Literatura científica selecionada sobre o tema "Activité axonale"
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Artigos de revistas sobre o assunto "Activité axonale"
Satkeviciute, Ieva, George Goodwin, Geoffrey M. Bove e Andrew Dilley. "Time course of ongoing activity during neuritis and following axonal transport disruption". Journal of Neurophysiology 119, n.º 5 (1 de maio de 2018): 1993–2000. http://dx.doi.org/10.1152/jn.00882.2017.
Texto completo da fonteWang, Jack T., Zachary A. Medress, Mauricio E. Vargas e Ben A. Barres. "Local axonal protection by WldS as revealed by conditional regulation of protein stability". Proceedings of the National Academy of Sciences 112, n.º 33 (24 de julho de 2015): 10093–100. http://dx.doi.org/10.1073/pnas.1508337112.
Texto completo da fonteChen, Yanmin, e Zu-Hang Sheng. "Kinesin-1–syntaphilin coupling mediates activity-dependent regulation of axonal mitochondrial transport". Journal of Cell Biology 202, n.º 2 (15 de julho de 2013): 351–64. http://dx.doi.org/10.1083/jcb.201302040.
Texto completo da fonteTang, Bor. "Why is NMNAT Protective against Neuronal Cell Death and Axon Degeneration, but Inhibitory of Axon Regeneration?" Cells 8, n.º 3 (21 de março de 2019): 267. http://dx.doi.org/10.3390/cells8030267.
Texto completo da fonteCorna, Andrea, Timo Lausen, Roland Thewes e Günther Zeck. "Electrical imaging of axonal stimulation in the retina". Current Directions in Biomedical Engineering 8, n.º 3 (1 de setembro de 2022): 33–36. http://dx.doi.org/10.1515/cdbme-2022-2009.
Texto completo da fonteTigerholm, Jenny, Marcus E. Petersson, Otilia Obreja, Angelika Lampert, Richard Carr, Martin Schmelz e Erik Fransén. "Modeling activity-dependent changes of axonal spike conduction in primary afferent C-nociceptors". Journal of Neurophysiology 111, n.º 9 (1 de maio de 2014): 1721–35. http://dx.doi.org/10.1152/jn.00777.2012.
Texto completo da fonteHwang, Jinyeon, e Uk Namgung. "Phosphorylation of STAT3 by axonal Cdk5 promotes axonal regeneration by modulating mitochondrial activity". Experimental Neurology 335 (janeiro de 2021): 113511. http://dx.doi.org/10.1016/j.expneurol.2020.113511.
Texto completo da fonteJamann, Nora, Merryn Jordan e Maren Engelhardt. "Activity-Dependent Axonal Plasticity in Sensory Systems". Neuroscience 368 (janeiro de 2018): 268–82. http://dx.doi.org/10.1016/j.neuroscience.2017.07.035.
Texto completo da fonteSusuki, Keiichiro, e Hiroshi Kuba. "Activity-dependent regulation of excitable axonal domains". Journal of Physiological Sciences 66, n.º 2 (13 de outubro de 2015): 99–104. http://dx.doi.org/10.1007/s12576-015-0413-4.
Texto completo da fonteGanguly, Archan, Xuemei Han, Utpal Das, Lina Wang, Jonathan Loi, Jichao Sun, Daniel Gitler et al. "Hsc70 chaperone activity is required for the cytosolic slow axonal transport of synapsin". Journal of Cell Biology 216, n.º 7 (30 de maio de 2017): 2059–74. http://dx.doi.org/10.1083/jcb.201604028.
Texto completo da fonteTeses / dissertações sobre o assunto "Activité axonale"
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.
Texto completo da fonteGlioblastoma (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.
Texto completo da fonteThroughout 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.
Texto completo da fonteUne 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.
Texto completo da fonteDuring 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.
Texto completo da fonteReis, 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.
Texto completo da fonteTitle 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.
Texto completo da fonteGoganau, 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.
Texto completo da fonteFerraro, 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.
Texto completo da fonteLa 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.
Texto completo da fonteLivros sobre o assunto "Activité axonale"
1953-, Angelov D. N., ed. Axonal branching and recovery of coordinated muscle activity after transection of the facial nerve in adult rats. Berlin: Springer, 2005.
Encontre o texto completo da fontePark, Susanna B., Cindy S.-Y. Lin e Matthew C. Kiernan. Axonal excitability: molecular basis and assessment in the clinic. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199688395.003.0009.
Texto completo da fonteAxonal Branching and Recovery of Coordinated Muscle Activity after Transection of the Facial Nerve in Adult Rats. Berlin/Heidelberg: Springer-Verlag, 2005. http://dx.doi.org/10.1007/3-540-29931-9.
Texto completo da fonteBhargava, Pavan, e Peter A. Calabresi. Multiple Sclerosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0087.
Texto completo da fonteAngelov, D. N., O. Guntinas-Lichius, K. Wewetzer, W. F. Neiss e M. Streppel. Axonal Branching and Recovery of Coordinated Muscle Activity after Transsection of the Facial Nerve in Adult Rats (Advances in Anatomy, Embryology and Cell Biology). Springer, 2005.
Encontre o texto completo da fonteRoze, Emmanuel, e Frédéric Sedel. Gangliosidoses (GM1 and GM2). Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0050.
Texto completo da fonteAngelov, Doychin N., Orlando Guntinas-Lichius, Konstantin Wewetzer, Wolfram Neiss e Michael Streppel. Axonal Branching and Recovery of Coordinated Muscle Activity after Transsection of the Facial Nerve in Adult Rats (Advances in Anatomy, Embryology and Cell Biology Book 180). Springer, 2006.
Encontre o texto completo da fonteGaetz, Michael B., e Kelly J. Jantzen. Electroencephalography. Editado por Ruben Echemendia e Grant L. Iverson. Oxford University Press, 2016. http://dx.doi.org/10.1093/oxfordhb/9780199896585.013.006.
Texto completo da fonteGuo, Yong, e Claudia F. Lucchinetti. Taking a Microscopic Look at Multiple Sclerosis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199341016.003.0005.
Texto completo da fonteColumb, Malachy O. Local anaesthetic agents. Editado por Michel M. R. F. Struys. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0017.
Texto completo da fonteCapítulos de livros sobre o assunto "Activité axonale"
Carr, Richard. "Nociceptors and Activity-Dependent Changes in Axonal Conduction Velocity". In Encyclopedia of Pain, 2244–49. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-28753-4_4984.
Texto completo da fonteBurke, David. "Effects of Activity on Axonal Excitability: Implications for Motor Control Studies". In Advances in Experimental Medicine and Biology, 33–37. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-0713-0_5.
Texto completo da fonteThanos, Solon. "Blockade of Proteolytic Activity Retards Retrograde Degeneration of Axotomized Retinal Ganglion Cells and Enhances Axonal Regeneration in Organ Cultures". In The Changing Visual System, 77–93. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3390-0_7.
Texto completo da fonteTroglio, Alina, Roberto de Col, Barbara Namer e Ekaterina Kutafina. "Modeling of Activity-Induced Changes in Signal Propagation Speed of Mechano-Electrically Stimulated Nerve Fiber". In Studies in Health Technology and Informatics. IOS Press, 2021. http://dx.doi.org/10.3233/shti210127.
Texto completo da fonte"THIAMINE TRIPHOSPHATE AS SPECIFIC OPERATING SUBSTANCE IN AXONAL CONDUCTION". In Molecular Basis of Nerve Activity, 401–16. De Gruyter, 1985. http://dx.doi.org/10.1515/9783110855630-035.
Texto completo da fonteLi, Sunan, e Zu-Hang Sheng. "Regulation of Synaptic Transmission through Mitochondrial Positioning and Metabolism". In The Oxford Handbook of Mitochondria. Oxford University Press, 2024. http://dx.doi.org/10.1093/oxfordhb/9780190932183.013.13.
Texto completo da fonteBenarroch, Eduardo E. "Growth Factors, Survival, and Regeneration". In Neuroscience for Clinicians, editado por Eduardo E. Benarroch, 213–30. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780190948894.003.0013.
Texto completo da fonteB.Levitan, Irwin, e Leonard K. Kaczmarek. "Diversity in the Structure and Function of Ion Channels". In The Neuron, 139–62. Oxford University PressNew York, NY, 2001. http://dx.doi.org/10.1093/oso/9780195145236.003.0007.
Texto completo da fonteBarresi, Michael J. F., e Scott F. Gilbert. "Neural Crest Cells and Axonal Specificity". In Developmental Biology. Oxford University Press, 2023. http://dx.doi.org/10.1093/hesc/9780197574591.003.0021.
Texto completo da fonteFilippi, Massimo, e Maria A. Rocca. "Multiple sclerosis". In Clinical Applications of Functional Brain MRI, 311–41. Oxford University PressOxford, 2007. http://dx.doi.org/10.1093/oso/9780198566298.003.0011.
Texto completo da fonteTrabalhos de conferências sobre o assunto "Activité axonale"
Masson, Jean-Baptiste, Martin-Pierre Sauviat, Jean-Louis Martin e Guilhem Gallot. "Ionic contrast terahertz near-field imaging of axonal activity and water fluxes". In Biomedical Optics (BiOS) 2007, editado por Daniel L. Farkas, Robert C. Leif e Dan V. Nicolau. SPIE, 2007. http://dx.doi.org/10.1117/12.698309.
Texto completo da fonteTamatani, Chie, Kenta Shimba, Kiyoshi Kotani e Yasuhiko Jimbo. "Activity- and Spatial-dependent Variations in Axonal Conduction Recorded from Microtunnel Electrodes". In 2023 15th Biomedical Engineering International Conference (BMEiCON). IEEE, 2023. http://dx.doi.org/10.1109/bmeicon60347.2023.10321980.
Texto completo da fonteXu, Gang, Kate S. Wilson, Ruth J. Okamoto, Jin-Yu Shao, Susan K. Dutcher e Philip V. Bayly. "The Apparent Flexural Rigidity of the Flagellar Axoneme Depends on Resistance to Inter-Doublet Sliding". In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80220.
Texto completo da fonteNakagawa, K., T. Takaki, Y. Morita e E. Nakamachi. "2D Phase-Field Analyses of Axonal Extension of Nerve Cell". In ASME 2013 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/imece2013-64281.
Texto completo da fonteParca, Leonardo Martins, Ahmad Abdallah Hilal Nasser, Gabriel Rodrigues Gomes da Fonseca, Gabriel Nogueira Noleto Vasconcelos, Grazielle de Oliveira Marques, Renato Sarnaglia Proença e Pablo Henrique da Costa Silva. "Guillain-barré syndrome (GBS): acute motor axonal neuropathy (AMAN) - case report". In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.139.
Texto completo da fonteNicholson, Kristen J., e Beth A. Winkelstein. "The Duration of a Nerve Root Compression Modulates Evoked Neuronal Responses in a Rat Model of Painful Injury". In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53082.
Texto completo da fonteBayly, Philip V., e Kate S. Wilson. "Unstable Oscillations and Wave Propagation in Flagella". In ASME 2015 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. American Society of Mechanical Engineers, 2015. http://dx.doi.org/10.1115/detc2015-46920.
Texto completo da fonte