Letteratura scientifica selezionata sul tema "Activité axonale"
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Articoli di riviste sul tema "Activité axonale":
1
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. 5 (1 maggio 2018): 1993–2000. http://dx.doi.org/10.1152/jn.00882.2017.
Abstract (sommario):
Local nerve inflammation (neuritis) leads to ongoing activity and axonal mechanical sensitivity (AMS) along intact nociceptor axons and disrupts axonal transport. This phenomenon forms the most feasible cause of radiating pain, such as sciatica. We have previously shown that axonal transport disruption without inflammation or degeneration also leads to AMS but does not cause ongoing activity at the time point when AMS occurs, despite causing cutaneous hypersensitivity. However, there have been no systematic studies of ongoing activity during neuritis or noninflammatory axonal transport disruption. In this study, we present the time course of ongoing activity from primary sensory neurons following neuritis and vinblastine-induced axonal transport disruption. Whereas 24% of C/slow Aδ-fiber neurons had ongoing activity during neuritis, few (<10%) A- and C-fiber neurons showed ongoing activity 1–15 days following vinblastine treatment. In contrast, AMS increased transiently at the vinblastine treatment site, peaking on days 4–5 (28% of C/slow Aδ-fiber neurons) and resolved by day 15. Conduction velocities were slowed in all groups. In summary, the disruption of axonal transport without inflammation does not lead to ongoing activity in sensory neurons, including nociceptors, but does cause a rapid and transient development of AMS. Because it is proposed that AMS underlies mechanically induced radiating pain, and a transient disruption of axonal transport (as previously reported) leads to transient AMS, it follows that processes that disrupt axonal transport, such as neuritis, must persist to maintain AMS and the associated symptoms. NEW & NOTEWORTHY Many patients with radiating pain lack signs of nerve injury on clinical examination but may have neuritis, which disrupts axonal transport. We have shown that axonal transport disruption does not induce ongoing activity in primary sensory neurons but does cause transient axonal mechanical sensitivity. The present data complete a profile of key axonal sensitivities following axonal transport disruption. Collectively, this profile supports that an active peripheral process is necessary for maintained axonal sensitivities.
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Wang, 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. 33 (24 luglio 2015): 10093–100. http://dx.doi.org/10.1073/pnas.1508337112.
Abstract (sommario):
The expression of the mutant Wallerian degeneration slow (WldS) protein significantly delays axonal degeneration from various nerve injuries and in multiple species; however, the mechanism for its axonal protective property remains unclear. Although WldS is localized predominantly in the nucleus, it also is present in a smaller axonal pool, leading to conflicting models to account for the WldS fraction necessary for axonal protection. To identify where WldS activity is required to delay axonal degeneration, we adopted a method to alter the temporal expression of WldS protein in neurons by chemically regulating its protein stability. We demonstrate that continuous WldS activity in the axonal compartment is both necessary and sufficient to delay axonal degeneration. Furthermore, by specifically increasing axonal WldS expression postaxotomy, we reveal a critical period of 4–5 h postinjury during which the course of Wallerian axonal degeneration can be halted. Finally, we show that NAD+, the metabolite of WldS/nicotinamide mononucleotide adenylyltransferase enzymatic activity, is sufficient and specific to confer WldS-like axon protection and is a likely molecular mediator of WldS axon protection. The results delineate a therapeutic window in which the course of Wallerian degeneration can be delayed even after injures have occurred and help narrow the molecular targets of WldS activity to events within the axonal compartment.
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Chen, Yanmin, e Zu-Hang Sheng. "Kinesin-1–syntaphilin coupling mediates activity-dependent regulation of axonal mitochondrial transport". Journal of Cell Biology 202, n. 2 (15 luglio 2013): 351–64. http://dx.doi.org/10.1083/jcb.201302040.
Abstract (sommario):
Axonal mitochondria are recruited to synaptic terminals in response to neuronal activity, but the mechanisms underlying activity-dependent regulation of mitochondrial transport are largely unknown. In this paper, using genetic mouse model combined with live imaging, we demonstrate that syntaphilin (SNPH) mediates the activity-dependent immobilization of axonal mitochondria through binding to KIF5. In vitro analysis showed that the KIF5–SNPH coupling inhibited the motor adenosine triphosphatase. Neuronal activity further recruited SNPH to axonal mitochondria. This motor-docking interplay was induced by Ca2+ and synaptic activity and was necessary to establish an appropriate balance between motile and stationary axonal mitochondria. Deleting snph abolished the activity-dependent immobilization of axonal mitochondria. We propose an “Engine-Switch and Brake” model, in which SNPH acts both as an engine off switch by sensing mitochondrial Rho guanosine triphosphatase-Ca2+ and as a brake by anchoring mitochondria to the microtubule track. Altogether, our study provides new mechanistic insight into the molecular interplay between motor and docking proteins, which arrests axonal mitochondrial transport in response to changes in neuronal activity.
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Tang, Bor. "Why is NMNAT Protective against Neuronal Cell Death and Axon Degeneration, but Inhibitory of Axon Regeneration?" Cells 8, n. 3 (21 marzo 2019): 267. http://dx.doi.org/10.3390/cells8030267.
Abstract (sommario):
Nicotinamide mononucleotide adenylyltransferase (NMNAT), a key enzyme for NAD+ synthesis, is well known for its activity in neuronal survival and attenuation of Wallerian degeneration. Recent investigations in invertebrate models have, however, revealed that NMNAT activity negatively impacts upon axon regeneration. Overexpression of Nmnat in laser-severed Drosophila sensory neurons reduced axon regeneration, while axon regeneration was enhanced in injured mechanosensory axons in C. elegans nmat-2 null mutants. These diametrically opposite effects of NMNAT orthologues on neuroprotection and axon regeneration appear counterintuitive as there are many examples of neuroprotective factors that also promote neurite outgrowth, and enhanced neuronal survival would logically facilitate regeneration. We suggest here that while NMNAT activity and NAD+ production activate neuroprotective mechanisms such as SIRT1-mediated deacetylation, the same mechanisms may also activate a key axonal regeneration inhibitor, namely phosphatase and tensin homolog (PTEN). SIRT1 is known to deacetylate and activate PTEN which could, in turn, suppress PI3 kinase–mTORC1-mediated induction of localized axonal protein translation, an important process that determines successful regeneration. Strategic tuning of Nmnat activity and NAD+ production in axotomized neurons may thus be necessary to promote initial survival without inhibiting subsequent regeneration.
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Corna, Andrea, Timo Lausen, Roland Thewes e Günther Zeck. "Electrical imaging of axonal stimulation in the retina". Current Directions in Biomedical Engineering 8, n. 3 (1 settembre 2022): 33–36. http://dx.doi.org/10.1515/cdbme-2022-2009.
Abstract (sommario):
Abstract Stimulation of axons or its avoidance plays a central role for neuroprosthetics and neural-interfaces research. One peculiar example constitutes retinal implants. Retinal implants aim to artificially activate retinal ganglion cells (RGCs) via electrical stimulation. Such stimulation, however, often generates undesired stimulation of RGC axon bundles, which leads to distorted visual percepts. In order to establish stimulation strategies avoiding axonal stimulation it is necessary to image the evoked activity in single axons. In this work we electrically imaged axonal stimulation in ex vivo mouse retina using a high-density CMOS-based microelectrode array. We demonstrate signal propagation tracking via stimulus triggered average during high frequency (100 Hz) sinusoidal electrical stimulation.
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Tigerholm, 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. 9 (1 maggio 2014): 1721–35. http://dx.doi.org/10.1152/jn.00777.2012.
Abstract (sommario):
Action potential initiation and conduction along peripheral axons is a dynamic process that displays pronounced activity dependence. In patients with neuropathic pain, differences in the modulation of axonal conduction velocity by activity suggest that this property may provide insight into some of the pathomechanisms. To date, direct recordings of axonal membrane potential have been hampered by the small diameter of the fibers. We have therefore adopted an alternative approach to examine the basis of activity-dependent changes in axonal conduction by constructing a comprehensive mathematical model of human cutaneous C-fibers. Our model reproduced axonal spike propagation at a velocity of 0.69 m/s commensurate with recordings from human C-nociceptors. Activity-dependent slowing (ADS) of axonal propagation velocity was adequately simulated by the model. Interestingly, the property most readily associated with ADS was an increase in the concentration of intra-axonal sodium. This affected the driving potential of sodium currents, thereby producing latency changes comparable to those observed for experimental ADS. The model also adequately reproduced post-action potential excitability changes (i.e., recovery cycles) observed in vivo. We performed a series of control experiments replicating blockade of particular ion channels as well as changing temperature and extracellular ion concentrations. In the absence of direct experimental approaches, the model allows specific hypotheses to be formulated regarding the mechanisms underlying activity-dependent changes in C-fiber conduction. Because ADS might functionally act as a negative feedback to limit trains of nociceptor activity, we envisage that identifying its mechanisms may also direct efforts aimed at alleviating neuronal hyperexcitability in pain patients.
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Hwang, Jinyeon, e Uk Namgung. "Phosphorylation of STAT3 by axonal Cdk5 promotes axonal regeneration by modulating mitochondrial activity". Experimental Neurology 335 (gennaio 2021): 113511. http://dx.doi.org/10.1016/j.expneurol.2020.113511.
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Jamann, Nora, Merryn Jordan e Maren Engelhardt. "Activity-Dependent Axonal Plasticity in Sensory Systems". Neuroscience 368 (gennaio 2018): 268–82. http://dx.doi.org/10.1016/j.neuroscience.2017.07.035.
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Susuki, Keiichiro, e Hiroshi Kuba. "Activity-dependent regulation of excitable axonal domains". Journal of Physiological Sciences 66, n. 2 (13 ottobre 2015): 99–104. http://dx.doi.org/10.1007/s12576-015-0413-4.
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Ganguly, 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. 7 (30 maggio 2017): 2059–74. http://dx.doi.org/10.1083/jcb.201604028.
Abstract (sommario):
Soluble cytosolic proteins vital to axonal and presynaptic function are synthesized in the neuronal soma and conveyed via slow axonal transport. Our previous studies suggest that the overall slow transport of synapsin is mediated by dynamic assembly/disassembly of cargo complexes followed by short-range vectorial transit (the “dynamic recruitment” model). However, neither the composition of these complexes nor the mechanistic basis for the dynamic behavior is understood. In this study, we first examined putative cargo complexes associated with synapsin using coimmunoprecipitation and multidimensional protein identification technology mass spectrometry (MS). MS data indicate that synapsin is part of a multiprotein complex enriched in chaperones/cochaperones including Hsc70. Axonal synapsin–Hsc70 coclusters are also visualized by two-color superresolution microscopy. Inhibition of Hsc70 ATPase activity blocked the slow transport of synapsin, disrupted axonal synapsin organization, and attenuated Hsc70–synapsin associations, advocating a model where Hsc70 activity dynamically clusters cytosolic proteins into cargo complexes, allowing transport. Collectively, our study offers insight into the molecular organization of cytosolic transport complexes and identifies a novel regulator of slow transport.
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.
Abstract (sommario):
Le glioblastome (GB), une tumeur cérébrale d'origine gliale, est la tumeur primaire du système nerveux central la plus fréquente et la plus agressive chez l'adulte, avec un taux de survie médian de moins de 18 mois après un traitement standard. Ce mauvais pronostic est principalement lié au caractère invasif des cellules tumorales gliales, responsable des échecs thérapeutiques. Les faisceaux de substance blanche constituent une voie majeure d'invasion des gliomes, mais les mécanismes impliqués dans l'invasion des gliomes sont encore mal compris. Dans ce travail de thèse, des cellules de GB humain U87 ont été injectées dans des souris adultes Nude immunodéficientes. Cette lignée présente une masse tumorale circonscrite avec des colonnes d'invasion collective dans le parenchyme sain. L’invasion tumorale est majoritairement périvasculaire mais les cellules U87 contactent également les axones au sein de la substance blanche. Des dommages spécifiques de la substance blanche incluant des dommages axonaux avec une démyélinisation, ainsi qu’une hyperexcitabilité axonale péritumorale ont été mis en évidence. La modulation de l’activité axonale par une approche optogénétique indique que l’augmentation de l’activité axonale favorise l’invasion tumorale. Pour conclure, les dommages tissulaires et fonctionnels des faisceaux de fibres de la substance blanche constitue un microenvironnement favorable à la progression tumoraleGlioblastoma (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
2
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.
Abstract (sommario):
Au cours du développement du système nerveux, l'activité des cibles post-synaptiques permet le raffinement du nombre et de la force des connexions neuronales. En employant la jonction neuromusculaire de Caenorhabditis elegans comme système modèle, nous avons étudié deux aspects de la mise en place de ces connexions. D'une part, nous montrons que le nombre de récepteurs présents à la jonction neuromusculaire est contrôlé par l'activité musculaire : une augmentation de l'activation synaptique entraîne une régulation différentielle des trois types de récepteurs présents à la jonction neuromusculaire. D'autre part, nous avons étudié les changements de la morphologie de certains motoneurones de la tête du ver, appelés neurones SAB, en fonction de l’activité musculaire. Une diminution de l’activité musculaire durant une période critique du développement entraîne une surcroissance axonale des neurones SAB. À travers différentes approches, nous avons pu identifier la suppression de la surcroissance axonale dans des mutants où la biosynthèse des neuropeptides est perturbée. Enfin, nous avons mis en évidence que la surcroissance axonale apparait également lors de perturbations plus générales de la physiologie cellulaire, telles qu'un choc thermique ou la surexpression d'un transgène, ce qui suggère que le système SAB est plastique et particulièrement sensible au cours du développementThroughout 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
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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.
Abstract (sommario):
Les lésions du Système Nerveux Central, qu'elles soient accidentelles ou liées à une maladie, sont à l'origine de dégâts irréversibles. En effet, suite à la section des axones, il s'en suit un processus de cicatrisation. Cette « cicatrice gliale » constitue une barrière physique et chimique sollicitant de nombreux acteurs cellulaires et moléculaires. Les principales cellules la constituant sont les astrocytes, les oligodendrocytes, les microgliocytes et les fibroblastes. Ces cellules surexpriment les protéines de myéline et la sémaphorine 3A (Sema3A), des agents très inhibiteurs de la régénération nerveuse et de la croissance axonale. Par ailleurs, l'hyperactivité des microgliocytes est à l'origine de l'augmentation considérable de la quantité de radicaux libres oxygénés néfastes pour les neurones.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.
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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.
Abstract (sommario):
Pendant le développement, les projections axonales à longue distance se ramifient pour se connecter à leurs cibles. L’établissement et le remodelage de ces connexions est notamment régulé par l’activité neuronale. L’adaptation de la morphologie de l’axone nécessite alors des quantités importantes de matériel sécrétoire et de facteur trophiques comme le BDNF (brain derived neurotrophic factor). Ce matériel est transporté dans des vésicules le long de l’axone depuis le corps cellulaire où il est synthétisé, vers les sites actifs à l’extrémité de l’axone. Si le relargage de vésicules sécrétoires à la synapse est bien étudié, les mécanismes régulant le transport axonal par l’activité sont encore méconnus.Dans ce travail de thèse, nous avons dans un premier temps développé des outils permettant d’étudier les dynamiques intracellulaires dans des réseaux neuronaux. Nous avons ainsi développé une chambre microfluidique permettant de reconstruire in vitro des réseaux neuronaux physiologiques et compatibles avec de la vidéomicroscopie à haute résolution. Nous avons caractérisé l’établissement et la maturation du réseau et validé l’intérêt de ce dispositif microfluidique dans le contexte de la maladie de Huntington. Nous avons ensuite étudié l’évolution des dynamiques intracellulaires avec la maturation du réseau. Nous avons notamment observé une augmentation du transport axonal de vésicules sécrétoires en fonction de l'état de maturation du réseau neuronal. Ces premières observations ont renforcé l’hypothèse d’une régulation directe du transport axonal de vésicules sécrétoires par l’activité neuronale au cours du développement du réseau.Nous avons ainsi fait évoluer la plateforme microfluidique par l’ajout d’un réseau d’électrodes (MEA) qui permet d'étudier les dynamiques intracellulaires tout en contrôlant l’activité neuronale. A l’aide de ce système, nous avons identifié un groupe de vésicules sécrétoires ancré le long de l’axone et recruté en réponse à une haute activité neuronale en direction des sites présynaptiques actifs. Nous avons alors identifié les acteurs impliqués dans ce mécanisme dépendant de l’activité. Nous avons montré que la myosine Va permettait l’attachement des vésicules le long de l’axone dans des structures d’actine dynamique. L’activité neuronale induit une augmentation de calcium le long de l’axone, via l’activation des canaux calciques dépendant du voltage, qui régule la myosine Va et entraine le recrutement des vésicules stockées dans l’axone sur les microtubules. Une fois les acteurs identifiés, nous avons pu mettre en évidence le rôle de ce mécanisme dépendant de l’activité dans la formation de branches axonales pendant le développement. Enfin, nous avons confirmé l’existence de ce groupe de vésicules dépendant de l’activité et résidant dans l’axone in vivo grâce à la mise au point d'un système d’étude du transport axonal sur tranches aigües de cerveau en microscopie biphotonique.L’ensemble de ce travail propose de nouveaux outils in vitro et in vivo pour comprendre les régulations des dynamiques intracellulaires dans des réseaux neuronaux physiologiques. Grâce à ces outils, nous avons identifié un mécanisme de régulation local qui permet l'adressage rapide de facteurs trophiques vers les branches en développement en réponse à l’activité neuronaleDuring 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
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Leterrier, Christophe. "Activité constitutive et adressage axonal du récepteur cannabinoïque neurotal". Paris 6, 2006. https://tel.archives-ouvertes.fr/tel-00250338.
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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.
Abstract (sommario):
Thesis (Ph. D.)--University of California, San Diego, 2008.Title from first page of PDF file (viewed Nov. 5, 2008). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references.
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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.
Abstract (sommario):
L'activité constitutive est une propriété pharmacologique que possèdent de nombreuxrécepteurs couplés aux protéines G. Cependant, son rôle biologique reste largement inconnu.Nous avons étudié les relations entre la pharmacologie et le trafic intracellulaire du récepteurcannabinoïque CB1, un récepteur abondamment exprimé dans le cerveau qui possède uneactivité constitutive avérée. Exprimé dans les cellules HEK-293, l'activité constitutive durécepteur CB1 provoque un cycle continu d'endocytose et de recyclage du récepteur entre lamembrane plasmique et les endosomes intracellulaires : à l'équilibre, le récepteur CB1 estmajoritairement présent dans les endosomes. Le cycle fait intervenir une endocytose par puitsrecouverts de clathrine et un trafic intracellulaire dépendant de Rab5 et de Rab4, mais pas deRab11. Dans les neurones d'hippocampe en culture, ce cycle d'endocytose/recyclage durécepteur CB1 est limité au compartiment somatodendritique, et le récepteur est stable à lasurface de l'axone. Ce cycle dépend de l'activité constitutive du récepteur CB1 etl'endocytose sélective du récepteur dirige l'établissement de l'expression axonale durécepteur CB1 à la surface du neurone.
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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.
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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.
Abstract (sommario):
The complex wiring of the mammalian brain is established by accurate axonal guidance and synaptogenesis. These developmental processes are highly regulated by ligands and their corresponding cell surface receptors expressed on neurons. Unfortunately, the mature central nervous system (CNS) severely restricts neurite outgrowth following injury in part due to the presence of inhibitory ligands and receptors. The Nogo66 receptor (NgR1) is expressed by mature neurons and inhibits the regrowth of injured CNS neurons by binding to multiple inhibitory ligands. Further, NgR1 is highly expressed in synaptogenic areas such as the cortex and hippocampus where it regulates synaptic plasticity and restricts experience-dependent plasticity. Interestingly, NgR1 levels in neurons can be altered by proteolytic activity termed shedding, which is mediated by metalloproteinases. This process reduces cell surface full length NgR1 and generates a soluble dominant negative fragment, which has the potential to impact NgR1 function in the brain. My thesis focused on studying the impact of metalloproteinase induced shedding on NgR1 function. Herein I provide evidence that membrane anchored metalloproteinases can cleave NgR1 from neurons and attenuate responses to inhibitory cues. Membrane type metalloproteinases are expressed in the adult mouse brain and promote NgR1 shedding until late adulthood. NgR1 is shed from synaptosomes suggesting that this mechanism may regulate NgR1 function at the synapse. These results prompted us to investigate whether metalloproteinase activity can regulate axonal outgrowth through other cell surface proteins. We determined that membrane anchored metalloproteinases promote axonal outgrowth from CNS and PNS neurons. We identified several candidate targets by mass spectroscopy, which include the adhesive protein family IgLONs that are known to regulate axonal outgrowth. Together, the data presented here extends our understanding of metalloproteinase-dependent regulation of neurite outgrowth during development. In addition, our observations with NgR1 shedding by metalloproteinases suggest that this process is conserved in neurite outgrowth inhibition and restriction of synaptic plasticity.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.
10
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.
Libri sul tema "Activité axonale":
1
1953-, Angelov D. N., a cura di. Axonal branching and recovery of coordinated muscle activity after transection of the facial nerve in adult rats. Berlin: Springer, 2005.
2
Park, 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.
Abstract (sommario):
Axonal excitability techniques were developed to assess axonal resting membrane potential and ion channel function in vivo, and thereby provide greater molecular understanding of the activity of voltage gated ion channels and ion pumps underlying nerve and membrane function. Axonal excitability studies provide complimentary information to conventional nerve conduction studies, using submaximal stimuli to examine the properties underlying the excitability of the axon. Such techniques have been developed both as a research technique to examine disease pathophysiology and as a clinical investigation technique. This chapter provides an overview of axonal excitability techniques, addressing the role of key ion channels and pumps in membrane function and highlighting examples of clinical case studies, where such techniques have been utilized, including motor neuronopathies, tracking progression of chemotherapy-induced peripheral neuropathy, and assessing treatment response in chronic inflammatory demyelinating polyneuropathy.
3
Axonal 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.
4
Bhargava, Pavan, e Peter A. Calabresi. Multiple Sclerosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0087.
Abstract (sommario):
Multiple sclerosis is a chronic demyelinating neurological disorder of the brain and spinal cord, with both inflammatory and degenerative components. Current treatment strategies utilize immunomodulatory and immunosuppressive agents to reduce the inflammatory disease activity and retard accumulation of disability. Future challenges for treatment include identifying agents that will promote remyelination and axonal protection to help impact progressive forms of multiple sclerosis. This chapter discusses currently available disease modifying therapies, agents currently in phase 2/3 trials, and future directions in the treatment of multiple sclerosis.
5
Angelov, 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.
6
Roze, Emmanuel, e Frédéric Sedel. Gangliosidoses (GM1 and GM2). Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0050.
Abstract (sommario):
GM1 gangliosidosis is due to beta-galactosidase deficiency. The adult-onset form is characterized by progressive generalized dystonia, often associated with akineto-rigid Parkinsonism. Mild skeletal dysplasia and short stature are good diagnostic clues. GM2 gangliosidosis is due to beta-hexosaminidase deficiency. The adult-onset form is characterized by complex neurological disorders, in which features resulting from cerebellar and motor neuron dysfunction are the most frequent. Movement disorders, psychotic symptoms, mild pyramidal signs, axonal polyneuropathy, autonomic dysfunction, and vertical supranuclear palsy can also be observed. Clinical severity and the rate of progression both vary widely from one patient to another. Diagnosis is based on measurements of enzyme activity and molecular analysis. Physiotherapy, speech therapy and management of swallowing are crucial for these patients’ quality of life and prognosis.
7
Angelov, 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.
8
Gaetz, Michael B., e Kelly J. Jantzen. Electroencephalography. A cura di Ruben Echemendia e Grant L. Iverson. Oxford University Press, 2016. http://dx.doi.org/10.1093/oxfordhb/9780199896585.013.006.
Abstract (sommario):
Axonal injury is currently considered to be the structural substrate behind most concussion-related neurological dysfunction. Because the principal generators of EEG fields are graded excitatory and inhibitory synaptic potentials of pyramidal neurons, the EEG is well suited for characterizing large-scale functional disruptions associated with concussion induced metabolic and neurochemical changes, and for connecting those disruptions to deficits in behavior and cognition. This essay provides an overview of the use of EEG and newly developed analytical procedures for the measurement of functional impairment related to sport concussion. Elevations in delta and theta activity can be expected in a percentage of athletes and change in asymmetry and coherence may also be present. Newer techniques are likely to be of critical importance for understanding the anatomical and physiological basis of cognitive deficits and may provide additional insight into susceptibility to future injury. Computational modeling may advance our understanding of concussion.
9
Guo, 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.
Abstract (sommario):
The pathology of multiple sclerosis is complex, extends beyond the white matter plaque, and is influenced by stage of demyelinating activity, clinical course, disease duration, and treatment. Technological advances in immunology, molecular biology, and “omic” biology have provided novel insights into the mechanisms for development of white matter plaques, axonal damage, cortical demyelination, and disease progression. Detailed, systematic, and statistically rigorous pathological studies on clinically well-characterized MS cohorts have helped define the heterogeneous pathological substrates of MS and unravel the complex molecular pathogenic mechanisms, with the ultimate goal of identifying targets for therapeutic interventions. It is increasingly clear that the use of human tissues is imperative to improve current diagnostic, prognostic, and therapeutic modalities. Preclinical animal models have been invaluable for discovery of key immune processes, basic disease mechanisms, and candidate immune targeting strategies, but the conclusions have yet be reconciled with the essential features of the human disease.
10
Columb, Malachy O. Local anaesthetic agents. A cura di Michel M. R. F. Struys. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0017.
Abstract (sommario):
Local anaesthetic agents cause a pharmacologically induced reversible neuropathy characterized by axonal conduction blockade. They act by blocking the sodium ionophore and exhibit membrane stabilizing activity by inhibiting initiation and propagation of action potentials. They are weak bases consisting of three components: a lipophilic aromatic ring, a link, and a hydrophilic amine. The chemical link classifies them as esters or amides. Local anaesthetics diffuse through the axolemma as unionized free-base and block the ionophore in the quaternary ammonium ionized form. The speed of onset of block is therefore dependent on the pKa of the agent and the ambient tissue pH. Esters undergo hydrolysis by plasma esterases and amides are metabolized by hepatic microsomal mixed-function oxidases. Local anaesthetics are bound in the blood to α1-acid glycoproteins. Pharmacological potency is dependent on the lipid solubility of the drug as is the potential for systemic toxicity. The blood concentrations required to cause cardiovascular system (CVS) collapse and early central nervous system (CNS) toxicity are used to quantify the CVS:CNS toxicity ratio. Local anaesthetics also have the potential to induce direct neuronal damage. Intravenous lipid emulsion is used for the treatment of systemic toxicity but the scientific evidence is inconsistent. With regard to the pipecoloxylidine local anaesthetics, early evidence indicated that the S- was less toxic than the R-enantiomer. However, clinical research using minimum local analgesic concentration designs suggests that reduced systemic toxicity and motor block sparing is mainly explained by potency rather than enantiomerism.
Capitoli di libri sul tema "Activité axonale":
1
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.
2
Burke, 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.
3
Thanos, 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.
4
Troglio, 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.
Abstract (sommario):
One of the important questions in the research on neural coding is how the preceding axonal activity affects the signal propagation speed of the following one. We present an approach to solving this problem by introducing a multi-level spike count for activity quantification and fitting a family of linear regression models to the data. The best-achieved score is R2=0.89 and the comparison of different models indicates the importance of long and very short nerve fiber memory. Further studies are required to understand the complex axonal mechanisms responsible for the discovered phenomena.
5
"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.
6
Li, 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.
Abstract (sommario):
Abstract This chapter provides an overview of axonal mitochondrial trafficking/anchoring and their metabolic function in modulating synaptic efficacy and plasticity. Synaptic transmission is a key neuronal information process. Mitochondria are commonly localized at presynaptic terminals, where they sustain presynaptic function by producing ATP and buffering calcium. Given their extremely polarized geometry, neurons face exceptional challenges maintaining local ATP and Ca2+ homeostasis at distal presynapses that are constantly changing with altered synaptic activity. Mitochondrial transport in axons and their distribution at presynapses are correlated with synaptic activity. Therefore, precise control of axonal mitochondrial trafficking and positioning and their capacity in buffering calcium and supplying presynaptic energy or “synaptoenergetics” are critical for neurons to adapt to dynamic synaptic activity. Mitochondrial dysfunction and impaired trafficking have been implicated in major neurological disorders associated with bioenergetic failure. Investigation into the roles of mitochondria in synaptic transmission is an important research frontier.
7
Benarroch, Eduardo E. "Growth Factors, Survival, and Regeneration". In Neuroscience for Clinicians, a cura di Eduardo E. Benarroch, 213–30. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780190948894.003.0013.
Abstract (sommario):
Neurotrophic factors and hypoxia-inducible factors participate in fundamental processes including growth, differentiation, survival, and plasticity in the nervous system. They activate downstream cascades that promote protein synthesis and inhibit cell death mechanisms of apoptosis and autophagy. Axonal injury triggers retrograde neurotrophic signaling to the nucleus to regulate transcription of genes involved in axonal repair. Hypoxia induces expression of genes that control angiogenesis, erythropoiesis, and glycolysis. Growth factor and hypoxia-inducible signals are regulated by products of tumor suppressor genes. Excessive activation of these pathways lead to genetic tumor syndromes, many of them associated with epilepsy. Experimental models indicate that growth factors have neuroprotective effects against neurodegeneration. However, several human studies using growth factors administered systemically or via genetic methods have so far failed to show consistent beneficial effects. This has been attributed to inadequate dosing and delivery and enrollment of patients at late stage of disease. Approaches to promote axonal regeneration by targeting are an active area of research.
8
B.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.
Abstract (sommario):
Abstract Thus far we have been discussing the axonal membrane as if it had only two kinds of ion currents, a voltage—dependent potassium current that is responsible for the axon’s electrical activity (or rather its lack of activity) at rest, and a voltage-dependent sodium current that underlies the large and rapid membrane depolarization during the action potential. Although the work of Hodgkin and Huxley demonstrated that these two currents could provide a reasonably accurate picture of the electrical activity of the squid giant axon, it is now evident that there is a considerable diversity of ion currents in axons, and even greater diversity in neuronal cell bodies and dendrites.
9
Barresi, 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.
Abstract (sommario):
This chapter considers the neural crest as a transitory structure as its cells migrate to become many different cell types. The path a neural crest cell takes depends on the extracellular environment it meets. The chapter discusses the cranial neural crest cells that enter the pharyngeal arches to become the cartilage of the jaw and the bones of the middle ear and form the bones of the frontonasal process, odontoblasts, and cranial nerves. The chapter also highlights the fates of the cranial neural crest cells which are influenced by Hox genes, and are acquired by expression pattern through interaction with neighboring cells. The chapter covers proteins and shows how they are generally permissive to neuron adhesion and provide substrates on which axons can migrate. It stresses how the lack of synapse formation and neuronal activity can lead to induction apoptosis, which unleashes a cascade of caspase enzymes that result in cell death.
10
Filippi, 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.
Abstract (sommario):
Abstract Multiple sclerosis (MS) is the most common chronic inflammatory demyelinating disease affecting the central nervous system (CNS) of young adults in the western countries, leading, in the majority of the cases, to severe and irreversible clinical disability. Since its clinical introduction, conventional magnetic resonance imaging (cMRI — dual-echo and post-contrast T1-weighted scans) has greatly improved our ability to diagnose MS and to monitor its evolution, either natural or modified by treatment. CMRI-derived measures have indeed shown several advantages over clinical assessment, including their more objective nature and increased sensitivity to MS-related changes. Nevertheless, the magnitude of the relationship between cMRI measures of disease activity or burden and the clinical manifestations of the disease is weak (Fig. 11.1). This necessarily limits the role of cMRI for the understanding of MS pathophysiology and monitoring of experimental treatment. Several factors are likely to be responsible for this clinical/MRI discrepancy. First, dualecho imaging lacks specificity with regard to the heterogeneous pathological substrates of individual lesions and, as a consequence, does not allow an accurate quantification of tissue damage. Specifically, oedema, inflammation, demyelination, remyelination, gliosis, and axonal loss all lead to a similar appearance of hyperintensity on T2-weighted images. This is a major issue now that there is compelling evidence that: (a) inflammatory demyelination is not enough to explain ‘fixed’ neurological deficits in MS; (b) irreversible axonal damage does occur in inflamed MS lesions; and (c) axonal damage is the main contributor to the clinical manifestations of the disease and to its clinical worsening over time. Secondly, T2-weighted images do not delineate tissue damage occurring in the normal-appearing white matter (NAWM), which usually represents a large portion of the brain tissue from MS patients and which is known to be damaged in MS patients. Post-mortem studies have shown subtle changes in the NAWM from MS patients, which not only include diffuse astrocytic hyperplasia, patchy oedema, and perivascular cellular infiltration, but also axonal damage. Finally, dual-echo imaging does not provide an accurate picture of gray matter (GM) damage, which several pathological studies have shown to be prominent in MS and which is likely to be associated with some clinical manifestations of the disease, such as cognitive impairment and fatigue.
Atti di convegni sul tema "Activité axonale":
1
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, a cura di Daniel L. Farkas, Robert C. Leif e Dan V. Nicolau. SPIE, 2007. http://dx.doi.org/10.1117/12.698309.
2
Tamatani, 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.
3
Xu, 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.
Abstract (sommario):
Cilia are thin subcellular organelles that bend actively to propel fluid. The ciliary cytoskeleton (the axoneme) consists of nine outer microtubule doublets surrounding a central pair of singlet microtubules. Large bending deformations of the axoneme involve relative sliding of the outer doublets, driven by the motor protein dynein. Ciliary structure and function have been studied extensively, but details of the mechanics and coordination of the axoneme remain unclear. In particular, dynein activity must be switched on and off at specific times and locations to produce an oscillatory, propulsive beat. Leading hypotheses assert that mechanical feedback plays a role in the control of dynein activity, but these ideas remain speculative.
4
Nakagawa, 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.
Abstract (sommario):
In this study, we aimed to develop a computer-aided simulation technique to predict the axonal extension in the neuronal network evolution processes for design new scaffolds to activate the nerve cell and promote the nerve regeneration. We developed a mathematical model of axonal extension by using phase-field method and evaluated the validity of the mathematical model by comparison with the experiments. In the previous experimental studies, the peripheral nerve scaffold has been introduced to guide the axonal extension. Damaged part of nerve was replaced by the artificial tube as the scaffold to induce the axonal growth through the artificial tube and regenerate the nerve network. However, the scaffold made of biodegradable materials has a problem that it is degraded and absorbed before the nerve regenerate, and then the nerve cannot regenerate. Therefore, there is a need for the design and development of a scaffold for nerve regeneration to promote nerve regeneration. For that purpose, it is necessary to understand the difference between the axonal extensions by the surrounding environment, such as the shape or materials of the scaffold for nerve regeneration. In particular, the numerical technique to analyze the remodeling process of the nerve in the scaffold is strongly required to be established because the in-vivo experimental observation technology at the micro scale, bioethical issues in the animal experiment and requires time and money are also remained as unresolved problems. In this study, we developed a new simulation code which employed the phase-field method to predict the two-dimensional dendritic and axonal growth processes of nerve cells on cultivation scaffolds. We curried out the phase-field analyses to make clear how the parameters of Kobayashi–Warren–Carter (KWC) phase-field model affected on the morphologic growths of dendrite and axon. Simultaneously, we had observed the axonal extension process by using the PC-12D cells with nerve growth factor (NGF) on two-dimensional cultivation dish. Based on these axonal extension observation results, we approximated the morphological changes and establish the phenomenological model for phase-field analysis. Finally, we confirmed the validity of our newly developed phase-field simulation scheme in two dimensions by comparison with the experiments.
5
Parca, 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.
Abstract (sommario):
Background: GBS is an acute inflammatory polyneuropathy resulting from an immune response after infection. Characterized as an ascetic, progressive, selflimiting flaccid tetraparesis. It has several phenotypic presentations, which one is AMAN. The treatment’s based on use of intravenous immunoglobulin (IGIV) and plasmapheresis (PLEX). Methods: A literature review of the PubMed and UpToDate databases using descriptors “GBS” and “AMAN” between 2014-2020. Objectives: Report a case of GBS, addressing AMAN variant; a literature review with therapeutic and diagnostic possibilities. Case report: DTS, 32y, male, admitted with a picture of flaccid, limp asymmetrical tetraparesis, with an asymmetrical pattern, predominant in lower limbs, without sensory symptoms. Progressive evolution, onset of motor symptoms on the 8th day after self-limited diarrhea. CSF on 3rd day of onset of motor symptoms without dissociation cytological protein - CN: 62 / Ptn: 80.1mg / dl. Repeated CSF on the 10th day with CN: 27 / Ptn: 215 mg / dl. electroneuromyography 16/04: electrophysiological examination shows motor neuropathy of axonal pattern with signs of denervation in activity, findings compatible with axonal neuropathy. IGIV was performed for 5 days, without complications. Results: The diagnosis of GBS is based on CSF clinical criteria and findings on electroneuromyography. AMAN is a phenotypic variant characterized by purely motor and axonal impairment. The therapeutic options proven effectiveness are PLEX, and IGIV. Conclusion: Studies demonstrates that there’s no difference in effectiveness between PLEX and IGIV, the choice of treatment being dependent on socioeconomic and patient-related factors.
6
Nicholson, 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.
Abstract (sommario):
The annual incidence for neck pain in the adult population is 30–50% [1]. The cervical nerve roots are at risk for mechanical injury due to impingement of surrounding structures which can result in pain and numbness [2]. During nerve root compression, an immediate, brief increase in spontaneous afferent activity and a gradual decrease in electrically evoked axonal conduction have been reported [3,4]. Although previous studies demonstrate that a transient cervical nerve root compression induces persistent behavioral sensitivity [5,6], it is not known how the tissue mechanics during loading modulate neuronal function or how they relate to the onset of pain. Therefore, the goal of this study was to quantify neuronal activity in the spinal cord as a function of the duration of applied compression by measuring both electrically-evoked and spontaneous afferent activity during a transient compression of the cervical nerve root in a rat model of pain [5,6].
7
Bayly, 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.
Abstract (sommario):
Flagella are active, beam-like, sub-cellular organelles that use wavelike oscillations to propel the cell. The mechanisms underlying the coordinated beating of flagella remain incompletely understood despite the fundamental importance of these organelles. The axoneme (the cytoskeletal structure of flagella) consists of microtubule doublets connected by passive and active elements. The motor protein dynein is known to drive active bending, but dynein activity must be regulated to generate oscillatory, propulsive waveforms. Mathematical models of flagella motion generate quantitative predictions that can be analyzed to test hypotheses concerning dynein regulation. Here we investigate the emergence of unstable modes in a mathematical model of flagella motion with feedback from inter-doublet separation (the “geometric clutch” or GC model). The unstable modes predicted by the model may be used to critically evaluate the underlying hypothesis. The least stable mode of the GC model exhibits switching at the base and robust base-to-tip propagation.