kinetics and modes of the variety of neuronal translocation events. Most of our knowledge about neuronal translocation has been gained using fixed tissue or ex vivo imaging, which is not ideal for such a dynamic process heavily dependent on the surrounding environment. To avoid these limitations, I combined translucent zebrafish embryos with light sheet fluorescence microscopy, which together enabled gentle in toto imaging of neuronal translocation. I studied the translocation of retinal ganglion cells (RGCs) across the developing zebrafish retina. RGCs are the first neurons that differentiate in the vertebrate retina and are born in a proliferative zone at the retinal apical side. From here, they move basally, spanning the complete apico-basal length of the tissue. They are destined to occupy the most basal layer, where their axons form the optic nerve. Although it was described that RGCs move their soma while being attached to both apical and basal sides of the retina, the kinetics and cell biological mechanisms of somal translocation remained unknown. Extracting single cell behavior of RGCs from high-resolution movies of their translocation allowed for quantitative analysis of RGC movement. I revealed that RGCs cross the retina in less than two hours in a directionally persistent manner. The movement of RGC soma is a cell autonomously generated process, which requires intact microtubules and actin-dependent basal attachment of cells for speed and efficiency. Unexpectedly, interference with somal translocation leads to a shift towards a multipolar migratory mode, previously not observed for RGCs, in which they temporarily lose both apical and basal attachment and apico-basal polarity. The multipolar mode is overall slower and less directionally persistent, but still allows RGCs to reach the basal retina. However, when RGC translocation is inhibited completely, they differentiate ectopically in the center of the retina, which in turn triggers the formation of ectopic layers of later born neurons. These results highlight the importance of establishing the basal layer of ganglion cells for ensuing retinal lamination. Overall, I generated important advances in the understanding of neuronal translocation and lamination, which might be relevant for other parts of the CNS.
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6

Atkinson, Joana. "Manipulation of retinal neuronal outgrowth." Thesis, University of Cambridge, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.311308.

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7

Schneider, Nicole [Verfasser]. "Glutamate transporters in retinal neurons / Nicole Schneider." Hannover : Bibliothek der Tierärztlichen Hochschule Hannover, 2013. http://d-nb.info/1037880625/34.

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8

Holt, M. G. "Exocytosis and endocytosis in a retinal neurone." Thesis, University of Cambridge, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.604197.

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The synaptic vesicle cycle in the nerve terminal consists of exocytosis and neurotransmitter release, endocytosis and vesicle regeneration. However, the exact mechanisms which underlie this cycle are still largely unknown. This dissertation describes the use of fluorescence microscopy to study aspects of vesicle cycling in the synaptic terminal of retinal depolarizing bipolar cells isolated from goldfish retina. Endocytosis at the synapse may proceed via one of two pathways: through the direct reformation of small vesicles, or through the formation of large cisternae. However, the mechanisms responsible for forming these larger compartments are unclear. In chapter 3, it is shown that following exocytosis membrane is retrieved via small vesicles and large vacuoles in bipolar cells. Vacuoles were heterogeneous in size and their formation was dependent on P1 3-kinase and F-actin, whereas formation of small synaptic vesicles was not. Vacuoles were also transported away from the plasma membrane by an actin-dependent mechanism, stimulated by calcium influx. Bulk membrane retrieval in the bipolar cell therefore exhibits the properties of macropinocytosis observed in non-neuronal cells. The bipolar cell can maintain high levels of neurotransmitter release over periods of many minutes, in response to sustained stimulation. The bipolar cell also contains high amounts of PKCα. A role for this enzyme in continuous exocytosis was investigated and the results presented in chapter 4. To maintain continuous exocytosis required an elevated free Ca2+ level in the synaptic terminal of approximately 1 μM. Inhibition of PKC led to a reduced Ca2+ level during stimulation, blocking exocytosis. In addition, PKCα may also have other roles in the exocytic process, such as modulating the mobility of synaptic vesicles or regulating the sensitivity of the exocytic machinery to Ca2+. In conclusion to the chapter, experiments are described which could help distinguish between these possible functions of PKCα in the bipolar cell. The mobility of synaptic vesicles is likely to play an important role in the regulation of synaptic transmission. This is especially true in the bipolar cell, because of its ability to support continuous exocytosis.
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9

Wali, Naheed. "Three-dimensional reconstruction of mudpuppy retinal neurons /." The Ohio State University, 1988. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487595712160115.

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10

Sardo, Giacomo. "Caratteristiche morfologiche della retina nei Cetacei." Master's thesis, Alma Mater Studiorum - Università di Bologna, 2015. http://amslaurea.unibo.it/8130/.

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Le caratteristiche strutturali dell’occhio dei Cetacei sono state in passato oggetto di studio. Tuttavia, i dati relativi alla stratigrafia della retina ed alle caratteristiche morfologiche dei neuroni gangliari in essa presenti sono piuttosto ridotti; per questo motivo, l’obiettivo della presente ricerca è stato quello di studiare, mediante metodiche di immunoistochimica, l’uso della microscopia ottica e di opportuni software di analisi immagine, le caratteristiche morfologiche della retina e delle cellule gangliari in essa presenti in differenti specie di Cetacei. Per la presente ricerca sono stati utilizzate come specie di riferimento i seguenti Delfinidi: tursiope (Tursiops truncatus) e stenella striata (Stenella coeruleoalba). Le analisi sulle sezioni interessano l’area, la densità dei neuroni gangliari, la stratigrafia della retina e l’analisi morfometrica degli strati e dei neuroni. I risultati ottenuti indicano come la retina del tursiope e della stenella striata, nonostante un'organizzazione di base assai simile a quella degli altri Mammiferi, mostri caratteristiche qualitative sue proprie. Gli strati retinici sono quelli che si osservano in tutti i Mammiferi e lo spessore totale della retina è, nel tursiope (101,23 µm ) e nella stenella striata (108.35 µm ), pressochè simile ai Mammiferi terrestri (110-220 µm). Nell'ambito della retina, lo strato che presento lo spesso medio maggiore è quello dei granuli interni (SNE); tale dato non coincide con quanto osservato in altri Mammiferi. I neuroni gangliari presenti nella retina di tursiope e stenella striata mostrano, analogamente a quanto osservato in altri Cetacei, una bassa densità cellulare. Nel tursiope e nella stenella striata le aree a maggiore densità cellulare presentano neuroni multipolari di dimensioni minori rispetto a quelle con bassa densità. Questo dato potrebbe indicare una "cellularità" (quantità di superficie occupata da cellule) costante nei differenti distretti retinici. I neuroni gangliari presenti nella retina di tursiope e stenella striata sono disposti in un unico strato, come osservato in numerosi altri Cetacei, ma differisce da quanto osservato nel capodoglio (Physeter macrocephalus) dove tali cellule si dispongono in strati multipli. Neuroni gangliari di grandi dimensioni sono stati osservati sia nel tursiope che nella stenella striata. Tale dato coincide con quanto osservato in altri Odontoceti ed in alcuni Misticeti. Allo stato attuale non è ancora stato dato un chiaro significato funzionale alle cellule gangliari giganti. Un possibile ruolo potrebbe essere quello di condurre, in animali di grossa mole, l'impulso nervoso molto velocemente, grazie alla presenza di un assone provvisto di un diametro notevole. Tale interpretazione non è da tutti accettata in quanto Mammiferi terrestri di grandi dimensioni non presentano nella loro retina neuroni gangliari giganti.
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11

Montgomery, Rick. "Fractal Electrodes for Interfacing Neurons to Retinal Implants." Thesis, University of Oregon, 2015. http://hdl.handle.net/1794/18714.

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With life expectancy on the rise, age-related ailments are a significant strain on the welfare of individuals and the economy. Progress is being made towards combating the leading cause of unavoidable blindness, age-related macular degeneration (AMD). AMD affects ten million Americans and costs the world economy $343 billion annually. Retinal implants promise to restore sight by replacing the eye's damaged photoreceptors with electronic photodiodes. Clinical trials succeed at restoring some vision, but are limited by the stimulating electrodes. We study the electrode-neuron interface with a focus on the geometrical dependence of the electrode. The functionality of neurons is intimately connected to their branching and curving shape, described by fractal geometry. We examine the morphology of neurons using fractal analysis. The results inform our electrode designs, which are fabricated using top-down lithographic and bottom-up self-assembly techniques. A novel technique for fabricating a fractal electrode is presented. Heating and cooling a film of poly(methyl methacrylate) on a SiO2 substrate causes fractal structures to form on the surface. The geometry of the structures is temperature dependent, producing crystalline branches at lower temperatures and diffusion-limited aggregates at higher temperatures. Subsequent deposition of antimony nanoclusters shows preferred diffusion to the fractal surface features. The dependence of a photodiode's performance on its top contact geometry is explored using modified nodal analysis. The results reinforce the need to balance a low mean semiconductor-metal separation distance with an adequate contact width for low resistance, all while maximizing light input. Future designs will benefit from the spatial voltage maps produced by the simulation. The electric field emanating from an electrode is also dependent on the geometry of the electrode. The Faraday cage effect is exploited to achieve similar electric field responses to traditional electrode shapes. A preliminary study of neural adhesion to SU-8 fractal electrodes is promising. The neuron grows along the electrode even at 90° turns. The role the fractal geometry plays in neuron and electrode functionality is shown to be significant. Continued study of, and experimentation with, new electrode designs is sure to produce exciting possibilities in the future. This dissertation includes previously unpublished co-authored material.
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12

Mazurier, Nicolas. "Etude des mécanismes de maintenance et de spécification des cellules souches et progénitrices de la rétine du xénope." Phd thesis, Université Paris Sud - Paris XI, 2012. http://tel.archives-ouvertes.fr/tel-00980574.

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Au cours de ma thèse, mes projets de recherche ont visé à mieux comprendre les mécanismes moléculaires contrôlant la prolifération et la spécification des cellules progénitrices dans la rétine du xénope à travers trois projets principaux. Le réseau de régulation qui contrôle la spécification des cellules progénitrices vers les sous-types neuronaux est à ce jour très peu connu. C'est dans ce contexte que j'ai étudié le rôle du facteur de transcription à domaine bHLH, Ascl1, dans la détermination des sous-types rétiniens au cours du développement. Par des approches in vivo de gain et perte de fonction d'Ascl1, des expériences d'épistasie et la recherche de ses cibles transcriptionnelles, j'ai pu mettre en évidence qu'Ascl1 (i) est impliqué dans la genèse des neurones GABAergiques rétiniens, (ii) qu'il est épistatique sur des facteurs glutamatergiques tels que Neurog2, NeuroD1 ou Atoh7, (iii) que son activité GABAergique est conférée par son domaine basique de liaison à l'ADN et (iv) que cette activité implique la régulation directe du facteur de transcription Ptf1a. Ces données ajoutent donc une nouvelle pièce au réseau transcriptionnel gouvernant la spécification des sous-types GABAergiques au cours du développement de la rétine. La mise en place correcte des types et sous-types cellulaires de la rétine nécessite une coordination avec le moment de sortie du cycle cellulaire des progéniteurs rétiniens. Dans ce contexte, j'ai contribué à l'avancée d'un projet visant à étudier le réseau de signalisation contrôlant la prolifération des précurseurs de la rétine. Par des approches in vivo, génétiques et pharmacologiques, cette étude a montré que les voies Wnt et Hedgehog s'antagonisent pour réguler l'activité proliférative des cellules souches et progénitrices rétiniennes. Nos données préliminaires suggèrent que ces voies agissent de façon opposée à la fois sur la sortie et sur la cinétique du cycle cellulaire. Ce travail nous a conduit à proposer un modèle selon lequel ces voies Wnt et Hedgehog réguleraient la balance entre prolifération et différenciation dans la rétine post-embryonnaire. Enfin, dans le but d'élargir nos connaissances sur les réseaux de signalisation et les réseaux transcriptionnels impliqués dans le contrôle de la prolifération et de la détermination cellulaire dans la rétine, j'ai également contribué à la recherche de nouveaux marqueurs spécifiques des différentes populations cellulaires rétiniennes au travers d'un crible à grande échelle par hybridation in situ. De nombreux gènes spécifiquement exprimés dans les cellules souches ou les cellules progénitrices constituent des gènes candidats pour de futures approches fonctionnelles.
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13

McCabe, Kathryn Leigh. "The transition from progenitor cell to neuron : fibroblast growth factors and their role in retinal ganglion cell neurogenesis /." Thesis, Connect to this title online; UW restricted, 2000. http://hdl.handle.net/1773/10640.

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14

Mendl, Christian. "Neuronal coding in the retina." Diss., lmu, 2012. http://nbn-resolving.de/urn:nbn:de:bvb:19-139015.

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15

Cooke, Anne Christina. "Exocytosis and endocytosis at the synapse of retinal bipolar neurons." Thesis, University of Cambridge, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.620706.

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16

Moshiri, Ala. "Sonic hedgehog in the vertebrate retina /." Thesis, Connect to this title online; UW restricted, 2004. http://hdl.handle.net/1773/10669.

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17

Prince, Deborah Josephine. "Neuronal interactions in the fish retina." Thesis, Imperial College London, 1987. http://hdl.handle.net/10044/1/47703.

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18

Williams, Peter. "Retinal neuronal remodelling in a model of optic atrophy." Thesis, Cardiff University, 2011. http://orca.cf.ac.uk/20050/.

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The heterozygous mutation, B6;C3-Opa1Q285STOP, leads to a 50% reduction in Opa1 transcript and protein in the mouse retina and neural tissues and models autosomal dominant optic atrophy and presents with visual dysfunction and structural changes in the retina and optic nerve. This thesis explores the intimate relationship between retinal ganglion cell dendritic architecture, health and synaptic connectivity as influenced by the mitochondrial fusion protein Opa1. Using a range experimental paradigms it is reported here retinal ganglion cell dendritic atrophy which is exacerbated with age and localised exclusively to sublamina b of the inner plexiform layer. There is a marked reduction in the number of glutamatergic synaptic sites and PSD95 levels on ON-centre retinal ganglion cells. In addition, there is a significant increase in synaptic vesicle number and density in both ON and OFF bipolar cells. These processes cast light on the intimate relationship between normal mitochondrial fusion and fission balances, as influenced by the OPA1 protein, in neural cell connectivity in the mammalian retina and the changes shown here serve as an exciting biomarker for disease and rescue and recovery therapeutics.
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19

Amemiya, Kaori. "Adult human retinal pigment epithelial cells capable of differentiating into neurons." Kyoto University, 2007. http://hdl.handle.net/2433/135754.

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20

Randlett, Owen Myles. "Orienting and organizing neuronal morphogenesis in the retina." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610174.

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21

Akagi, Tadamichi. "Requirement of multiple bHLH genes for retinal neuronal subtype specification." Kyoto University, 2005. http://hdl.handle.net/2433/144719.

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22

Rakowicz, Wojciech Piotr. "The regulation of death in retinal ganglion cells and spinal motor neurons." Thesis, University of Cambridge, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.621305.

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23

Zhang, Shen. "Protective effects of ifenprodil against glutamate-induced neurotoxicity in cultured retinal neurons." Kyoto University, 2001. http://hdl.handle.net/2433/150508.

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24

Yasuyoshi, Hiroki. "Protective Effect of Bradykinin Against Glutamate Neurotoxicity in Cultured Rat Retinal Neurons." Kyoto University, 2000. http://hdl.handle.net/2433/180887.

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25

游思維 and Siwei You. "Neuronal survival and axonal regeneration of retinal ganglion cells inadult hamsters." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1998. http://hub.hku.hk/bib/B3123799X.

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26

Ghaffari, Mithra. ""Glial Islands" promote survival and regeneration of neurites from chick embryo retinal neurons." CSUSB ScholarWorks, 1997. https://scholarworks.lib.csusb.edu/etd-project/1458.

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27

Saadi, Anisse. "The signal transducing receptor gp130 is essential for protection of retinal neurons from stress-induced cell death but not for retinal development." Oklahoma City : [s.n.], 2009.

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28

You, Siwei. "Neuronal survival and axonal regeneration of retinal ganglion cells in adult hamsters /." Hong Kong : University of Hong Kong, 1998. http://sunzi.lib.hku.hk/hkuto/record.jsp?B19859946.

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29

Mao, Weiming. "The role of bHLH gene ash1 in the developing chick eye." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2008. https://www.mhsl.uab.edu/dt/2009r/mao.pdf.

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30

Chow, Wei-Yan. "Inhibitory neuron lamination in the developing zebrafish retina." Thesis, University of Cambridge, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708976.

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31

Edqvist, Per-Henrik. "Neuronal Development in the Embryonic Retina : Focus on the Characterization, Generation and Development of Horizontal Cell Subtypes." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-7128.

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32

Gregory, Linda Jane. "The effects of barbiturates and other sedatives on fish retina neurones : an electrophysiological study." Thesis, Imperial College London, 1988. http://hdl.handle.net/10044/1/47089.

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33

Binley, Kate E. "The retinal explant as a model to investigate neuronal pathology and neuroprotective strategies." Thesis, Cardiff University, 2016. http://orca.cf.ac.uk/94882/.

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Despite the association of neuronal cell loss with a wide range of neurodegenerative disorders, the mechanisms leading to this cell death remain poorly understood. In this thesis I have investigated these mechanisms and tested whether they represent viable targets for therapeutic intervention. The adult mouse retinal explant is a popular model of axotomy-induced neuronal degeneration but has been limited by the lack of morphometric data. Since dendritic pruning is well-evidenced to precede cell loss in neurodegenerative diseases, including glaucoma and Alzheimer’s disease, I investigated whether the quantification of dendritic morphology of retinal ganglion cells in the retinal explant could be used as a more sensitive measure of neuronal health after axotomy. I report here that retinal ganglion cell dendrite loss precedes cell loss by at least 7 days and that this retraction is substantially retarded following treatment with brain-derived neurotrophic factor applied at the time of explantation. Perhaps most importantly, I demonstrate for the first time in this model that delayed application of brain-derived neurotrophic factor significantly protects against dendritic retraction of retinal ganglion cells. The work outlined in this thesis thus supports the targeting of dendritic outgrowth and/or synaptic connectivity for the treatment of neurodegenerative disorders.
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34

Suzuki, Takuya. "Chondroitinase ABC treatment enhances synaptogenesis between transplant and host neurons in model of retinal degeneration." Kyoto University, 2009. http://hdl.handle.net/2433/126424.

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35

Martin-Martinelli, Elisabeth. "Evolution de la morphologie et de la distribution des neurones catecholaminergiques dans la retine de rat albinos au cours du developpement postnatal." Paris 6, 1988. http://www.theses.fr/1988PA066399.

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36

Moore-Dotson, Johnnie M., Jamie J. Beckman, Reece E. Mazade, Mrinalini Hoon, Adam S. Bernstein, Melissa J. Romero-Aleshire, Heddwen L. Brooks, and Erika D. Eggers. "Early Retinal Neuronal Dysfunction in Diabetic Mice: Reduced Light-Evoked Inhibition Increases Rod Pathway Signaling." Association for Research in Vision and Ophthalmology (ARVO), 2016. http://hdl.handle.net/10150/604678.

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Recent studies suggest that the neural retinal response to light is compromised in diabetes. Electroretinogram studies suggest that the dim light retinal rod pathway is especially susceptible to diabetic damage. The purpose of this study was to determine whether diabetes alters rod pathway signaling.
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37

Boije, Henrik. "Generation of Retinal Neurons : Focus on the Proliferation and Differentiation of the Horizontal Cells and their Subtypes." Doctoral thesis, Uppsala universitet, Medicinsk utvecklingsbiologi, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-150886.

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We have used the chicken retina as a model for investigating cell cycle regulation and cell fate commitment during central nervous system development. This thesis focuses on the characterization of and commitment to the horizontal cell fate in the retina. Horizontal cells are interneurons that provide intraretinal signal processing prior to information relay to the brain. We have identified molecular markers that selectively distinguish the three subtypes of horizontal cells, previously described in the chicken retina based on morphology. Subtype specific birth-dating revealed that horizontal cell subtypes are generated consecutively by biased progenitors that are sensitive to the inhibitory effects of follistatin. Follistatin stimulates proliferation in progenitors by repressing the differentiation signal of activin. Initially, injection of follistatin led to a decrease in committed horizontal cells but as the inhibitory effect dissipated it resulted in an increased number of horizontal cells. During development committed horizontal cell progenitors migrate to the vitreal side of the retina where they become arrested in G2-phase for approximately two days. When the arrest is overcome the horizontal cell progenitors undergo ectopic mitosis followed by migration to their designated layer. The G2-phase arrest is not triggered or maintained by any of the classic G2-arrest pathways such as DNA damage or stress. Nevertheless, we show that the cyclin B1-Cdk1 complex has a central role in maintaining this G2-phase arrest. Two transcription factors, FoxN4 and Ptf1a, are required for the generation of horizontal cells. We show that these factors are also sufficient to promote horizontal cell fate. Overexpression of FoxN4 and Ptf1a resulted in an overproduction of horizontal- and amacrine cells at the expense of ganglion- and photoreceptor cells. We identified Atoh7, a transcription factor required for the generation of ganglion cells, as a Ptf1a transcriptional target for downregulation. Our data support a common horizontal/amacrine lineage separated from the ganglion/photoreceptor lineage by the action of Ptf1a. In conclusion, these data describe several novel characteristics of horizontal cells enhancing our understanding of neural development and cell fate commitment.
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38

Joyal, Jean Sebastien. "Retinal neurons govern angiogenesis by regulating opposing actions of Semaphorin 3A and nuclear Protease-activated receptor 2." Thesis, McGill University, 2012. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=106266.

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Proliferative retinopathies (PRs), such as proliferative diabetic retinopathy and retinopathy of prematurity, are leading causes of blindness in children and working age adults. PRs are characterized by initial microvascular degeneration, followed by a compensatory albeit pathological hyper-vascularization mounted by the hypoxic retina attempting to reinstate metabolic equilibrium. Paradoxically, this secondary revascularization fails to grow into the most ischemic regions of the retina. Instead, the new vessels are misdirected towards the vitreous, suggesting that vaso-repulsive forces operate in the avascular hypoxic retina. Here we demonstrate that the neuronal guidance cue Semaphorin3A (Sema3A) secreted by severely hypoxic neurons participates in hindering revascularization of ischemic zones within the retina by deviating vessels away from these avascular areas. Using a rodent model of oxygen induced retinopathy, we provide evidence that Sema3A produced by ischemic retinal ganglion neurons contributes to microvascular decay and later forms a chemical barrier that impedes normal revascularization by repelling neo-vessel towards the vitreous. Conversely, silencing Sema3A expression enhances normal vascular regeneration within the ischemic retina, thereby preserving retinal neuronal function, and consequently diminishing aberrant neovascularization. Protease-activated receptor 2 (PAR2) partakes in retinal angiogenesis and was found to inhibit the production of Sema3A in ischemic retinal ganglion cells (RGCs). In light of the newly recognized contribution of RGCs in regulating retinal angiogenesis, we studied the expression and function of PAR2 in these neurons. Interestingly, we detected PAR2 at the cell nucleus of RGCs. To date, many G-protein coupled receptors (GPCRs), like PAR2, have been reported at the cell nucleus where they evoke in situ gene induction. However, the sub-cellular origin of nuclear GPCRs, the mechanisms governing this localization and their nuclear function, as well as the in vivo physiologic manifestation of nuclear GPCRs are not known. We show that PAR2 translocates from the plasma membrane to the nucleus, requiring specific receptor domains (C-terminus and nuclear localization signals) as well as the recruitment of Importin-β1 and Sorting nexin 11 (SNX11), which interact with microtubules. In turn, nuclear PAR2 recruits transcription factor Sp1 to trigger angiogenic genes and ensued neovascularization. This is the first demonstration of the in vivo physiologic manifestation governed by the nuclear localization of a GPCR. The sub-cellular localization and function of a receptor should therefore be considered in order to achieve more selective therapeutic goals. Approaches that foster normal retinal revascularization and in turn counter pathological neovascularization could prevent or delay the onset of blindness in patients afflicted with ischemic proliferative retinopathies.
Les rétinopathies prolifératives (RPs), telles que la rétinopathie diabétique ou du prématuré, sont les principales causes de cécité chez l'enfant et les adultes en âge de travailler. Les RPs sont caractérisées par une phase initiale de dégénérescence microvasculaire, suivie d'une surcompensation pathologique donnant lieu à une hyper-vascularisation initiée par la rétine hypoxique tentant de rétablir l'équilibre métabolique. Paradoxalement, cette revascularisation secondaire ne parvient pas à pénétrer les régions les plus ischémiques de la rétine. Au contraire, ces nouveaux vaisseaux croissent de façon inappropriée vers le corps vitré, ce qui suggère la présence de forces répulsives libérées dans la rétine avasculaire hypoxique. Cette thèse démontre que le signal de guidage neuronal Semaphorin3A (Sema3A) sécrété par les neurones hypoxiques participe à entraver la revascularisation des zones ischémiques de la rétine en repoussant les vaisseaux vers le corps vitré. En utilisant le modèle murin de rétinopahtie induite par l'oxygène, nous démontrons que Sema3A sécrété par les neurones ganglionnaires de la rétine ischémique contribue à la dégénérescence microvasculaire et forme une barrière chimique qui empêche la revascularisation normale de la rétine. À l'inverse, lorsque l'on inhibe l'expression de Sema3A, la revascularisation de la rétine ischémique est accélérée, préservant ainsi la fonction neuronale rétinienne et diminuant la néovascularisation pathologique.Le récepteur activé par les protéases 2 (PAR2) contribue au développement de nouveaux vaisseaux sanguins rétiniens et diminue l'expression de Sema3A. À la lumière de la contribution des cellules ganglionnaires de la rétine dans la régulation de l'angiogenèse rétinienne, nous avons par la suite étudié l'expression et la fonction de PAR2 dans ces neurones. Nous détectons la présence de PAR2 aux noyaux des neurones rétiniens. Plusieurs récepteurs couplés aux protéines G (GPCRs) ont été identifiés au noyau de la cellule, où ils induisent localement différents gènes. Toutefois, l'origine subcellulaire des GPCRs nucléaires, les mécanismes qui gouvernent cette localisation et leur fonction au noyau, de même que leur contribution physiologique demeurent inconnus. Notre travail démontre que PAR2 migre de la membrane plasmatique jusqu'au noyau par l'entremise des microtubules et nécessitant certains domaines spécifiques (région C-terminale et signaux de localisation nucléaire), de même que le recrutement d'importin-β1 et Sorting nexin 11 (SNX11). Ensuite, PAR2 nucléaire recrute le facteur de transcription Sp1 pour déclencher l'expression de gènes pro-angiogéniques et une néovascularization rétinienne. Il s'agit de la première description des manifestations physiologiques in vivo régis par la localisation nucléaire d'un GPCR. La distribution subcellulaire et son influence sur la fonction d'un récepteur doivent être pris en considération afin d'identifier des cibles thérapeutiques plus spécifiques. Des approches thérapeutiques favorisant la revascularization normale des régions ischémiques, et par le fait même freinant la néovascularization pathologique, pourrait prévenir ou retarder l'apparition de la cécité chez les patients souffrant d'une rétinopathie proliférative.
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39

HEIDINGER, VALERIE. "Excitotoxicite retinienne : reponses cellulaires et implication des interactions neurones-glies (doctorat : sciences)." Strasbourg 1, 1998. http://www.theses.fr/1998STR15040.

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40

Granado, Bertrand. "Architecture des systemes electroniques pour les reseaux de neurones. Conception d'une retine connexionniste." Paris 11, 1998. http://www.theses.fr/1998PA112296.

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Aujourd'hui les vitesses de traitements des micro-processeurs remettent en cause le developpement d'architectures de systemes electroniques dedies a une application specifique notamment pour la simulation des algorithmes neuronaux ou le traitement d'image en temps reel. Il est necessaire de pouvoir juger scientifiquement de la validite de tels systemes face aux micro-processeurs. Dans une premiere partie nous presentons une methodologie originale d'evaluation des architectures des systemes electroniques pour la simulation des reseaux de neurones qui permet d'analyser finement les concepts architecturaux mis en oeuvre et leur validite dans le domaine concerne. Nous validons et demontrons la pertinence de cette methodologie en l'appliquant a plusieurs modeles neuronaux (pmc et rbf) et en l'appliquant a plusieurs architectures specifiques (zisc), specialisees (cnaps) et generalistes (sparc et pentium). Mais une faible latence de simulation n'est pas la seule contrainte qui peut etre imposee a un systeme electronique : des contraintes spatiales, des contraintes de consommation et des contraintes de debit d'entrees-sorties interviennent lors de la realisation de systemes embarques. Pour les contraintes de surface et de consommation, il apparait que les micro-processeurs sont inadequats. Dans une deuxieme partie nous presentons maharadja, une architecture electronique originale satisfaisant aux contraintes des systemes embarques et a la simulation des reseaux de neurones en temps reel, qui constitue le coeur d'une retine connexionniste.
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41

Tegland, Alex Christopher. "DESIGNING A NOVEL VECTOR THAT EXPRESSES A MODIFIED mGFP IN CRE EXPRESSING NEURONS." University of Akron / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=akron1479117669266643.

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42

Siniša, Babović. "Značaj optičke koherentne tomografije makule kod glaukoma otvorenog ugla." Phd thesis, Univerzitet u Novom Sadu, Medicinski fakultet u Novom Sadu, 2016. http://www.cris.uns.ac.rs/record.jsf?recordId=100017&source=NDLTD&language=en.

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Cilj ovog istraživanja je bio da se utvrdi da li postoji razlika u debljini makule kod pacijenata sa glaukomom otvorenog ugla (POAG) u odnosu na zdravu populaciju i u zavisnosti od stepena progresije bolesti, kao i da se utvrdi da li postoji povezanost između promene debljine makule i stepena oštećenja vidnog polja i debljine peripapilarnog sloja nervnih vlakana u zavisnosti od stepena progresije bolesti. Materijal i metode: U ovu kliničku prospektivnu studiju je uključeno 186 pacijenata. Na osnovu kliničkog nalaza formirane su tri grupe. Prva grupa (kontrolna – grupa zdravih): 68 pacijenata bez očnih oboljenja, sa najboljom korigovanom vidnom oštrinom ≥ 0.9, intraokularnim pritiskom (IOP) ≤ 21 mmHg, normalnim odnosom ekskavacije i površine glave vidnog živca i normalnim nalazom vidnog polja. Druga grupa (rani glaukom): 78 pacijenata sa klinički dijagnostikovanim primarnim glaukomom otvorenog ugla (sa karakterističnim oštećenjem glave vidnog živca i sloja nervnih vlakana retine i kod kojih je srednja vrednost devijacije standardne automatske perimetrije MD > -6 dB, prema Hodap klasifikaciji), bez drugih očnih ili sistemskih oboljenja, koja bi imala uticaj na nastanak glaukoma i sa najboljom korigovanom vidnom oštrinom ≥ 0.5. Treća grupa (glaukom srednjeg stepena): 40 pacijenata sa klinički dijagnostikovanim primarnim glaukomom otvorenog ugla (sa karakterističnim oštećenjem glave vidnog živca i sloja nervnih vlakana retine i kod kojih je srednja vrednost devijacije standardne automatske perimetrije -6 dB > MD > -12 dB, prema Hodap klasifikaciji), bez drugih očnih ili sistemskih oboljenja, koja bi imala uticaj na nastanak glaukoma i sa najboljom korigovanom vidnom oštrinom ≥ 0.5. Svim pacijentima je bio urađen kompletan oftalmološki pregled, kompjuterizovano vidno polje (Humphrey Field Analyzer, Carl Zeiss Meditec, Jena, Germany, SITA Standard, test C 24-2) i optička koherentna tomografija sloja nervnih vlakana peripapilarno i u predelu makule (SOCT Copernicus HR, Optopol Tech. SA, Zawiercie, Poland). Rezultati: Perifovea i parafovea, pokazuju statistički značajno smanjenje debljine i zapremine sloja nervnih vlakana u odnosu na stepen progresije glaukoma otvorenog ugla, pri čemu je ono naglašenije u perifovei (p<0,05). U svim segmentima makule (TPeriF, IPeriF, SPeriF, NPeriF, TParaF, SParaF, IParaF i NParaF) dolazi do smanjenja debljine i zapremine sloja nervnih vlakana sa progresijom bolesti (p<0,05). Segmenti makule TPeriF, IPeriF, a potom i SPeriF, prema navedenom redosledu, predstavljaju segmente sa najvećim potencijalom za predikciju ranih glaukomskih oštećenja s obzirom na uočeno najveće smanjenje debljine i zapremine nervnih vlakana (p<0,05). Segmenti makule SParaF i NParaF predstavljaju segmente sa najvećim potencijalom za predikciju napredovanja glaukomskih oštećenja srednjeg stepena s obzirom na uočeno najveće smanjenje debljine i zapremine nervnih vlakana (p<0,05). Debljina RNFL glave vidnog živca se statistički značajno smanjuje sa progresijom bolesti u svim posmatranim segmentima (p<0,05). Međusobni odnos između grupe zdravih i grupe pacijenata sa ranim glaukomom ukazuje da je statistički značajno smanjenje debljine RNFL prisutno u svim segmentima osim u segmentima P3 i P4 (p>0,05). Merenja debljine RNFL u segmentu P6 imaju najbolji potencijal za predikciju ranog glaukoma s obzirom na najizraženije smanjenje debljine nervnih vlakana upravo u ovom segmentu (p<0,05). Merenja debljine RNFL u segmentu P1 ima najbolji potencijal za predikciju dalje progresije bolesti. Debljina sloja nervnih vlakana makule srazmerna je smanjenju debljine RNFL na glavi vidnog živca, pri čemu je ona uočljivija na nivou segmenata koji su okarakterisani kao dobri prediktori za nastanak, odnosno progresiju bolesti (P6 sa IPeriF i TPeriF, odnosno P1 sa SPeriF), što dodatno naglašava njihovu važnost u dijagnostici glaukoma otvorenog ugla. Debljina makule kod pacijenata sa glaukomom otvorenog ugla je opisana umerenom do dobrom povezanošću sa stepenom oštećenja vidnog polja, pri čemu je ona najjača kod TPeriF, IPeriF i SPeriF segmenata i srazmerna je stepenu oštećenja vidnog polja. Koeficijenti korelacije između vrednosti srednje devijacije vidnog polja i debljine RNFL, odnosno  sloja nervnih vlakana makule, pokazuju snažniju povezanost u odnosu na parametre dobijenog smanjenja debljine nervnih vlakana u makuli, što otvara mogućnost za dalja istraživanja. Segmenti glave vidnog živca i makule, koji su pokazali najbolju diskriminaciju u smislu predikcije nastanka POAGa, kao i oni koji sugerišu na njegovu progresiju, smešteni su na lokacijama koje su međusobno povezane opisanim prirodnim tokom nervnih vlakana.  Zaključak: Optička koherentna tomografija makule je važna pomoćna metoda u dijagnostici glaukoma kojom je moguće izdvojiti pacijente sa ranim glaukomom u odnosu na zdravu populaciju, odnosno utvrditi progresiju glaukoma otvorenog ugla.
All patients underwent complete ophthalmologic examination, SAP (Humphrey Field Analyzer, Carl Zeiss Meditec, Jena, Germany, SITA Standard, test C 24-2) and optical coherent tomography scans of RNFL and macula (SOCT Copernicus HR, Optopol Tech. SA, Zawiercie, Poland). Results: Perifoveal and parafoveal nerve fiber layer have shown significant reduction of thickness and volume compared to stage of POAG progression, where perifovea showed higher significance (p<0,05). All macular segments (TPeriF, IPeriF, SPeriF, NPeriF, TParaF, SParaF, IParaF i NParaF) showed reduction in thickness and volume compared to disease progression (p<0,05). Macular segments TPeriF, IPeriF, as well as SPeriF, represent segments with highest potential to predict early glaucomatous damage according to the most significant reduction of nerve fiber layer thickness and volume (p<0,05). Macular segments SParaF and NParaF represent segments with highest potential to predict progression of POAG according to the most significant reduction of nerve fiber layer thickness and volume (p<0,05). Optic nerve head (ONH) RNFL thickness showed reduction compared to POAG progression in all segments (p<0,05). All ONH segments except P3 and P4 showed significant reduction of RNFL comparing control group to early glaucoma group patients (p>0,05). ONH segment P6 was found to be the highly specific for early glaucoma prediction according to the most significant reduction of RNFL thickness (p<0,05), while segment P1 was found to have highest potential for POAG progression. Macular nerve fiber layer thickness reduction follows ONH RNFL thickness reduction and there is mutual relation between both macular and ONH segments (P6 to IPeriF and TPeriF, P1 to SPeriF) with highest specificity for early defects and POAG progression. It was shown that macular thickness changes have moderate to good correlation with visual filed changes and it was highest in TPeriF, IPeriF and SPeriF segments. This correlation was found to be higher in macula then in ONH RNFL thickness changes, compared to visual field changes. Both macular and ONH RNFL segments, which were found to have highest specificity to POAG prediction and progression, are located in areas which mutually connect following natural course of nerve fiber layer between them. Conclusion: Optical coherence tomography of macula represents important ancillary method in POAG diagnosis and follow up, allowing to differentiate between early glaucoma patients and healthy individuals, as well as to determine progression of glaucomatous disease.
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43

Close, Jennie L. "The role of the TGF beta superfamily and EGF in postnatal retinal proliferation and Müller Glial differentiation /." Thesis, Connect to this title online; UW restricted, 2005. http://hdl.handle.net/1773/10672.

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44

Lau, Yuk-fan Silvania, and 劉玉芬. "The neuroprotective effect of lycium barbarum polysaccharides on retinal neurons in a novel acute glaucoma attack animal model." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B47309325.

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Acute glaucoma is an ocular emergency and sight -threatening disease which is caused by a sudden increase in intraocular ocular pressure (IOP) due to blockage of aqueous humor outflow. Acute glaucoma can result in permanent loss of visual acuity and visual field (VF). Prophylactic or therapeutic medicine is rare for acute glaucoma. In animal studies, a well-established model to investigate this acute IOP spike is by fluid infusion and adjustment of the fluid level to induce high IOP within a few seconds. However, there is no blockage of aqueous outflow and the increase in intraocular pressure is unrealistically rapid. To mimic the IOP profile in human acute glaucoma attack, we propose the use of an ophthalmic viscosurgical device (OVD), Healon 5 (AMO, Santa Ana, CA, USA) which is injected intracamerally to block aqueous outflow. The IOP is allowed to increase naturally inside the globe. We found that Healon 5 can induce an acute elevation in IOP with very similar characteristics to those observed in humans. For example, the IOP profile during the attack, changes in the anterior segment and retinal nerve fibre layer (RNFL) thinning are all consistent with findings in human acute angle closure glaucoma (AACG). We believed that our new model can more accurately reflect acute glaucoma than other animal models. Based on these findings we further tested the neuroprotective effect of Lycium barbarum polysaccharides (LBP) on retinal neurons against an acute rise in IOP (attack) with the new model. L. barbarum is an herb that has been used in Chinese medicine for thousands of years. The fruit of this plant is believed to be good for the health of the eyes. In our study we found that oral administration of LBP preceding an acute glaucoma attack can preserve the visual function of the animals despite the loss of neurons in the retinal ganglion cell layer (RGCL). L. barbarum intake seems to inhibit secondary cell death and progression of the disease. In conclusion, we had successfully established a new acute glaucoma attack animal model by intracameral injection of Healon 5. This model more closely resembles the condition observed in human acute glaucoma. We also found that LBP has a prophylactic neuroprotective effect against an acute glaucoma attack in animals. It can protect the visual function and possibly inhibit secondary cell death. Oral consumption of LBP as a health supplement may provide extra benefit to people who are at high risk of developing acute glaucoma, in addition to the protective effects of LBP against other diseases.
published_or_final_version
Anatomy
Master
Master of Philosophy
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45

Eldred, Megan. "Investigating cellular and molecular mechanisms of neuronal layering in self-organising aggregates of zebrafish retinal cells." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/284080.

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The central nervous system is a complex, yet well-organised, often laminated, tissue. This robust organisation is evident in the architecture of the retina: consisting of 5 different neuronal types organised into distinct layers: Retinal Ganglion Cell (RGC), Amacrine Cell (AC), Bipolar Cell (BP), Horizontal Cell (HC) and Photoreceptor cell (PR) layers. This remarkable organisation is evolutionarily conserved in vertebrates, yet little is known about the mechanisms by which these cells form the correct layers. Live imaging has revealed overlapping periods of birth and extensive inter-digitation followed by cells sorting out into their appropriate positions, suggesting cell-cell interactions are important. To investigate possible cellular and molecular mechanisms responsible for the establishment of the tissue architecture I developed an organoid culture system for zebrafish retinal cells. To identify the cells in culture I used a Spectrum of Fates fish line which is a multiply transgenic line in which each retinal cell type can be identified based on expression of a combination of fluorescently tagged cell fate markers. The development of the protocol by which I cultured the cells and observed their cell-cell interactions involved establishing the best methods to dissociate and culture zebrafish retinal cells in a non-adhesive environment, then imaging the resulting reaggregates to examine the position of the different retinal cell types. By doing this I observed their inherent self-organising properties, in the absence of extrinsic cues or scaffolds. These cells appeared to be arranged in an inside-out layering, although all cell types are layered in the same relative order as they are in vivo. To analyse the organization in these aggregates I developed a Matlab script in collaboration with Leila Muresan which analyses the relative positioning of cells in concentric rings from the periphery to the centre of the aggregates according to the cell fate-tagged fluorescent markers. The script then fits this data as an empirical cumulative distribution function for different groups of cells to determine how spatially distinct populations of cells are. This gave me my measure of organisation. I then investigated the cell-cell interactions involved in this self-organisation by genetically or pharmacologically removing individual cell types and assaying the resulting organisation of the reaggregated, cell-type deficient, retinal organoids. I revealed that Müller Glia are important for retinal cell self-organisation. I also investigated the role of Retinal Pigment Epithelial (RPE) cells and Retinal Ganglion Cells and found they had no impact on the ability of the remaining cell types to organize. I began to investigate the role of Amacrine Cells but found that retinas void of ACs were susceptible to disaggregating in our dissection setup, preventing me from collecting the material needed for culture. I also investigated the role of candidate molecules in this system and revealed that R-Cognin is critical for retinal cells to reaggregate. Not only can I remove cells or molecules from the system, but I show how it can also be manipulated to replace molecules of interest such as laminin, by coating beads with the substance of choice and placing it amongst the cells to see if their organisational behaviour is affected. In summary, I have developed a system which provides a simple and easy platform to manipulate in various ways to help us potentially reveal some of the important players in neuronal patterning.
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46

Hasegawa, Tomoko. "Branched chain amino acids attenuate major pathologies in mouse models of retinal degeneration and glaucoma." Kyoto University, 2019. http://hdl.handle.net/2433/242384.

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47

SIMON, AXELLE. "Etude des neurones catecholaminergiques de la retine de rat et de primates par l'immunohistochimie." Paris 7, 1992. http://www.theses.fr/1992PA077186.

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Dans la retine, les neurones dopaminergiques sont des neurones modulateurs, appartenant aux classes des cellules amacrines et interplexiformes. Ils sont mis en evidence par l'immunohistochimie grace a un anticorps anti-tyrosine hydroxylase (th). Nous avons demontre, par une technique de double marquage, que les petites cellules th-immunoreactives, non dopaminergiques, ne sont pas pnmt-i, et ne synthetisent donc pas l'adrenaline. Nous avons montre, par cette meme technique, que les cellules dopaminergiques contiennent aussi du gaba. L'etude des prolongements externes des cellules interplexiformes dopaminergiques, aux microscopes optique et electronique, chez le rat, le macaque et l'homme, dans la retine peripherique et la fovea, montre que ces prolongements atteignent la couche nucleaire externe ou se trouvent les corps cellulaires des photorecepteurs; des prolongements dopaminergiques longent et entourent les capillaires retiniens, et presentent des contacts avec la lame basale, face aux pericytes, suggerant un role sur leur vasomotricite. Des recepteurs dopaminergiques ont ete localises a l'aide d'un anticorps anti-idiotypique anti anti-dopamine sur les segments externes des photorecepteurs et les parois vasculaires, ce qui confirme que ces structures sont les cibles de la dopamine
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48

Wong, Sharon Tsau-Yuen. "Effects of induced myopia and hyperopia on dopaminergic and serotonergic amacrine neurons in chick retina." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/NQ32867.pdf.

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49

Ocampo, Daza Daniel. "Evolution of Vertebrate Endocrine and Neuronal Gene Families : Focus on Pituitary and Retina." Doctoral thesis, Uppsala universitet, Farmakologi, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-191829.

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The duplication of genes followed by selection is perhaps the most prominent way in which molecular biological systems gain multiplicity, diversity and functional complexity in evolution. Whole genome duplications (WGDs) therefore have the potential of generating an extraordinary amount of evolutionary innovation. It is now accepted that the vertebrate lineage has gone through two rounds of WGD in its early stages, after the divergence of invertebrate chordates and before the emergence of jawed vertebrates. These basal vertebrate WGDs are called 2R for two rounds of whole genome duplication. An additional WGD called 3R occurred early in the evolution of teleost fishes, before the radiation of this species-rich group. This thesis describes the evolution of several endocrine and neuronal gene families in relation to the vertebrate WGDs, through a comparative genomic approach including both phylogenetic analyses and chromosomal location data across a wide range of vertebrate taxa. These results show that numerous endocrine gene families have expanded in 2R and in several cases also in 3R. These include the gene families of oxytocin and vasopressin receptors (OT/VP-R), somatostatin receptors (SSTR) and insulin-like growth factor binding proteins (IGFBP). For the OT/VP-R and SSTR families, previously undescribed subtypes were identified. The protein hormone family that includes growth hormone (GH), prolactin (PRL) and somatolactin (SL) acquired a new PRL gene in 2R, however the origins of GH, PRL and SL likely predate 2R. The corresponding family of receptors diversified during different time periods through a combination of local duplications and 3R. Neuronal gene families of the visual system have also expanded in 2R and 3R. The results presented here demonstrate that the vertebrate repertoire of visual opsin genes arose in 2R as part of chromosomal blocks that also include the OT/VP-R genes. The gene families including the transducin alpha, beta and gamma subunits also arose in 2R, hinting at the importance of these events in the diversification and specialization of phototransduction cascades for rods and cones. Thus, the whole genome duplications have been important contributors to the evolution of both vision and endocrine regulation in the vertebrates.
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50

Nasser, Hassan. "Analyse des trains de spike à large échelle avec contraintes spatio-temporelles : application aux acquisitions multi-électrodes rétiniennes." Phd thesis, Université Nice Sophia Antipolis, 2014. http://tel.archives-ouvertes.fr/tel-00990744.

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Abstract:
L'évolution des techniques d'acquisition de l'activité neuronale permet désormais d'enregistrer simultanément jusqu'à plusieurs centaines de neurones dans le cortex ou dans la rétine. L'analyse de ces données nécessite des méthodes mathématiques et numériques pour décrire les corrélations spatiotemporelles de la population neuronale. Une méthode couramment employée est basée sur le principe d'entropie maximale. Dans ce cas, le produit N×R, où N est le nombre de neurones et R le temps maximal considéré dans les corrélations, est un paramètre crucial. Les méthodes de physique statistique usuelles sont limitées aux corrélations spatiales avec R = 1 (Ising) alors que les méthodes basées sur des matrices de transfert, permettant l'analyse des corrélations spatio-temporelles (R > 1), sont limitées à N×R≤20. Dans une première partie, nous proposons une version modifiée de la méthode de matrice de transfert, basée sur un algorithme de Monte-Carlo parallèle, qui nous permet d'aller jusqu'à N×R=100. Dans la deuxième partie, nous présentons la bibliothèque C++ Enas, dotée d'une interface graphique développée pour les neurobiologistes. Enas offre un environnement hautement interactif permettant aux utilisateurs de gérer les données, effectuer des analyses empiriques, interpoler des modèles statistiques et visualiser les résultats. Enfin, dans une troisième partie, nous testons notre méthode sur des données synthétiques et réelles (rétine, fournies par nos partenaires biologistes). Notre analyse non exhaustive montre l'avantage de considérer des corrélations spatio-temporelles pour l'analyse des données rétiniennes; mais elle montre aussi les limites des méthodes d'entropie maximale.
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