Dissertationen zum Thema „Transport neuronal“
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MacAskill, A. F. N. „Control of neuronal mitochondrial transport“. Thesis, University College London (University of London), 2010. http://discovery.ucl.ac.uk/19495/.
Der volle Inhalt der QuelleMahato, Deependra. „Mutation of Polaris, an Intraflagellar Transport Protein, Shortens Neuronal Cilia“. Thesis, University of North Texas, 2005. https://digital.library.unt.edu/ark:/67531/metadc4856/.
Der volle Inhalt der QuelleChen, Liang. „Single molecule and single particle studies of neuronal axonal transport /“. May be available electronically:, 2009. http://proquest.umi.com/login?COPT=REJTPTU1MTUmSU5UPTAmVkVSPTI=&clientId=12498.
Der volle Inhalt der QuelleJohnson, Christopher M. „Investigating the Slow Axonal Transport of Neurofilaments: A Precursor for Optimal Neuronal Signaling“. Ohio University / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1452018547.
Der volle Inhalt der QuellePekergin, Mehmet Ferhan. „Optimisation combinatoire par le calcul neuronal et parallelisme optimal“. Paris 5, 1992. http://www.theses.fr/1992PA05S017.
Der volle Inhalt der QuelleCoats, Charles Jason. „Development of primary neuronal culture of embryonic rabbit dorsal root ganglia for microfluidic chamber analysis of axon mediated neuronal spread of Bovine Herpesvirus type 1“. Thesis, Manhattan, Kan. : Kansas State University, 2010. http://hdl.handle.net/2097/4115.
Der volle Inhalt der QuelleLi, Yunyun [Verfasser], und Peter [Akademischer Betreuer] Hänggi. „Noise assisted transport in artificial channels and neuronal membranes / Yunyun Li. Betreuer: Peter Hänggi“. Augsburg : Universität Augsburg, 2011. http://d-nb.info/1077700296/34.
Der volle Inhalt der QuelleCopp, Steven Wesley. „Enzymatic regulation of skeletal muscle oxygen transport: novel roles for neuronal nitric oxide synthase“. Diss., Kansas State University, 2013. http://hdl.handle.net/2097/15512.
Der volle Inhalt der QuelleDepartment of Anatomy and Physiology
Timothy I. Musch
Nitric oxide (NO) is synthesized via distinct NO synthase (NOS) enzymes and constitutes an essential cardiovascular signaling molecule. Whereas important vasomotor contributions of endothelial NOS (eNOS) have been well-described, the specific vasomotor contributions of nNOS-derived NO in healthy subjects during exercise are unknown. The purpose of this dissertation is to test the global hypothesis that nNOS-derived NO is a critical regulator of exercising skeletal muscle vascular control. Specifically, we utilized the selective nNOS inhibitor S-methyl-L-thiocitrulline (SMTC) to investigate the effects of nNOS-derived NO on skeletal muscle vascular function within established rodent models of exercise performance. The first investigation (Chapter 2) identifies that nNOS inhibition with SMTC increases mean arterial pressure (MAP) and reduces rat hindlimb skeletal muscle blood flow at rest whereas there are no effects during low-speed (20 m/min) treadmill running. In Chapter 3 it is reported that nNOS inhibition with SMTC reduces blood flow during high-speed treadmill running (>50 m/min) with the greatest relative effects found in highly glycolytic fast-twitch muscles and muscle parts. Chapter 4 demonstrates that nNOS-derived NO modulates contracting skeletal muscle blood flow (increases), O2 consumption (VO2, increases), and force production (decreases) in the rat spinotrapezius muscle and thus impacts the microvascular O2 delivery-VO2 ratio (which sets the microvascular partial pressure of O2, PO2mv, and represents the pressure head that drives capillary-myocyte O2 diffusion). In Chapter 5 we report that systemic administration of the selective nNOS inhibitor SMTC does not impact lumbar sympathetic nerve discharge. This reveals that the SMTC-induced peripheral vascular effects described herein reflect peripheral nNOS-derived NO signaling as opposed to centrally-derived regulation. In conclusion, nNOS-derived NO exerts exercise-intensity and muscle fiber-type selective peripheral vascular effects during whole-body locomotor exercise. In addition, nNOS-derived NO modulates skeletal muscle contractile and metabolic function and, therefore, impacts the skeletal muscle PO2mv. These data identify novel integrated roles for nNOS-derived NO within healthy skeletal muscle and have important implications for populations associated with reduced NO bioavailability and/or impaired nNOS structure and/or function specifically (e.g., muscular dystrophy, chronic heart failure, advanced age, etc.).
Naudon, Laurent. „Recherche d'une participation du transporteur neuronal de la dopamine et du transporteur vésiculaire à l'adaptation neuronale“. Rouen, 1994. http://www.theses.fr/1994ROUES066.
Der volle Inhalt der QuelleDaoust, Alexia. „IRM du manganèse (MEMRI) : couplage à l'imagerie chimique par microsonde synchrotron pour optimiser l'imagerie fonctionnelle du transport neuronal“. Phd thesis, Université de Grenoble, 2012. http://tel.archives-ouvertes.fr/tel-00770158.
Der volle Inhalt der QuelleTomac, Andreas C. „Glial cell line-derived neurotrophic factor : expression patterns, neuronal transport, regulation, effects and receptor dependence /“. Stockholm, 1998. http://diss.kib.ki.se/search/diss.se.cfm?19980618toma.
Der volle Inhalt der QuelleHeber, Simone [Verfasser]. „Molecular aspects of RNA-recognition by the neuronal mRNA transport factor Staufen 2 / Simone Heber“. Ulm : Universität Ulm, 2018. http://d-nb.info/116675653X/34.
Der volle Inhalt der QuelleLalli, Giovanna. „The binding fragment of tetanus neurotoxin : a probe to study neuronal endocytosis and retrograde transport“. Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.272379.
Der volle Inhalt der QuelleMoutaux, Eve. „Régulation du transport axonal par l'activité neuronale : Implication pour le développement des réseaux neuronaux Neuronal activity recruits an axon-resident pool of secretory vesicles to regulate axon branching Reconstituting Corticostriatal Network on-a-Chip Reveals the Contribution of the Presynaptic Compartment to Huntington’s Disease Neuronal network maturation differently affects secretory vesicles and mitochondria transport in axons ALG-2 interacting protein-X (Alix) is required for activity-dependent bulk endocytosis at brain synapses An integrated microfluidic/microelectrode array for the study of activity-dependent intracellular dynamics in neuronal networks“. Thesis, Université Grenoble Alpes, 2020. https://thares.univ-grenoble-alpes.fr/2020GRALV024.pdf.
Der volle Inhalt der QuelleDuring postnatal development, long-distance axonal projections form branches to connect with their targets. Establishment and remodeling of these projections are tightly regulated by neuronal activity and require a large amount of secretory material and trophic factors, such as brain derived neurotrophic factor (BDNF). Axonal transport is responsible for addressing trophic factors packed into vesicles to high demand sites where mechanisms of secretion are well-known. However, mechanisms controlling the preferential targeting of axonal vesicles to active sites in response to neuronal activity are unknown.In this work, we first developed tools to study intracellular dynamics in neuronal networks. We thus developed a microfluidic chamber to reconstruct physiologically-relevant networks in vitro which is compatible with high resolution videomicroscopy. We characterized the formation and maturation of reconstructed networks and we validated the relevance of the microfluidic platform in the context of Huntington’s disease. We then studied the evolution of intracellular dynamics with the maturation of reconstructed neuronal networks in microfluidic chambers. We observed an increase of anterograde axonal transport of secretory vesicles during maturation. These first results lead us to think that neuronal activity could regulate axonal transport of secretory vesicles over maturation of the network.Therefore, we improved the in vitro microfluidic system with a designed microelectrode array (MEA) substrate allowing us to record intracellular dynamics while controlling neuronal activity. Using this system, we identified an axon-resident reserve pool of secretory vesicles recruited upon neuronal activity to rapidly distribute secretory materials to presynaptic sites. We identified the activity-dependent mechanism of recruitment of this axonal pool of vesicles along the axon shaft. We showed that Myosin Va ensures the tethering of vesicles in the axon shaft in axonal actin structures. Specifically, neuronal activity induces a calcium increase after activation of Voltage Gated Calcium Channels along the axon, which regulates Myosin Va and triggers the recruitment of tethered vesicles on microtubules. We then showed the involvement of this activity-dependent pool for axon branches formation during axon development. By developing 2-photon live microscopy of axonal transport in acute slices, we finally confirmed that a pool of axon-resident static vesicles is recruited by neuronal activity in vivo with a similar kinetic.Altogether, this work provides new in vitro and in vivo tools to study intracellular dynamics in physiological networks. Using these tools, we identified the existence of a local mechanism of axonal transport regulation along the axon shaft, allowing rapid supply of trophic factors to developing branches
Vijayakumar, Jeshlee Cyril. „Rôle du domaine de type prion de Imp dans la régulation des granules RNP neuronaux“. Thesis, Université Côte d'Azur (ComUE), 2018. http://www.theses.fr/2018AZUR4099/document.
Der volle Inhalt der QuelleEukaryotic mRNAs are bound by RNA Binding Proteins (RBP) and packaged into diverse range of macromolecular assemblies named RNP granules. In neurons, transport RNP granules are implicated in the transport of specific mRNAs to axons or dendrites, and in their local translation in response to external cues. Although little is known about the assembly and regulation of these granules in vivo, growing evidence indicates that the presence of Prion Like domains (PLD) within RBPs favours multivalent protein–protein and protein-RNA interactions, promoting the transition of soluble complexes into RNP granules. The conserved RBP Imp is as a core component of RNP granules that are actively transported to axons upon neuronal remodelling in Drosophila. Furthermore, Imp function was shown to be required for axonal remodelling during Drosophila nervous system maturation. Analyses of the domain architecture of the Imp protein revealed that, in addition to four RNA binding domains (RBD), Imp contains a Cterminal domain showing a striking enrichment in Glutamines and Serines, which is one of the characteristics of a PLD. During my PhD, I explored the function of the PLD in the context of granule assembly and transport. In cultured cells, I observed that Imp granules assembled in the absence of the PLD, however their number and size were increased. Proteins with scrambled PLD sequence accumulated in granules of normal size and number, implying that the degree of disorder of this domain, and not its sequence, is essential for granule homeostasis. Moreover, FRAP experiments, performed on cultured cells and in vivo, revealed that Imp PLD is important to maintain the turnover of these granules. In vivo, this domain is both necessary and sufficient for efficient transport of Imp granules to axons. These defects are associated with a reduction on the number of motile granules in axons. Furthermore, mutant forms lacking the PLD do not rescue the axon remodelling defects observed upon imp loss of function. Finally, a swapping experiment in which I moved Imp PLD from the C-terminus to the N-terminus of the protein revealed that the functions of Imp PLD in granule transport and homeostasis are uncoupled, and that PLD-dependent modulation of Imp granule properties is dispensable in vivo. Together, my results show that Imp PLD of is not required for the assembly of RNP granules, but rather regulates granule number and dynamics. Furthermore, my work uncovered an unexpected in vivo function for a PLD in axonal transport and remodelling during nervous system maturation
Precht, Thomas A. „Regulation of neuronal apoptosis by the mitochondria /“. Connect to full text via ProQuest. Limited to UCD Anschutz Medical Campus, 2008.
Den vollen Inhalt der Quelle findenTypescript. Includes bibliographical references (leaves 112-125). Free to UCD Anschutz Medical Campus. Online version available via ProQuest Digital Dissertations;
Asselin, Laure. „Etude du rôle de la kinésine KIF21B au cours du développement cortical“. Thesis, Strasbourg, 2019. http://www.theses.fr/2019STRAJ032/document.
Der volle Inhalt der QuelleThe development of the cerebral cortex is a highly regulated process that is crucial for the establishment of functional cortical networks. Disruption of one or several of these steps can lead severe neurodevelopmental disorders that are associated with intellectual disabilities, epilepsies and cognitive impairment. Over the past few years, several genetic mutations in genes encoding either tubulin or microtubule-associated motors such as kinesins, have been found in individuals with neurodevelopmental disorders. Although kinesins have been found to be essential for a proper cortical development, the exact functions of kinesins in these processes are still poorly understood. My work clearly identified Kif21b, a poorly-known kinesin, as a novel key regulator of cortical development both in mouse and human. We show that Kif21b regulates both radial and tangential migration of cortical neurons, and identify four KIF21B variants in individuals presenting neurodevelopmental disorders. We show that ectopic expression of variants recapitulate phenotypes both in mice and zebrafish
Workinger, Paul M., und Paul M. Workinger. „Familial Amyotrophic Lateral Sclerosis with a focus on C9orf72 Hexanucleotide GGGGCC Repeat Expansion Associated ALS with Frontotemporal Dementia“. Thesis, The University of Arizona, 2017. http://hdl.handle.net/10150/625350.
Der volle Inhalt der QuellePARISI, BARBARA. „Role of the novel neuronal protein APache in autophagy“. Doctoral thesis, Università degli studi di Genova, 2022. http://hdl.handle.net/11567/1090471.
Der volle Inhalt der QuelleBideaux, Eric. „Stan : systeme de transport a apprentissage neuronal. application de la vision omnidirectionnelle a la localisation d'un robot mobile autonome“. Besançon, 1995. http://www.theses.fr/1995BESA2008.
Der volle Inhalt der QuelleBrumback, Audrey Christine. „Thermodynamic regulation of NKCC1-mediated chloride transport underlies plasticity of GABAA signaling /“. Connect to full text via ProQuest. Limited to UCD Anschutz Medical Campus, 2006.
Den vollen Inhalt der Quelle findenTypescript. Includes bibliographical references (leaves 86-96). Free to UCDHSC affiliates. Online version available via ProQuest Digital Dissertations;
Ganesan, Sundar. „Local protein turnover as a regulatory mechanism of growth and collapse of neuronal growth cones“. Doctoral thesis, [S.l.] : [s.n.], 2005. http://deposit.ddb.de/cgi-bin/dokserv?idn=976327376.
Der volle Inhalt der QuelleChane, Kuang Sang Laurent. „Stratégie de contrôle hybride d'un magnétron verrouillé par injection pour un Transport d'Energie Sans Fil par onde hyperfréquence“. Phd thesis, Université de la Réunion, 2002. http://tel.archives-ouvertes.fr/tel-00464105.
Der volle Inhalt der QuelleDo, Rego Marie Jean-Claude. „Etude du site et du mode de liaison des inhibiteurs du transporteur neuronal de la dopamine ; caractérisation et utilisation d'un inhibiteur irréversible afin de mesurer la vitesse de renouvellement du transporteur“. Rouen, 2000. http://www.theses.fr/2000ROUES017.
Der volle Inhalt der QuelleVaillant-Beuchot, Loan. „Étude des mécanismes liés aux dysfonctions mitochondriales, à l'altération de la mitophagie et aux défauts du transport mitochondrial dans la maladie d'Alzheimer“. Electronic Thesis or Diss., Université Côte d'Azur, 2022. http://www.theses.fr/2022COAZ6019.
Der volle Inhalt der QuelleMitochondria are essential organelles in cells, ensuring energy production with ATP synthesis, calcium buffering, apoptosis regulation. These functions are altered at early stages of Alzheimer's disease (AD) and are essentially induced by the Amyloid (Aβ), produced after the sequential cleavage of amyloid precursor protein (APP) by β- and γ-secretase. Aβ is a major actor of AD development but all the treatments targeting this peptide remain ineffective. C-terminal APP fragments (APP-CTFs: C83 and C99 (Aβ precursor) are other fragments presenting specific toxicity in AD and new potential therapeutic targets. My project is focus on the study of APP-CTFs toxicity, independently of Aβ, on the structure, function of mitochondria, their degradation by mitophagy and on mitochondrial transport proteins. They constitute the complex allowing mitochondrial transport in cells, especially in neurons, closely linked to mitochondrial renewal, particularly in neurons.First axe: APP-CTFs impact on mitochondrial structure, function and mitophagy. We described APP-CTFs accumulation in mitochondrial fraction in vitro (human neuroblastoma cells expressing APP Swedish double mutation (SH-SY5Y-APPswe) or C99 fragment (SH-SY5Y-C99)) and in vivo (3xTgAD mice expressing APPswe, TauP301L, PS1 (M146V) or C99 fragment after viral injection). We inhibit the cleavage of APP-CTFs and the production of Aβ by pharmacological approaches, to abolish γ-secretase activity. Ours results show for the first time in vitro and in vivo, that high concentration of APP-CTFs independently of Aβ, impact mitochondrial structure, function and alter mitophagy process, resulting in an accumulation of altered mitochondria producing high levels of toxic reactive oxygen species. In addition, our results in patient brains of sporadic AD (SAD) patients show altered mitophagic protein levels correlating with APP-CTFs accumulation (1-2).Second axe: study of the effects of APP, APP-CTFs and Aβ peptide on mitochondrial transport machinery. I reported the specific regulation of mitochondrial transport protein by endogenous APP (Mice fibroblasts APP WT and KO) and the overexpression of APPswe (and in SH-SY-5Y-APPswe cells). APP-CTFs and Aβ differentially regulate mitochondrial transport protein levels in treated SH-SY-5Y-APPswe cells with γ-secretase inhibitor. These results were validated in mice fibroblasts KO for presenilins (catalytic compounds of γ-secretase) avoiding APP-CTFs degradation. APP-CTFs and Aβ impair the recruitment of mitochondria to its transport machinery in differentiated SHSY-5Y. The progression of the disease deregulates the levels of mitochondrial transport protein in vivo (3xTgAD and WT mice brains, C99 injected mice brains) and in SAD patients brains. The analyses of young and old mice brains and of SAD patients samples at different stages of the disease, allowed us to demonstrate an impact of aging in the regulation of mitochondrial transport protein levels. This phenomenon occurs also in addition with AD progression (3).These studies highlight new molecular mechanisms impacting mitochondrial homeostasis during AD progression. Our findings will bring new therapeutic research to slow down mitochondrial dysfunctions and/or to stimulate their renewal in AD context.(1). Vaillant-Beuchot L.*, Mary A.* et al. Acta Neuropathologica 2020.(2). Mary A.*, Vaillant-Beuchot L.* et al. Médecine/sciences 2021.(3). Vaillant-Beuchot et al. En cours de soumission
Gabriel, Luke R. „Dynamic Regulation at the Neuronal Plasma Membrane: Novel Endocytic Mechanisms Control Anesthetic-Activated Potassium Channels and Amphetamine-Sensitive Dopamine Transporters: A Dissertation“. eScholarship@UMMS, 2013. http://escholarship.umassmed.edu/gsbs_diss/725.
Der volle Inhalt der QuelleVijayakumar, Jeshlee Cyril. „Rôle du domaine de type prion de Imp dans la régulation des granules RNP neuronaux“. Electronic Thesis or Diss., Université Côte d'Azur (ComUE), 2018. http://www.theses.fr/2018AZUR4099.
Der volle Inhalt der QuelleEukaryotic mRNAs are bound by RNA Binding Proteins (RBP) and packaged into diverse range of macromolecular assemblies named RNP granules. In neurons, transport RNP granules are implicated in the transport of specific mRNAs to axons or dendrites, and in their local translation in response to external cues. Although little is known about the assembly and regulation of these granules in vivo, growing evidence indicates that the presence of Prion Like domains (PLD) within RBPs favours multivalent protein–protein and protein-RNA interactions, promoting the transition of soluble complexes into RNP granules. The conserved RBP Imp is as a core component of RNP granules that are actively transported to axons upon neuronal remodelling in Drosophila. Furthermore, Imp function was shown to be required for axonal remodelling during Drosophila nervous system maturation. Analyses of the domain architecture of the Imp protein revealed that, in addition to four RNA binding domains (RBD), Imp contains a Cterminal domain showing a striking enrichment in Glutamines and Serines, which is one of the characteristics of a PLD. During my PhD, I explored the function of the PLD in the context of granule assembly and transport. In cultured cells, I observed that Imp granules assembled in the absence of the PLD, however their number and size were increased. Proteins with scrambled PLD sequence accumulated in granules of normal size and number, implying that the degree of disorder of this domain, and not its sequence, is essential for granule homeostasis. Moreover, FRAP experiments, performed on cultured cells and in vivo, revealed that Imp PLD is important to maintain the turnover of these granules. In vivo, this domain is both necessary and sufficient for efficient transport of Imp granules to axons. These defects are associated with a reduction on the number of motile granules in axons. Furthermore, mutant forms lacking the PLD do not rescue the axon remodelling defects observed upon imp loss of function. Finally, a swapping experiment in which I moved Imp PLD from the C-terminus to the N-terminus of the protein revealed that the functions of Imp PLD in granule transport and homeostasis are uncoupled, and that PLD-dependent modulation of Imp granule properties is dispensable in vivo. Together, my results show that Imp PLD of is not required for the assembly of RNP granules, but rather regulates granule number and dynamics. Furthermore, my work uncovered an unexpected in vivo function for a PLD in axonal transport and remodelling during nervous system maturation
Lee, Han Kyu Verfasser], und Matthias [Akademischer Betreuer] [Kneussel. „Analysis of the adaptor proteins, gephyrin and GRIP1, in KIF5-driven neuronal transport in Mus musculus, (Linnaeus, 1758) / Han Kyu Lee. Betreuer: Matthias Kneussel“. Hamburg : Staats- und Universitätsbibliothek Hamburg, 2011. http://d-nb.info/1020458259/34.
Der volle Inhalt der QuelleCORICH, LUCIA. „USE OF A TETRALCYCLINE-INDUCIBLE SILENCING SYSTEM TO INVESTIGATE THE ROLE OF MRP1 AND MDR1 IN THE TRANSPORT OF ORGANIC ANIONS IN NEURONAL CELLS“. Doctoral thesis, Università degli studi di Trieste, 2007. http://thesis2.sba.units.it/store/handle/item/12294.
Der volle Inhalt der QuelleVitet, Hélène. „Conséquences de la régulation du transport axonal par la huntingtine sur l'homéostasie de réseaux neuronaux et sur le comportement, en conditions saine et pathologique Traffic signaling: new functions of huntingtin and axonal transport in neurological disease Presynaptic APP levels and synaptic homeostasis are regulated by Akt phosphorylation of Huntingtin“. Thesis, Université Grenoble Alpes, 2020. http://www.theses.fr/2020GRALV038.
Der volle Inhalt der QuelleNeuronal circuits are at the basis of behaviors such as motor coordination or learning and memory. As being part of a network, neurons communicate at synapses through finely tuned molecular and cellular processes. One key mechanism regulating synapse homeostasis involves transport of vesicles within axons and dendrites which is dysregulated in many neurological disorders such as Rett syndrome, Alzheimer’s (AD) and Huntington’s diseases (HD). Thus, deciphering the regulation of vesicular transport within neurites in physiological context is crucial to understand, and potentially restore, the consequences of these dysregulations in pathological contexts.Huntingtin (HTT) protein, known for its devastating role in HD when mutated, is a key actor of axonal transport. It promotes and regulates vesicular transport in neurites by scaffolding adaptors and molecular motors. Particularly, HTT phosphorylation status on S421 regulates the directionality of BDNF, APP and VAMP-7 vesicles within neurites in cultured and transfected neurons. However, several questions remain to be elucidated regarding the mechanisms and the consequences of this HTT-dependent regulation of axonal transport such as the neuritic specificity (axons or dendrites) and the behavioral consequences of such modifications. Finally, we do not know whether transport regulation can be influenced in pathological conditions to restore disease-associated phenotypes in vivo.This thesis aims at characterizing in vivo the mechanisms and the consequences of axonal transport regulation of three different vesicles through the phosphorylation of Huntingtin at S421 and to investigate its propensity to restore disease-associated phenotypes in mouse models of human neurological disorders.In order to reproduce in vitro the in vivo networks associated to neurological disorders we used microfluidic devices. We investigated the transport of Amyloid Precursor Protein (APP) vesicles, precursors of synaptic vesicles (SVPs) or dense-core vesicles (DCVs) in neurons in which the HTT phosphorylation status was modified. These neurons came from mice in which Serine 421 has been replaced by an aspartic acid to mimic the phosphorylated form of HTT (HTTS421D) or by an alanine to mimic the unphosphorylatable form of HTT (HTTS421A).Transport of APP vesicles is impaired in AD. We investigated APP transport and accumulation at synapses within a corticocortical circuit. We found that Akt-mediated HTT phosphorylation at S421 regulates the directionality of APP containing vesicles in axons but not in dendrites: the phospho-defective form of HTT decreases axonal anterograde flux of APP and reduces its levels at presynaptic zones both in vitro and in vivo. Reducing anterograde flux of APP in familial AD mouse model restored synapse homeostasis in vivo and memory deficits (Publication 21; Bruyere*, Abada*, Vitet* et al., eLife, 2020).SVP axonal transport regulates the number of SVs at the synapse, which, within a corticostriatal synapse, is essential for motor skill learning. We found that HTT phosphorylation increases the recruitment of the molecular motor KIF1A on SVPs, thus promoting anterograde transport and the probability of release. Silencing KIF1A in the corticostriatal network of HTTS421D mice, we found that pHTTS421 increases the number of SVs at the synapse and impairs procedural memory through a specific HTT-KIF1A dependent mechanism. This study defines a pathway by which axonal transport of SVP impact the behavioral phenotype. (Publication 2; Vitet et al, in prep)Finally, it has been shown that BDNF transport within DCVs is dysregulated in the corticostriatal network of Rett syndrome’s patients. We found that endogenous HTT phosphorylation at S421 or a chemical inhibitor of calcineurin (FK506) rescue BDNF transport in the corticostriatal network, neuronal communication, and behaviors of Rett Syndrome mice (Publication 3; Ehinger et al., Embo Mol Med,2020)
Corera, Amadou Tidjane. „Effets des ions sur la capture de [3H]dopamine et sur la liaison des substrats et des inhibiteurs au transporteur neuronal de la dopamine marqué avec le [3H]WIN 35428 ou le [3H]Mazindol“. Rouen, 2000. http://www.theses.fr/2000ROUES008.
Der volle Inhalt der QuelleAmejdki-Chab, Nassira. „Effets des ions sur le transport neuronal de la dopamine et sur la liaison des inhibiteurs et des substrats au transporteur, étudiée à l'aide d'un marqueur spécifique, le [3H] GBR 12783“. Rouen, 1991. http://www.theses.fr/1991ROUES042.
Der volle Inhalt der QuelleIzquierdo, Villalba Ismael. „Gαq regulates mitochondrial motility and interacts with ALEX3, MIRO1 and TRAK proteins“. Doctoral thesis, Universitat de Barcelona, 2020. http://hdl.handle.net/10803/668465.
Der volle Inhalt der QuelleHenaff, Daniel. „Adenovirus biology : receptors and intracellular trafficking“. Thesis, Montpellier 2, 2010. http://www.theses.fr/2010MON20138/document.
Der volle Inhalt der QuelleAdenoviruses have a dual nature as ubiquitous pathogens that occasionally cause life-threatening disease and their use as gene transfer vectors. To the best of our current knowledge, the first 30 min from binding to nuclear pore docking of both wild-type virus and vector are identical. The goal of my thesis is to understand different mechanisms involved in receptor binding, internalization, endosomal escape and trafficking to the MTOC. First I studied the mechanism involved in hemagglutination of CAR-tropic and SA-tropic viruses. I identified the presence of CAR on human erythrocytes and showed that it was the main responsible for the agglutination mediated by CAR-tropic viruses. Moreover, I show that CAR on erythrocytes can sequester virus in the bloodstream and block liver infection. In a second part I participated to the characterization of the role of the protein VI and the translocation of HAd to the MTOC. We showed that Nedd4 was involved in the targeting of the virus to MTOC through ubiquitination of this protein VI. Finally, I worked on the neurotropism of CAV-2 and characterize its subcellular localization at the synapse. I showed that a part of CAR was localized in lipid raft at the synapse and enter through the synaptic vesicle-recycling pathway
Ammar, Mohamed Raafet. „Rôle de la phospholipase D1 dans le trafic membranaire : implication dans le développement neuronal et l'exocytose régulée“. Phd thesis, Université de Strasbourg, 2013. http://tel.archives-ouvertes.fr/tel-00998047.
Der volle Inhalt der QuelleNegatsch, Alexandra. „Vergleichende Analysen zur Replikation und zum intraaxonalen Transport des Pseudorabiesvirus und des Herpes Simplex Virus Typ 1 in primären Rattenneuronen“. Doctoral thesis, Universitätsbibliothek Leipzig, 2015. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-144375.
Der volle Inhalt der QuelleBertrand, Anne. „Etude morphologique et fonctionnelle par IRM à très haut champ de modèles animaux de la maladie d'Alzheimer : micro-IRM du cerveau du primate Microcebus Murinus, et caractérisation par MEMRI du transport neuronal chez différents modèles murins transgéniques“. Paris 6, 2013. http://www.theses.fr/2013PA066011.
Der volle Inhalt der QuelleKomissarov, Artem 1992. „Reconstitution of FMRP-mediated mRNA transport system in vitro“. Doctoral thesis, Universitat Pompeu Fabra, 2020. http://hdl.handle.net/10803/670058.
Der volle Inhalt der QuelleEl aprendizaje y la formación de la memoria se basan en los mecanismos de plasticidad sináptica. La plasticidad sináptica modula el desarrollo y el fortalecimiento de nuevas conexiones neuronales, o sinapsis, al aprender y se basa en la síntesis local de proteínas al lado de las espinas neuronales activadas. Miles de especies de ARNm son transportadas desde el soma de la neurona a las dendritas, para ser traducidas bajo demanda. Los mecanismos de este transporte de ARNm siguen siendo poco conocidos. Las mutaciones de la proteína Fragile X-mental Retardation (FMRP) causan un espectro de trastornos de retraso mental. Entre otras funciones, FMRP media el transporte de ARNm inducido por señal y la traducción local en las dendritas. En múltiples intentos de comprender cómo FMRP está implicada en el transporte de ARNm, se identificaron algunos candidatos de proteínas motoras. Además de la controversia en la bibliografía, no se demostró que ninguna de estas proteínas se uniera directamente y transportara FMRP. En mis estudios de doctorado, he utilizado ensayos de reconstitución in vitro, junto con la microscopía de reflexión interna total (TIRF), para probar cuál de los motores candidatos propuestos puede transportar FMRP a lo largo de los microtúbulos y si FMRP puede co-transportar moléculas de ARNm. Para comprender la bioquímica del transporte de ARNm mediado por FMRP, he purificado y probado proteínas motoras de tres subfamilias de kinesina. En esta tesis doctoral, presento que FMRP se une directamente y es transportada por el motor Kinesin-2 (heterodímero KIF3A/C), pero no por los otros motores probados. El análisis de mutaciones de FMRP sugiere que su región C-terminal juega el papel más importante en la unión con Kinesin-2, y que esta interacción no depende de la región de RGG box, conocida por identificar la estructura de G.quadruplexde de los ARNm diana de FMRP. Estos resultados sugieren que FMRP es capaz de unirse al motor y transportar ARNm simultáneamente. También muestro una observación de que el motor KIF3A/C se une a varios ARNms, con y sin estructura de G-quadruplex, y que el ARNm con G-quadruplex compite con FMRP por la interacción con la proteína motora. Estos resultados plantean muchas preguntas que abordo en la parte de Discusión de esta tesis. Este trabajo es el primero de su tipo, en mi conocimiento, para probar sistemáticamente la interaccion directa de FMRP con las proteínas motoras de kinesina y para reconstruir un complejo de transporte de FMRP. Concluyo que FMRP se une directamente al motor Kinesin-2 y que este complejo se mueve procesivamente a lo largo de los microtúbulos. A este complejo todavía le falta su carga, ARNm, que se investigará más allá del alcance de esta tesis doctoral. Analizo las velocidades de los motores de kinesina utilizados y los comparo con la bibliografía. Al final, discuto las posibles razones de por qué FMRP no se estaba uniendo el ARNm de G-quadruplex en mis condiciones experimentales y describo los escollos en utiliza de los ensayos de reconstitución in vitro.
Ashley, James A. „The Role of Cell Adhesion, the Cytoskeleton, and Membrane Trafficking during Synapse Outgrowth: A Dissertation“. eScholarship@UMMS, 2006. http://escholarship.umassmed.edu/gsbs_diss/302.
Der volle Inhalt der QuelleAckerley, Steven. „Neurofilament transport and phosphorylation“. Thesis, King's College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.289881.
Der volle Inhalt der QuelleLeary, Gregory Patrick. „STRUCTURE AND FUNCTION OF A NEURONAL GLUTAMATE TRANSPORTER“. The University of Montana, 2009. http://etd.lib.umt.edu/theses/available/etd-03262009-135837/.
Der volle Inhalt der QuelleGlutamate transporters have a homotrimeric subunit structure with a large central water-filled cavity that extends partially into the plane of the lipid bilayer (Yernool et al., 2004). In addition to uptake of glutamate, the transporters also mediate a chloride conductance that is gated by Na+ and glutamate. Our data indicate that glutamate binding sites, transport pathways, and chloride channels reside in individual subunits in the trimer and function independently and that the anion channel is gated by alkali cations binding from either side of the membrane. We also investigated conformational changes during glutamate binding by incorporating a fluorescent probe into a site near the postulated external gate (HP2) of a mutant transporter that can bind but not transport L-Glu. Fluorescence changes were observed upon ligand binding that strongly depended on the number of subunits labeled; this suggests quenched fluorophore dimers form at the center of the trimer that are subject to HP2 loop closure upon substrate binding. This supports a model of gate motion that is also consistent with recent x-ray structural data (Boudker et al., 2007). Finally, we propose that the large aqueous central cavity in the trimeric complex (Yernool et al., 2004) may function to restrict the diffusion of molecules near the three ligand binding sites, resulting in an increase in the probability of rebinding.
Tennant, Maria Elizabeth. „Axonal transport in motor neurone disease“. Thesis, King's College London (University of London), 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.424667.
Der volle Inhalt der QuelleHaziza, Simon. „Quantification du transport intraneuronal par suivi de nanodiamants fluorescents. Application à l’étude de l’impact fonctionnel de facteurs de risque génétiques associés aux maladies neuropsychiatriques“. Thesis, Université Paris-Saclay (ComUE), 2015. http://www.theses.fr/2015SACLN013/document.
Der volle Inhalt der QuelleThe identification of molecular biomarkers of brain diseases as diverse as autism, schizophrenia and Alzheimer’s disease, is of crucial importance not only for an objective diagnosis but also to monitor response to treatments. The establishment and maintenance of sub-cellular neuronal functions, such as synaptic plasticity, are highly dependent on intracellular transport, which is essential to deliver important materials to specific locations. Abnormalities in such active transport are thought to be partly responsible for synaptic plasticity and neuronal morphology impairment found in many neuropsychiatric and neurodegenerative diseases. This thesis reports (i) the development of a quantification technic of intraneuronal transport based on fluorescent nanodiamonds (fNDs) tracking; (ii) the application of this simple and minimally invasive approach to the functional analysis of neuropsychiatric disease-related genetic variants.This manuscript falls into four chapters. The first one details the complex polygenic architecture of mental disorders and demonstrates the disease relevance of monitoring the intraneuronal transport. The second and the third chapters are dedicated to the nanodiamond-tracking assay and describe the fNDs internalisation strategies, the spatiotemporal quantitative readouts and the validation of the technic. The high brightness, the perfect photostability and the absence of cytotoxicity make fNDs a tool of choice to perform high throughput long-term bioimaging at high spatiotemporal resolution. Finally, in the fourth chapter, we apply this new functional analysis method to study the effect of genetic variants associated to autism and schizophrenia. We established transgenic mouse lines in which MARK1 and SLC25A12 genes were slightly overexpressed, and AAV-shRNA to induce AUTS2 gene haploinsufficiency. Our molecular diagnosis assay proves sufficiently sensitive to detect fine changes in intraneuronal transport dynamic, paving the way for future development in translational nanomedicine
Babic, Milos. „Molecular Mechanisms of Mitochondrial Transport in Neurons“. Diss., The University of Arizona, 2015. http://hdl.handle.net/10150/556433.
Der volle Inhalt der QuelleBodakuntla, Satish. „La régulation de transport neuronale par la polyglutamylation des microtubules“. Thesis, Paris Sciences et Lettres (ComUE), 2019. http://www.theses.fr/2019PSLET036.
Der volle Inhalt der QuelleIntracellular transport involves transporting various vesicles and organelles by molecular motors along the microtubules, and is thus a crucial process in all eukaryotic cells. Highly differentiated, complex and long-lived cells such as neurons pose a particular challenge for the maintenance of an efficient, tightly controlled transport. Defects in axonal transport have been implicated in many neurodegenerative disorders, and are currently considered as one of the early events in the pathogenic pathway. Mechanisms controlling intra-neuronal transport could thus be important players in neuronal homeostasis. A mechanism that was for many years proposed to control intracellular transport is the posttranslational modification of microtubule tracks. In my PhD thesis I tested the hypothesis that one tubulin modification that is particularly enriched in neurons, polyglutamylation, controls axonal transport.During my PhD, I have established all the necessary methods to obtain neurons with differential levels of polyglutamylation using different mouse models. I have then measured the transport of different cargoes in these neurons. First, I have measured mitochondria transport, and demonstrated that increased tubulin polyglutamylation, as found in neurons that degenerate, reduces the overall motility of mitochondria. Inversely, in neurons with decreased polyglutamylation, I have shown that mitochondria transport is increased. These results suggest that tubulin polyglutamylation is a dynamic regulator of mitochondrial transport. To investigate the specificity of transport regulation by tubulin polyglutamylation, I next measured the transport of other axonal cargoes. Transport of lysosomes, late endosomes and BDNF vesicles was, similar to mitochondria, negatively affected by hyperglutamylation.In conclusion, I have demonstrated that tubulin polyglutamylation could be a general tuning mechanism for axonal transport. Considering our earlier findings, which show that hyperglutamylation induces neurodegeneration, defects in axonal transport could be one of the key molecular mechanisms that induce degeneration of neurons with hyperglutamylation
Qin, Yan. „Studies of Zinc Transport and Its Contribution to Zinc Homeostasis in Cultured Cortical Neurons“. View abstract, 2008. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&res_dat=xri:pqdiss&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&rft_dat=xri:pqdiss:3339515.
Der volle Inhalt der QuelleCerruti, Catherine. „Etude, sur des neurones en culture primaire, du transporteur de la dopamine, au moyen d'un inhibiteur spécifique, la BTCP : pharmacologie, influence sur la maturation neuronale, neuroprotection“. Montpellier 2, 1991. http://www.theses.fr/1991MON20167.
Der volle Inhalt der QuelleWang, Jing, und 王景. „The study of KIF5B-mediated intracellular transport in neurons“. Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B41633763.
Der volle Inhalt der QuelleWang, Jing. „The study of KIF5B-mediated intracellular transport in neurons“. Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B41633763.
Der volle Inhalt der QuelleLe, Fablec Yann. „Prévision de trajectoires d'avions par réseaux de neurones“. Toulouse, INPT, 1999. http://www.theses.fr/1999INPT034H.
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