Tesi sul tema "Activité axonale"
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Lemercier, Quentin. "Dommages de la substance blanche et impact de l'activité axonale sur l'invasion tumorale dans un modèle murin de glioblastome". Electronic Thesis or Diss., Normandie, 2024. http://www.theses.fr/2024NORMR012.
Glioblastoma (GB), a brain tumor of glial origin, is the most common and most aggressive primary tumor of the central nervous system in adults, with a median survival rate of less than 18 months after standard treatment. This poor prognosis is mainly due to the invasive nature of the glial tumor cells, which is responsible for treatment failures. White matter tracts are a major pathway of glioma invasion, but the mechanisms involved in this process are still poorly understood. In this thesis work, the human glioblastoma U87 cell line was injected into immunodeficient adult Nude mice. This lineage presents a circumscribed tumor mass with collective invasion into the healthy parenchyma. U87 cell display predominantly a perivascular migration, and U87 cells also contact axons within the white matter. Specific damages of the white matter have been demonstrated. They include axonal damages and associated demyelination as well as a peritumoral axonal hyperexcitability. Modulation of axonal activity using optogenetic indicates that increased axonal activity promotes tumor invasion. To conclude, structural and functional damages of the white matter bundles therefore constitute a microenvironment suitable for tumor progression
Weinreb, Alexis. "Impact de l’activité postsynaptique sur le développement et le maintien de la jonction neuromusculaire de C. elegans". Thesis, Lyon, 2018. http://www.theses.fr/2018LYSE1137.
Throughout nervous system development, activity of the post-synaptic targets can regulate the connectivity of neural networks, affecting both the number and strength of synapses. Using the neuromuscular junction of Caenorhabditis elegans as a model system, we studied two processes displaying such plasticity. First, we show that the number of receptors present at the neuromuscular synapse is regulated by muscle activity: an increase in synaptic activity can lead to a differential regulation of the three types of receptors present at the neuromuscular junction. Second, we studied the activity-dependent morphological changes of one type of motor neurons in the worm’s head, called the SAB neurons. A decrease of muscle activity during a critical developmental phase leads to SAB axonal overgrowth. Using several approaches, we were able to observe suppression of SAB axonal overgrowth in mutants with a disruption of neuropeptides biosynthesis. Finally, we give evidence that axonal overgrowth also occurs following more general disruptions of cell physiology, such as a heat-shock or transgene overexpression, which suggest that the SAB system is plastic and sensitive during development
Hanbali, Mazen. "Composés hybrides w-alcanol / hydroquinone à activité neurotrophique. Synthèse et étude des propriétés physicochimiques et biologiques". Phd thesis, Université Louis Pasteur - Strasbourg I, 2005. http://tel.archives-ouvertes.fr/tel-00116946.
Une approche thérapeutique novatrice serait l'utilisation de composés hybrides portant deux activités distinctes. Une activité neurotrophique permettant la neuro-régénération et une activité antioxydante assurant la neuro-protection en piégeant les radicaux libres.
Dans cet objectif, cinq séries de molécules hybrides combinant une chaîne grasse Ω-hydroxylée et des noyaux quinol ont été synthétisés. Les alcools gras quinoliques (QFA) C-alkylés, comportant des noyaux quinol polyméthoxylés, ont été obtenu par couplage de Sonogashira entre des arylbromures et des alcynes vrais. Les homologues N- ou O-alkylés ont été obtenus par des réactions de type SN2.
Les molécules synthétisés possèdent de très bonnes activités antioxydantes sous leurs formes déméthylés dépassant d'un facteur 100 l'activité antioxydante du Trolox®. Par ailleurs, le QFA15 portant une chaîne latérale à 15 atomes de carbones, est capable de promouvoir une croissance axonale très importante, aussi bien sur substrat permissif que sur substrat inhibiteur tel les protéines de myéline ou la Sema3A. Des études préliminaires du mécanisme d'action ont permis de conclure que le QFA15 sollicite les nucléotides cycliques.
Moutaux, 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.
During 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
Leterrier, Christophe. "Activité constitutive et adressage axonal du récepteur cannabinoïque neurotal". Paris 6, 2006. https://tel.archives-ouvertes.fr/tel-00250338.
Reis, Gerald Feliz. "Mechanisms of motor activity regulation in axonal transport". Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2008. http://wwwlib.umi.com/cr/ucsd/fullcit?p3315202.
Title from first page of PDF file (viewed Nov. 5, 2008). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references.
Leterrier, Christophe. "Activité constitutive et adressage axonal du récepteur cannabinoïque neuronal CB1". Phd thesis, Université Pierre et Marie Curie - Paris VI, 2006. http://tel.archives-ouvertes.fr/tel-00250338.
Goganau, Ioana [Verfasser], e Armin [Akademischer Betreuer] Blesch. "Electrical stimulation and activity for axonal regeneration / Ioana Goganau ; Betreuer: Armin Blesch". Heidelberg : Universitätsbibliothek Heidelberg, 2016. http://d-nb.info/1180736885/34.
Ferraro, Gino. "Matrix metalloproteinase activity modulates neuronal response to myelin inhibition by cleaving NgR1 and basal axonal outgrowth". Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=114187.
La complexité du circuit du cerveau des mammifères est établie par le guidage axonal et la synaptogenèse. Ces processus de développement sont réglementés par des ligands et leurs récepteurs localisés à la surface cellulaire des neurones. Malheureusement, suite à une lésion, le système nerveux central (SNC) de mammifères adultes restreint sévèrement la croissance des neurites en partie par la présence de ligands et récepteurs inhibiteurs. Le récepteur de Nogo66 (NgR1), exprimé par les neurones matures, inhibe la repousse des neurones du SNC lésés par sa liaison à de multiples ligands inhibiteurs. En outre, NgR1 est fortement exprimé dans les zones synaptogeniques comme le cortex et l'hippocampe où il régule la plasticité synaptique et limite la plasticité dépendante d'expérience sensorielle. Les niveaux de NgR1 dans les neurones peuvent être altérés par l'activité protéolytique des métalloprotéinases. Celle-ci réduit les niveaux de NgR1 à la surface neuronale en générant un fragment soluble dominant négatif, qui peut avoir un impact sur la fonction de NgR1 dans le cerveau. Mon mémoire porte sur l'étude de l'impact de la protéolyse de NgR1 par les métalloprotéinases sur sa fonction dans le SNC. Ici, je présenterai des preuves que les métalloprotéinases membranaires peuvent cliver NgR1 à la surface neuronale et atténuer les réponses aux signaux inhibiteurs. Ces métalloprotéinases sont exprimées dans le cerveau de souris et peuvent promouvoir la protéolyse de NgR1 jusqu'à l'âge adulte. NgR1 est aussi clivé dans les synaptosomes suggérant que ce mécanisme peut réguler la fonction de NgR1 à la synapse. Ces résultats nous ont incités à rechercher si l'activité des métalloprotéinases peut réguler la croissance axonale par d'autres protéines de surface cellulaire. Nous avons déterminé que les métalloprotéinases membranaires peuvent promouvoir la croissance axonale du SNC et du système nerveux périphérique (SNP). Pour élucider le mécanisme sous-tendant ce phénotype, nous avons identifié des protéines candidates par spectrométrie de masse, qui comprennent les protéines adhésives IgLONs, une famille de protéines connues pour réguler la croissance axonale. Ensemble, les données présentées ici accroissent notre compréhension de la régulation par métalloprotéinases sur la croissance des neurites au cours du développement. En outre, nos observations avec la protéolyse de NgR1 par les métalloprotéinases suggèrent que ce processus est conservé dans l'inhibition de la croissance des neurites et la restriction de la plasticité synaptique.
Vernon, Geraint Grrffydd. "Mechanical activity and its propagation along the flagellar axoneme : studies using caged ATP". Thesis, University of Bristol, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.319140.
Tam, Siu Lin. "Neuromuscular activity, axonal sprouting and stability of chronically enlarged motor units in an animal model of motoneuron disease". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape9/PQDD_0021/MQ47104.pdf.
Kastanenka, Ksenia V. "IN VIVO ACTIVATION OF CHANNELRHODOPSIN-2 USED TO DETERMINE THE ROLE OF SPONTANEOUS NEURAL ACTIVITY IN AXONAL GUIDANCE". Case Western Reserve University School of Graduate Studies / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=case1307741269.
Hanbali, Mazen. "Composés hybrides [oméga]-Alcanol / Hydroquinone à activité neurotrophique : Synthèse et étude des propriétés physicochimiques et biologiques". Université Louis Pasteur (Strasbourg) (1971-2008), 2005. http://www.theses.fr/2005STR13116.
Roig, Puiggros Sergi. "Molecular mechanisms orchestrating commissural axon guidance Floor-plate-derived netrin-1 is dispensable for commissural axon guidance Synergistic Activity of Floor-Plateand Ventricular-Zone-Derived Netrin-1 in Spinal Cord Commissural Axon Guidance". Thesis, Sorbonne université, 2019. http://www.theses.fr/2019SORUS335.
Commissural neurons ensure the coordination of motor and somatosensory information between halves of the central nervous system. In the caudal part of the CNS, commissural axons, first grow toward the ventral midline, the floor plate, to cross it and reach their final target. The cellular and molecular mechanisms controlling midline crossing have been extensively studied. Ram—n y Cajal, in his neurotropic theory, suggested that floor plate cells could release diffusible factors chemo-attracting commissural axons to the ventral midline. Netrin-1, a protein discovered more than 2 decades ago, is a secreted protein expressed both by floor plate cells and ventricular zone progenitors and with long-range chemoattractive activity in vitro. Today, Netrin-1 is widely accepted as the textbook example of long-range chemoattractive guidance cue. However, our results, challenge this model by proposing a short-range mechanism of action for Netrin-1 during commissural axon guidance. Indeed, we determined that floor plate-derived netrin-1 is dispensable for commissural axon guidance. Instead, ventricular zone-derived netrin-1 is necessary and sufficient to promote the dorso-ventral extension of hindbrain commissural axons and midline crossing. We also confirmed that ventricular zone progenitors are the main Netrin-1 source for ventrally migrating precerebellar neurons. In addition, we observe that in absence of ventricular zone-derived netrin-1, commissural axons and precerebellar neurons cell bodies invade several cranial nerves. This appears to be a cell- autonomous and Dcc-dependent process. This mechanism is not conserved in the spinal cord, where both netrin-1 sources act synergistically to ensure commissural axon guidance and midline crossing. Commissural neurons are diverse and found throughout the nervous system. To analyse the molecular diversity of hindbrain and spinal cord commissural neurons, we used approaches combining mouse genetics and transcriptomics. We are currently working on some novel transcription factors that might play a role in the development of hindbrain and spinal cord commissural neurons
Feofilova, Maria [Verfasser], Jonathon [Akademischer Betreuer] Howard, Frank [Gutachter] Jülicher, Ivo [Gutachter] Sbalzarini e Jonathon [Gutachter] Howard. "Probing Dynein Motor Activity in the Intact Chlamydomonas Axoneme / Maria Feofilova ; Gutachter: Frank Jülicher, Ivo Sbalzarini, Jonathon Howard ; Betreuer: Jonathon Howard". Dresden : Technische Universität Dresden, 2019. http://d-nb.info/1230578102/34.
Auffarth, Benjamin. "Machine Learning Techniques with Specific Application to the Early Olfactory System". Doctoral thesis, KTH, Beräkningsbiologi, CB, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-90474.
QC 20120224
Feofilova, Maria. "Probing Dynein Motor Activity in the Intact Chlamydomonas Axoneme". 2017. https://tud.qucosa.de/id/qucosa%3A34182.
Rodrigues, Alexandra Lopes Ramos. "Dysfunctional dendritic and axonal activity in Alzheimer's disease - identifying possible therapeutic targets". Master's thesis, 2020. http://hdl.handle.net/10316/97747.
Alzheimer’s disease is the most common neurodegenerative disorder in the world, characterized by cognitive deficits and dementia. Amyloid-beta peptide and tau protein aggregate are the two disease hallmarks, forming plaques and neurofibrillary tangles, respectively. These insoluble structures have been recognized to cause synaptic and neuronal dysfunction, progressively leading to neurodegeneration. This review aims to describe the processing of these proteins and their modifications leading to aggregation, as well as synaptic-based mechanisms that result in behavioral changes and memory loss in AD. Part of these mechanisms include modifications in axonal transport and dendritic activity, due to hyperphosphorylation of tau protein, as well as activation of glutamate receptors preceding excitotoxic events, which involve calcium dyshomeostasis and mitochondrial dysfunction, closely linked to synaptic dysfunction. Understanding how these processes intricately work is expected to bring about new therapeutic strategies worth to be explored in the near future .
A doença de Alzheimer é a doença neurodegenerativa mais comum no mundo e é caraterizada por defeitos cognitivos e demência. As agregações de amilóide-beta e proteína tau são caraterísticas da doença e conduzem à formação de placas e estruturas insolúveis de tau, respetivamente. Estes depósitos foram reconhecidos como causadores de disfunção sinática e neuronal, conduzindo a neurodegeneração. Esta revisão tem como objetivo descrever os processos que estas proteínas sofrem até se tornarem agregados e os mecanismos que causam disfunção sinática até ao aparecimento de alterações no comportamento e perda de memória. Alguns destes processos patológicos, incluem modificações no transporte axonal e actividade dendrítica, devido à excessiva fosforilação da proteína tau e ativação dos recetores glutamatérgicos, que culminam em eventos excitotóxicos, que envolvem desregulação no balanço de cálcio no neurónio e disfunção mitocondrial. Perceber como estes mecanismos se relacionam é a base do desenvolvimento de novas estratégias terapêuticas que possam ser exploradas num futuro próximo .
Dedeagac, Asli. "Investigation of Molecular and Cellular Mechanism of Myelin – Induced Axonal Degeneration". Thesis, 2013. http://hdl.handle.net/1807/42811.
Ricardo, Catarina Eduarda Fernandes. "Study of the regulatory effect of neuronal electrical activity on mitochondria axonal transport dynamics". Master's thesis, 2021. https://hdl.handle.net/10216/136982.
Kurdakova, Anastasiia. "Quantitative analysis of neuropathological alterations in two transgenic mouse models of Alzheimer's disease". Doctoral thesis, 2016. http://hdl.handle.net/11858/00-1735-0000-002B-7C60-9.