Academic literature on the topic 'Membrane neuronale'
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Journal articles on the topic "Membrane neuronale"
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Simone, I. L., C. Tortorella, F. Federico, et al. "Contributo della risonanza magnetica spettroscopica del protone (1H-RMS) nella infezione da HIV." Rivista di Neuroradiologia 13, no. 1 (2000): 51–56. http://dx.doi.org/10.1177/197140090001300109.
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È stato condotto uno studio combinato di RMI e 1H-RMS (Magnetom Siemens 1,5 Tesla) in 60 pazienti sieropositivi per HIV (n. 25 encefalopatie-HIV correlate, n. 20 toxoplasmosi, n. 8 PML, n. 7 linfomi) e 22 controlli neurologici sieronegativi per HIV. Gli spettri sono stati acquisiti su volumi singoli localizzati su lesioni focali in toxoplasmosi, PML, linfomi o su lesioni diffuse nelle encefalopatie da HIV (sequenza Spin Echo, TE 135 ms). In tutti i sottogruppi HIV si è evidenziato un significativo decremento del rapporto NAA/Cr rispetto ai controlli neurologici, suggerendo un danno neuronale e/o assonale indipendentemente dall'eziologia. Tuttavia il rapporto NAA/Cr era più basso nelle PML e nei linfomi. Un significativo incremento del rapporto Cho/Cr era rilevato nelle encefalopatie da HIV, nelle PML e in particolare nei linfomi ove tale incremento era associato alla presenza del segnale dei lipidi, marker entrambi di un aumentato turnover e sintesi di membrane cellulari. Nelle PML si rilevava infine con elevata frequenza il segnale del lattato. I dati confermano una elevata sensibilità della 1H-RMS nel rilevare una compromissione metabolica cerebrale in corso di infezione da HIV. Nonostante una globale scarsa specificità nel discriminare lesioni di differente eziologia, determinati pattern metabolici possono risultare di supporto alla RMI per la diagnosi eziologica di alcune lesioni, per esempio di PML.
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Martínez-Reyes, Harold, and Antonio Eblen-Zajjur. "Evaluación in silico del efecto de benzodiacepinas, ketamina y termo-dependencia sobre los patrones de descarga neuronal pre-Bötzinger de control respiratorio." Archivos de Neurociencias 23, no. 2 (2020): 25–35. http://dx.doi.org/10.31157/an.v23i2.8.
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Introducción: la fiebre y el uso de drogas como las benzodiacepinas (agonistas GABAA) y la ketamina (antagonista NMDA) se presentan con relativa frecuencia en anestesiología. La respiración es un patrón generado en el tallo cerebral, producto de una red compleja de centros ponto-medulares, que controlan las motoneuronas respiratorias gracias a la interacción de las neuronas inspiratorias del complejo pre-Bötzinger y las espiratorias del complejo Bötzinger. Estas neuronas poseen receptores de membrana del tipo GABAA y NMDA, que muestran alta termodependencia, sin embargo; se desconoce los cambios en el patrón de descarga neuronal inducidos por estas drogas y los cambios de temperatura corporal.
 Materiales y métodos: se generó un modelo validado de neurona Pre-inspiratoria (complejo pre-Bötzinger) incrementándose el peso sináptico gabaérgico equivalente al efecto de las benzodiacepinas o se redujo el peso sináptico NMDA equivalente al efecto de la ketamina en condiciones de hipo (35°C), normo (37°C) e hipertermia (40°C); cuantificándose el número y amplitud de las descargas neuronales. 
 Resultados: el aumento del peso sináptico GABAA o la reducción del de NMDA a temperaturas de 35°C, 37°C o 40°C redujo proporcionalmente el número de espigas y la amplitud del potencial de acción de la neurona Pre-I, mostrando curvas dosis-respuesta polinomiales de 2do. Orden, siendo las pendientes mayores a 35°C y a 40°C. 
 Conclusión: el efecto de benzodiacepinas o de ketamina a través de sus receptores GABAA y NMDA modifican in silico el patrón de descarga de la neurona Pre-I del núcleo Pre-Bötzinger, mostrando predominio del efecto gabaérgico y mayor termodependencia en las curvas dosis-respuesta en hipo e hipertermia lo que respalda el interés clínico de los datos.
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Martínez-Reyes, Harold, and Antonio Eblen-Zajjur. "Evaluación in silico del efecto de benzodiacepinas, ketamina y termo-dependencia sobre los patrones de descarga neuronal pre-Bötzinger de control respiratorio." Archivos de Neurociencias 23, no. 2 (2020): 25–35. http://dx.doi.org/10.31157/archneurosciencesmex.v23i2.8.
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Introducción: la fiebre y el uso de drogas como las benzodiacepinas (agonistas GABAA) y la ketamina (antagonista NMDA) se presentan con relativa frecuencia en anestesiología. La respiración es un patrón generado en el tallo cerebral, producto de una red compleja de centros ponto-medulares, que controlan las motoneuronas respiratorias gracias a la interacción de las neuronas inspiratorias del complejo pre-Bötzinger y las espiratorias del complejo Bötzinger. Estas neuronas poseen receptores de membrana del tipo GABAA y NMDA, que muestran alta termodependencia, sin embargo; se desconoce los cambios en el patrón de descarga neuronal inducidos por estas drogas y los cambios de temperatura corporal.
 Materiales y métodos: se generó un modelo validado de neurona Pre-inspiratoria (complejo pre-Bötzinger) incrementándose el peso sináptico gabaérgico equivalente al efecto de las benzodiacepinas o se redujo el peso sináptico NMDA equivalente al efecto de la ketamina en condiciones de hipo (35°C), normo (37°C) e hipertermia (40°C); cuantificándose el número y amplitud de las descargas neuronales. 
 Resultados: el aumento del peso sináptico GABAA o la reducción del de NMDA a temperaturas de 35°C, 37°C o 40°C redujo proporcionalmente el número de espigas y la amplitud del potencial de acción de la neurona Pre-I, mostrando curvas dosis-respuesta polinomiales de 2do. Orden, siendo las pendientes mayores a 35°C y a 40°C. 
 Conclusión: el efecto de benzodiacepinas o de ketamina a través de sus receptores GABAA y NMDA modifican in silico el patrón de descarga de la neurona Pre-I del núcleo Pre-Bötzinger, mostrando predominio del efecto gabaérgico y mayor termodependencia en las curvas dosis-respuesta en hipo e hipertermia lo que respalda el interés clínico de los datos.
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Morelli, Sabrina, Antonella Piscioneri, Enrico Drioli, and Loredana De Bartolo. "Neuronal Differentiation Modulated by Polymeric Membrane Properties." Cells Tissues Organs 204, no. 3-4 (2017): 164–78. http://dx.doi.org/10.1159/000477135.
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In this study, different collagen-blend membranes were successfully constructed by blending collagen with chitosan (CHT) or poly(lactic-co-glycolic acid) (PLGA) to enhance their properties and thus create new biofunctional materials with great potential use for neuronal tissue engineering and regeneration. Collagen blending strongly affected membrane properties in the following ways: (i) it improved the surface hydrophilicity of both pure CHT and PLGA membranes, (ii) it reduced the stiffness of CHT membranes, but (iii) it did not modify the good mechanical properties of PLGA membranes. Then, we investigated the effect of the different collagen concentrations on the neuronal behavior of the membranes developed. Morphological observations, immunocytochemistry, and morphometric measures demonstrated that the membranes developed, especially CHT/Col30, PLGA, and PLGA/Col1, provided suitable microenvironments for neuronal growth owing to their enhanced properties. The most consistent neuronal differentiation was obtained in neurons cultured on PLGA-based membranes, where a well-developed neuronal network was achieved due to their improved mechanical properties. Our findings suggest that tensile strength and elongation at break are key material parameters that have potential influence on both axonal elongation and neuronal structure and organization, which are of fundamental importance for the maintenance of efficient neuronal growth. Hence, our study has provided new insights regarding the effects of membrane mechanical properties on neuronal behavior, and thus it may help to design and improve novel instructive biomaterials for neuronal tissue engineering.
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Dasgupta, Raktim, Markus S. Miettinen, Nico Fricke, Reinhard Lipowsky, and Rumiana Dimova. "The glycolipid GM1 reshapes asymmetric biomembranes and giant vesicles by curvature generation." Proceedings of the National Academy of Sciences 115, no. 22 (2018): 5756–61. http://dx.doi.org/10.1073/pnas.1722320115.
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The ganglioside GM1 is present in neuronal membranes at elevated concentrations with an asymmetric spatial distribution. It is known to generate curvature and can be expected to strongly influence the neuron morphology. To elucidate these effects, we prepared giant vesicles with GM1 predominantly present in one leaflet of the membrane, mimicking the asymmetric GM1 distribution in neuronal membranes. Based on pulling inward and outward tubes, we developed a technique that allowed the direct measurement of the membrane spontaneous curvature. Using vesicle electroporation and fluorescence intensity analysis, we were able to quantify the GM1 asymmetry across the membrane and to subsequently estimate the local curvature generated by the molecule in the bilayer. Molecular-dynamics simulations confirm the experimentally determined dependence of the membrane spontaneous curvature as a function of GM1 asymmetry. GM1 plays a crucial role in connection with receptor proteins. Our results on curvature generation of GM1 point to an additional important role of this ganglioside, namely in shaping neuronal membranes.
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Nakada, C., Kenneth Ritchie, T. Fujiwara, et al. "LS3A1 Diffusion barrier in the neuronal cell membrane : a single molecule study." Seibutsu Butsuri 42, supplement2 (2002): S223. http://dx.doi.org/10.2142/biophys.42.s223_4.
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SARRADIN, P., P. BERTHON, and F. LANTIER. "Le point sur l’épidémiologie et la physiopathologie des encéphalopathies spongiformes des ruminants." INRAE Productions Animales 10, no. 2 (1997): 123–32. http://dx.doi.org/10.20870/productions-animales.1997.10.2.3988.
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L’épidémie d’encéphalopathie spongiforme bovine (ESB) résulte de la consommation par les bovins de farines de viandes et d’os contaminées. En recyclant l’agent infectieux, ces farines ont permis d’amplifier la dissémination d’une maladie dont l’origine et l’agent responsable demeurent inconnus. Les hypothèses sur la nature protéique ou/et virale de l’agent sont évoquées, ainsi que l’éventualité d’une transmission à l’homme. Une grande partie de nos connaissances des encéphalopathies spongiformes résulte des études réalisées de longue date sur la tremblante des ovins. En particulier, l’idée que l’on peut se faire de la physiopathologie de l’infection des bovins est en grande partie extrapolée à partir du résultat d’infections expérimentales réalisées chez le mouton. Toutefois, la contamination des tissus lymphoïdes périphériques, qui est la règle au cours de la phase de dissémination dans l’organisme de l’agent de la tremblante, semble absente dans le cas de la maladie bovine. Il est donc possible que ce type de tissus, considéré comme infectieux en matière de tremblante, le soit peu au cours de la phase préclinique dans le cas de l’ESB. L’atteinte du système nerveux central des bovins pourrait alors résulter d’une dissémination empruntant les voies nerveuses.
 Les mécanismes conduisant à la mort neuronale responsable des symptômes observés restent mal connus. La protéine PrP, protéine normale de la membrane de nombreux types cellulaires, et qui s’accumule sous sa forme pathologique PrPSC au niveau des lésions est indispensable au processus pathologique. Son polymorphisme influence considérablement le devenir de l’infection, mais elle ne peut être tenue pour seule responsable de la transmission de la maladie.
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Chen, Yuejun, Feifei Wang, Hui Long, Ying Chen, Ziyan Wu, and Lan Ma. "GRK5 promotes F-actin bundling and targets bundles to membrane structures to control neuronal morphogenesis." Journal of Cell Biology 194, no. 6 (2011): 905–20. http://dx.doi.org/10.1083/jcb.201104114.
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Neuronal morphogenesis requires extensive membrane remodeling and cytoskeleton dynamics. In this paper, we show that GRK5, a G protein–coupled receptor kinase, is critically involved in neurite outgrowth, dendrite branching, and spine morphogenesis through promotion of filopodial protrusion. Interestingly, GRK5 is not acting as a kinase but rather provides a key link between the plasma membrane and the actin cytoskeleton. GRK5 promoted filamentous actin (F-actin) bundling at the membranes of dynamic neuronal structures by interacting with both F-actin and phosphatidylinositol-4,5-bisphosphate. Moreover, separate domains of GRK5 mediated the coupling of actin cytoskeleton dynamics and membrane remodeling and were required for its effects on neuronal morphogenesis. Accordingly, GRK5 knockout mice exhibited immature spine morphology and deficient learning and memory. Our findings identify GRK5 as a critical mediator of dendritic development and suggest that coordinated actin cytoskeleton and membrane remodeling mediated by bifunctional actin-bundling and membrane-targeting molecules, such as GRK5, is crucial for proper neuronal morphogenesis and the establishment of functional neuronal circuitry.
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Harrison, R., A. Jehanli, G. G. Lunt, and J. Rutter. "Autoantibodies to neuronal membranes in motor neurone disease." Journal of Neuroimmunology 16, no. 1 (1987): 71. http://dx.doi.org/10.1016/0165-5728(87)90238-4.
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Sotnikov, Oleg S., Svetlana S. Sergeeva, and Tat'yana I. Vasyagina. "NEURONAL-GLIAL MEMBRANE CONTACTS DURING PESSIMAL ELECTRICAL STIMULATION." Morphological newsletter 28, no. 3 (2020): 35–50. http://dx.doi.org/10.20340/mv-mn.2020.28(3):35-50.
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After the creation of a method for obtaining inter-neuronal gap junctions in a nervous system devoid of glia, it is expedient to reproduce gap neuronal-glial contacts on a model that also contains hybrid neuronal-glial gap junctions, which, as you know, are functionally fundamentally different from inter-neuronal contacts. The experiments were carried out on the truncus sympathicus ganglia of laboratory rats using pessimal electrical stimulation and transmission electron microscopy. Electrical activation of ganglia with a frequency of up to 100 Hz revealed local and widespread variants of various neuronal-glial connections (contacts, bridges), fringed with peri-membrane filamentous proteins. They had a blurred veil that masked two-layer neuro-membranes. Some of the contacts resembled slit or dense 5-layer structures without a visible inter-neuronal slit, but with an extreme decrease in the thickness of the contact slit. The main result of the experiments was the formation, in addition to slotted, multiple septate (ladder) contacts. Relatively independent aggregates of the electron-dense substance of the septa were located inside the intercellular gaps, crossing both adjacent membranes, and, possibly, permeate of them. Near-membrane, poorly outlined pyramid-like protein cones associated with both cell membranes were also formed. Such membranes appeared to be dotted-dashed, that is, not continuous. A significant number of septic contact membranes had endocytic invaginations (invaginations) facing neuroplasm with pyramid-like marginal projections. All reactive altered structures that have arisen de novo are considered by the authors as developed under the influence of frequency electrical stimulation of denaturation and aggregation of intrinsic and perimembrane proteins.
Dissertations / Theses on the topic "Membrane neuronale"
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Woiterski, Lydia. "Meeting at the Membrane – Confined Water at Cationic Lipids & Neuronal Growth on Fluid Lipid Bilayers." Doctoral thesis, Universitätsbibliothek Leipzig, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-132933.
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Die Zellmembran dient der Zelle nicht nur als äußere Hülle, sondern ist auch an einer Vielzahl von lebenswichtigen Prozessen wie Signaltransduktion oder Zelladhäsion beteiligt. Wasser als integraler Bestandteil von Zellen und der extrazellulären Matrix hat sowohl einen großen Einfluss auf die Struktur von Biomolekülen, als auch selbst besondere Merkmale in eingschränkter Geometrie. Im Rahmen dieser Arbeit wurden zwei Effekte an Modellmembranen untersucht: Erstens der Einfluss des Gegenions an kationischen Lipiden (DODAX, X = F, Cl, Br, I) auf die Eigenschaften des Grenzflächenwassers und zweitens das Vermögen durch Viskositätsänderungen das Wachstum von Nervenzellen anzuregen sowie die einzelnen Stadien der Bildung von neuronalen Netzwerken und deren Optimierung zu charakterisieren.
Lipidmultischichten und darin adsorbiertes Grenzflächenwasser wurden mittels Infrarotspektroskopie mit abgeschwächter Totalreflexion untersucht. Nach Charakterisierung von Phasenverhalten und Wasserkapazität der Lipide wurden die Eigenschaften des Wassers durch kontrollierte Hydratisierung bei einem Wassergehalt von einem Wassermolekül pro Lipid verglichen. Durch die geringe Wasserkapazität können in diesem besonderen System direkte Wechselwirkungen zwischen Lipiden und Wasser aus der ersten Hydratationsschale beobachtet werden. Bemerkenswert strukturierte OH-Streckschwingungsbanden in Abhängigkeit des Anions und niedrige IR-Ordnungsparameter zeigen, dass stark geordnete, in ihrer Mobilität eingeschränkte Wassermoleküle an DODAX in verschiedenen Populationen mit unterschiedlich starken Wasserstoffbrückenbindungen
existieren und sich vermutlich in kleinen Clustern anordnen.
Die zweite Fragestellung hatte zum Ziel, das Wachstum von Nervenzellen auf Membranen zu beleuchten. Auf der Ebene einzelner Zellen wurde untersucht, ob sich in Analogie zu den bisher verwendeten elastischen Substraten, die Viskosität von Membranen
als neuartiger physikalischer Stimulus dafür eignet, das mechanosensitive Verhalten von Neuronen zu modulieren. Das Wachstum der Neuronen wurde auf substrat- und
polymergestützten Lipiddoppelschichten mittels Phasenkontrastmikroskopie beobachtet. Die Quantifizierung der Neuritenlängen, -auswuchsgeschwindigkeiten und
-verzweigungen zeigten kaum signifikante Unterschiede. Diffusionsmessungen (FRAP) ergaben, dass entgegen der Erwartungen, die Substrate sehr ähnliche Fluiditäten aufweisen.
Die Betrachtung der zeitlichen Entwicklung des kollektiven Neuronenwachstums, also der Bildung von komplexen Netzwerken, offenbarte robuste „Kleine-Welt“-Eigenschaften und darüber hinaus unterschiedliche Stadien. Diese wurden durch graphentheoretische
Analyse beschrieben, um anhand typischer Größen wie dem Clusterkoeffizienten und der kürzesten Pfadlänge zu zeigen, wie sich die Neuronen in einem frühen Stadium vernetzen, im Verlauf eine maximale Komplexität erreichen und letztlich das Netzwerk durch effiziente Umstrukturierung hinsichtlich kurzer Pfadlängen
optimiert wird.
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Ferreira, Brigham Marco Paulo. "Nonstationary Stochastic Dynamics of Neuronal Membranes." Thesis, Paris 6, 2015. http://www.theses.fr/2015PA066111/document.
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Les neurones interagissent à travers leur potentiel de membrane qui a en général une évolution temporelle complexe due aux nombreuses entrées synaptiques irrégulières reçues. Cette évolution est mieux décrite en termes probabilistes, en raison de ces entrées irrégulières ou «bruit synaptique». L'évolution temporelle du potentiel de membrane est stochastique mais aussi déterministe: stochastique, car conduite par des entrées synaptiques qui arrivent de façon aléatoire dans le temps, et déterministe, car un neurone biologique a une évolution temporelle très similaire quand soumis à une même séquence d'entrées synaptiques. Nous étudions les propriétés statistiques d'un modèle simplifié de neurone soumis à des entrées à taux variable d'où en résulte l'évolution non-stationnaire du potentiel de membrane. Nous considérons un modèle passif de membrane neuronale, sans mécanisme de décharge neuronale, soumis à des entrées à courant ou à conductance sous la forme d'un processus de «shot noise». Les fluctuations du potentiel de membrane sont aussi modélisées par un processus stochastique similaire, de «shot noise» filtré. Nous avons analysé les propriétés statistiques de ces processus dans le cadre des transformations de processus ponctuels de Poisson. Des propriétés de ces transformations sont dérivées les statistiques non-stationnaires du processus. Nous obtenons ainsi des expressions analytiques exactes pour les moments et cumulants du processus filtré dans le cas général des taux d'entrée variables. Ce travail ouvre de nombreuses perspectives pour l'analyse de neurones dans les conditions in vivo, en présence d'entrées synaptiques intenses et bruitées<br>Neurons interact through their membrane potential that generally has a complex time evolution due to numerous irregular synaptic inputs received. This complex time evolution is best described in probabilistic terms due to this irregular or "noisy" activity. The time evolution of the membrane potential is therefore both stochastic and deterministic: it is stochastic since it is driven by random input arrival times, but also deterministic, since subjecting a biological neuron to the same sequence of input arrival times often results in very similar membrane potential traces. In this thesis, we investigated key statistical properties of a simplified neuron model under nonstationary input from other neurons that results in nonstationary evolution of membrane potential statistics. We considered a passive neuron model without spiking mechanism that is driven by input currents or conductances in the form of shot noise processes. Under such input, membrane potential fluctuations can be modeled as filtered shot noise currents or conductances. We analyzed the statistical properties of these filtered processes in the framework of Poisson Point Processes transformations. The key idea is to express filtered shot noise as a transformation of random input arrival times and to apply the properties of these transformations to derive its nonstationary statistics. Using this formalism we derive exact analytical expressions, and useful approximations, for the mean and joint cumulants of the filtered process in the general case of variable input rate. This work opens many perspectives for analyzing neurons under in vivo conditions, in the presence of intense and noisy synaptic inputs
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Morisset, Valérie. "Plasticité fonctionnelle dans la moelle épinière : caractéristiques et neuromodulation des propriétés membranaires intrinsèques des neurones de la corne dorsale." Bordeaux 2, 1999. http://www.theses.fr/1999BOR28644.
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Colin, Isabelle. "Formation de la membrane postsynaptique neuronale chez le rat : analyse morphologique de la mise en place des recepteurs glycinergiques centraux." Paris 6, 1997. http://www.theses.fr/1997PA066636.
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La formation des agregats de recepteurs de la glycine (rgly) postsynaptiques stabilises par une molecule associee (la gephyrine) a ete analysee par une etude immunocytochimique effectuee au cours du developpement in vitro et in vivo de la moelle epiniere de rat. Nous avons analyse ; i) les distributions cellulaires et subcellulaires des agregats de rgly et de gephyrine ; ii) les densites de leurs marquages postsynaptiques ; et ii) la nature des neurotransmetteurs inhibiteurs (glycine, gaba) presents dans les terminaisons presynaptiques a la gephyrine. In vitro nous avons caracterise l'etablissement de synapses morphologiquement definies et mis en evidence par immunofluorescence que la gephyrine est exprimee avant leur formation et avant le rgly. Elle forme des agregats cytoplasmiques des le premier jour in vitro (div) et membranaires des 3div. La quantification en microscopie confocale indique qu'a 5div la gephyrine est plus exprimee que le rgly. En microscopie electronique les agregats de gephyrine observes a 5div sont cytoplasmiques et membranaires, puis ils sont postsynaptiques des 7div. In vivo (cornes ventrales de moelle cervicale), comme in vitro, la gephyrine est exprimee en premier et a p0 elle est plus exprimee que le rgly. Chez l'embryon, elle forme des agregats cytoplasmiques et membranaires des e13 et est postsynaptique des e17. Nous avons evalue ; i) a 1,96 et 1,77 l'augmentation de leurs densites postsynaptiques respectives entre po et l'adulte ; et ii) a po 87% des terminaisons presynaptiques a la gpehyrine contiennent de la glycine et 50% egalement du gaba. Ceci indique que des po des synapses expriment la glycine et la gephyrine mais pas le rgly. Notre modele d'expression sequentielle du rgly et de la gephyrine conduisant a une complementarite fonctionnelle des elements pre et postsynaptiques propose que la gephyrine serait exprimee dans des synapses glycinergiques, le rgly s'accumulerait ensuite dans ces meme membranes postsynaptiques par une diffusion-trap ou par un transport specifique.
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Vigier, Maxime. "Influence des lipides membranaires sur les interactions protéiques liées aux anomalies endolysosomales dans un modèle neuronal de la maladie d'Alzheimer." Electronic Thesis or Diss., Université de Lorraine, 2022. http://www.theses.fr/2022LORR0331.
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La maladie d'Alzheimer (MA) est une pathologie complexe et multifactorielle pour laquelle il n'existe actuellement aucun traitement. Plusieurs hypothèses ont été proposées pour expliquer l'apparition et la progression de cette maladie, dont la cascade amyloïde, qui prédomine dans le domaine de la recherche depuis 30 ans. La voie amyloïdogène nécessite l'endocytose de la protéine APP dans les endosomes précoces où elle subit deux clivages protéolytiques, d'abord par la β-sécrétase pour produire le fragment C99, puis par la γ-sécrétase pour produire le peptide Aβ. L'une des hypothèses actuelles est que les anomalies de l'endocytose et le dysfonctionnement du système endolysosomal dans les neurones constitueraient un des mécanismes neuropathologiques précoces de la MA, bien avant la cascade neurotoxique générée par Aβ et les dépôts amyloïdes. Nous défendons l'hypothèse que des modifications de l'organisation membranaire, notamment au cours du vieillissement ou dues à des déséquilibres lipidiques, pourraient exacerber ou favoriser ces dysfonctionnements. Pour cette étude, nous avons utilisé un modèle de neuroblastome humain surexprimant la protéine mutante APPswe. Nous avons tout d'abord vérifié la présence d'anomalies endolysosomales typiques de la MA (endosomes hypertrophiés, trafic vésiculaire bloqué), auxquelles nous avons également associé une faible production d'exosomes, conditions de stress chronique que nous avons corrélées à la mort neuronale. Incriminant dans un premier temps une production continue d'Aβ dans ces cellules, nous avons cherché à réduire son impact en inhibant l'activité γ-sécrétase. Cela n'a pas amélioré le stress, mais l'a au contraire aggravé, ce qui nous a conduit à considérer que c'est le fragment C99 de l'APP, c'est-à-dire le substrat de la production d'Aβ, qui est le produit amyloïde central de la cascade neurotoxique observée dans les cellules surexprimant l'APP. Les effets délétères du C99 doivent se produire avant ceux de l'Aβ, expliquant la précocité connue des altérations endolysosomales. S'accumulant à la suite de l'inhibition de la γ-sécrétase, le fragment C99 interagit davantage avec la protéine Rab5, spécifique de l'endosome précoce. La maturation de cette dernière est ainsi empêchée, bloquant le trafic vésiculaire du système endolysosomal. Comme les interactions entre C99 et Rab5 se produisent au niveau de la membrane des endosomes, nous avons modifié la composition lipidique de la bicouche et exploré les conséquences sur ces interactions. À cette fin, nous avons traité des cellules SH-SY5Y-APPswe par de l'acide docosahexaénoïque (DHA, C22:6 n-3), le principal acide gras polyinsaturé des membranes neuronales et connu pour ses propriétés neuroprotectrices contre le stress amyloïde et la MA. L'effet bénéfique attendu sur la survie neuronale a bien été observé, en parallèle au déblocage du trafic endolysosomal et à la production d'exosomes. Tous ces changements ont été corrélés à une dispersion entre C99 et Rab5 dans la membrane, suggérant que le traitement par le DHA a pu initier un remodelage membranaire. Ce remodelage peut conduire à une relocalisation des protéines, les endosomes pouvant alors échanger Rab5 contre Rab7 et évoluer en endosomes tardifs, levant ainsi le blocage initial. À notre connaissance, il s'agit de la première preuve que le DHA peut corriger un phénotype directement lié à la MA, mais sa capacité à remodeler la membrane neuronale a déjà été démontrée par notre équipe pour préserver la signalisation par le facteur neurotrophique CNTF dans le cerveau de souris âgées. Nous ignorons quels principes mécanistiques pourraient régir ces effets bénéfiques, certainement non spécifiques, mais nous supposons qu'en préservant l'organisation des membranes des neurones âgés ou soumis à un stress chronique, ils pourraient prévenir ou restaurer une partie des dommages subis, augmenter les chances de survie des neurones et ainsi ralentir le développement de la MA<br>Alzheimer's disease (AD) is a complex and multifactorial pathology for which there is no current treatment. Several hypotheses have been proposed to explain the onset and progression of this disease, including the amyloid cascade, which predominates the field of research for the past 30 years. The amyloidogenic pathway requires the endocytosis of the APP protein in early endosomes where it undergoes two proteolytic cleavages, first by β-secretase to produce the C99 fragment, and then by γ-secretase to produce the Aβ peptide. One of the current hypotheses is that abnormalities of endocytosis and dysfunction of the endolysosomal system in neurons would constitute one of the early neuropathological mechanisms of AD, well before the neurotoxic cascade generated by Aβ and amyloid deposits. We advocate the hypothesis that changes in membrane organization, particularly during aging or due to lipid imbalances, may exacerbate or promote these dysfunctions. For this study, we used a human neuroblastoma model overexpressing the mutant protein APPswe. We first verified the presence of typical AD endolysosomal abnormalities (enlarged endosomes, blocked vesicular trafficking), to which we also associated low exosome production, chronic stress conditions that we correlated with neuronal death. Initially incriminating continuously produced Aβ in these cells, we sought to reduce its impact by inhibiting γ-secretase activity. This did not ameliorate the stress, but instead aggravated it, leading us to consider that it is the C99 fragment of APP, i.e. the substrate of Aβ production, that is the central amyloid product in the neurotoxic cascade seen in APP-overexpressing cells. The deleterious effects of C99 must occur before those of Aβ, explaining the known precocity of endolysosomal alterations. Accumulating as a result of γ-secretase inhibition, the C99 fragment interacts further with the early endosome-specific Rab5 protein. Maturation of the latter is thus prevented, blocking vesicular trafficking of the endolysosomal system. As the interactions between C99 and Rab5 occur at the membrane level of endosomes, we have modified the lipid composition of the bilayer and explored the consequences on these interactions. For this purpose, we treated SH-SY5Y-APPswe cells with docosahexaenoic acid (DHA, C22:6 n-3), the major polyunsaturated fatty acid in neuronal membranes and known for its neuroprotective properties against Aβ toxicity and AD. The expected beneficial effect on neuronal survival was indeed observed, in parallel with the unblocking of endolysosomal trafficking and exosomal production. All these changes were correlated with a dispersion between C99 and Rab5 in the membrane, suggesting that DHA treatment may initiate membrane remodeling. This remodeling may lead to protein relocalization, whereby endosomes may exchange Rab5 for Rab7 to evolve into late endosomes, thereby overcoming the initial blockage. To our knowledge, this is the first evidence that DHA can correct a phenotype directly related to AD, but its ability to remodel the neuronal membrane was previously demonstrated by our team to preserve the neurotrophic CNTF signaling in the brain of aged mice. We do not know what mechanistic principles might govern these beneficial effects, which are certainly non-specific, but we assume that by preserving the organization of the membranes of aged or chronically stressed neurons, they may prevent or restore some of the damage suffered, increase the chances of neuronal survival and thus slow AD development
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Colin, Julie. "Le vieillissement membranaire cérébral : conséquences fonctionnelles et protection par les acides gras polyinsaturés oméga-3 alimentaires." Thesis, Université de Lorraine, 2015. http://www.theses.fr/2015LORR0078/document.
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Un des phénomènes sociétaux marquants de ces dernières années est le vieillissement de la population et en conséquence, une hausse considérable du nombre de personnes âgées. Dans ce contexte, la recrudescence des pathologies chroniques liées au vieillissement, dont la maladie d’Alzheimer, est devenue un enjeu majeur de santé publique. L’impact de nombreux facteurs environnementaux modulables, l’aspect chronique et évolutif des mécanismes pathogènes mis en jeu, doivent inciter à développer des interventions préventives permettant de minimiser les risques de développer ces maladies liées au vieillissement. Ce travail nous a permis de mettre en évidence l’importance d’utiliser des modèles d’étude et des modes d’expérimentation adaptés au vieillissement pour espérer en ralentir ou retarder les processus délétères. Nos résultats ont aussi permis d’identifier les membranes comme des éléments essentiels au bon fonctionnement cérébral. L’altération de la composition et de l’architecture des membranes neuronales chez la souris âgée perturbe leurs fonctionnalités et diminue les capacités de réponse neuroprotectrices recherchées notamment lors des thérapies anti-Alzheimer. Nous avons aussi observé des modifications membranaires comparables chez les souris rendues dyslipidémiques par un régime alimentaire excessif en lipides saturés auquel nous avons pu clairement attribuer un rôle pro-vieillissement. Nous avons finalement démontré le potentiel préventif d’une supplémentation alimentaire en acide docosahexaénoïque, l’acide gras polyinsaturé à longue chaîne majoritaire dans le cerveau, et pu conclure en sa capacité de restaurer une réponse neuroprotectrice altérée chez la souris âgée<br>One of the marked societal phenomena in recent decades is the aging of populations due to continually increasing lifespans and as a result, a considerable surge in the number and proportion of elderly, particularly in Western countries. In this demographic context, the rise of chronic diseases related to aging, including Alzheimer’s disease and other types of dementia, has become a major public health issue. The impact of modifiable environmental factors, evolution of the pathogenic mechanisms involved, and the lack of curative treatments illustrates the need for the development of interventions to prevent or delay the onset of these aging-related diseases. The present work demonstrates the importance of using age-adapted study models and experimental methods with the goal towards slowing or delaying age-related deleterious processes. Secondly, our results have identified membranes as an essential part for normal brain function. The composition and architectural changes in the neuronal membranes of elderly mice disrupt their functionality and reduce neuroprotective responsiveness such as those sought by anti-Alzheimer’s therapies. We also observed similar pro-aging-type changes in brain membranes of dyslipidemic mice fed a high-fat diet. Thus, disturbances of lipid homeostasis are correlated with an increased risk of developing aging-related cardiovascular and metabolic as well as neurodegenerative diseases. We finally demonstrated the preventive potential of dietary supplementation with docosahexaenoic acid, the most abundant long-chain polyunsaturated fatty acid in the brain, and observed its ability to restore a neuroprotective response that was impaired in older mice
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Casellas, Díaz Sergi. "Regulación de la bioenergética mitocondrial por Mfn2 mediante los contactos RE-mitocondria y su implicación en la fisiología neuronal." Doctoral thesis, Universitat de Barcelona, 2021. http://hdl.handle.net/10803/673820.
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Las mitofusinas 1 y 2 son unas GTPasas que se encuentran en la membrana mitocondrial externa, donde llevan a cabo el proceso de fusión mitocondrial. La existencia de mutaciones en Mfn2 es la principal causa de la enfermedad de Charcot- Marie-Tooth tipo 2A, un grupo de distintas neuropatías caracterizadas por degeneración axonal. Por otro lado, otras alteraciones en Mfn2 también han sido descritas en múltiples enfermedades neurodegenerativas crónicas, en episodios traumáticos agudos como accidentes cerebrovasculares e incluso otras enfermedades no neurológicas como las cardiometabólicas. Un gran número de estudios han demostrado que Mfn2 está relacionada con la regulación del metabolismo y la bioenergética mitocondrial, ya que su supresión afecta negativamente ambos procesos y su sobreexpresión los estimula. Dado el papel del metabolismo mitocondrial en la fisiopatología de estas enfermedades, entender el mecanismo por el que Mfn2 regula la bioenergética mitocondrial resulta de gran importancia.
En esta tesis se demostró que la activación de la bioenergética mitocondrial por parte de Mfn2 requiere su localización en el retículo endoplasmático (RE) y es independiente a su función como proteína de fusión mitocondrial. A diferencia de Mfn1, Mfn2 se encuentra presente en el RE, concretamente en las membranas asociadas con las mitocondrias. Los contactos entre ambos orgánulos son de vital importancia en las células, ya que, entre otras funciones esenciales, crean micro-dominios que permiten la transferencia de Ca2+ del RE hacia las mitocondrias. Por su parte, el Ca2+ captado por las mitocondrias estimula diferentes enzimas del metabolismo mitocondrial y complejos encargados de mantener la bioenergética mitocondrial. En esta tesis, se observó que células carentes de Mfn2 también manifiestan defectos en la homeostasis del Ca2+ y en el mantenimiento de los contactos RE-mitocondrias. Mediante el uso de un enlazador artificial que mimetiza la función enlazadora de Mfn2 o diferentes formas de Mfn2 dirigidas a ambos orgánulos, se determinó que Mfn2 actúa como complejo enlazador de RE y mitocondrias, propiciando la formación de contactos óptimos para la transferencia de Ca2+ del RE a las mitocondrias. A su vez, el restablecimiento de la
captación de Ca2+ por las mitocondrias gracias a la función enlazadora de Mfn2 fue
capaz de estimular la bioenergética mitocondrial, definiendo de este modo un
mecanismo por el cual Mfn2 regula la bioenergética mitocondrial a través de los contactos RE-mitocondria.
La relevancia fisiológica de estos resultados se mostró en dos procesos neuronales. Por un lado, la falta de Mfn2 provocó alteraciones en el crecimiento neurítico y la formación de espinas dendríticas durante el periodo de desarrollo neuronal en modelos in vivo de ratón knockout para Mfn2. Estas alteraciones, fueron rescatadas in vitro mediante el enlazador artificial de RE-mitocondrias. Usando distintas formas de Mfn2 dirigidas específicamente a RE o mitocondria, se determinó que el mecanismo por el cual Mfn2 regula la bioenergética a través de los contactos RE-mitocondrias podría ser esencial durante el desarrollo neuronal para un correcto crecimiento y ramificación de sus neuritas.
Por otro lado, el restablecimiento de los contactos RE-mitocondria protegió contra la excitotoxicidad. Mfn2 destaca también por su capacidad neuroprotectora frente diferentes tipos de lesiones como daño al ADN, estrés oxidativo o privación de iones K+. Frente a una sobreactivación persistente de los receptores de NMDA, acontece un aumento continuo y acusado de Ca2+ intracelular que desencadena en muerte neuronal. Durante este proceso, los niveles de Mfn2 decrecen, hecho que correlaciona
con una mayor predisposición neuronal a la apoptosis. En este estudio, se determinó que la función enlazadora de Mfn2 podría estar relacionada con el reclutamiento de Bax hacia las mitocondrias, hecho típicamente definitorio de un proceso apoptótico. De este modo, se propone este mecanismo como una potencial diana terapéutica en procesos patológicos como los accidentes cerebrovasculares isquémicos, en los cuales aparecen eventos excitotóxicos y los niveles de Mfn2 se ven reducidos.
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Prado, Gustavo R. "Neuronal Plasma Membrane Disruption in Traumatic Brain Injury." Diss., Georgia Institute of Technology, 2004. http://hdl.handle.net/1853/7260.
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During a traumatic insult to the brain, tissue is subjected to large stresses at high rates which often surpass cellular thresholds leading to cell dysfunction or death. Cellular events that occur at the time of and immediately after an insult are poorly understood. Immediately following traumatic brain injury (TBI), the neuronal plasma membrane may become disrupted and potentiate detrimental pathways by allowing extracellular contents to gain access to the cytosol. In the current study, neuronal plasma membrane disruption was assessed in vivo following moderate unilateral controlled cortical impact in rats using a normally cell-impermeant fluorescent compound as a plasma membrane permeability marker. This fluorescent dye was injected into the cerebrospinal fluid and was allowed to diffuse into the brain. TBI caused a widespread acute disruption of neuronal membranes which was significantly different compared to uninjured brains. Affected cells were present in cortex and hippocampal regions. These findings were complemented by an in vitro model of TBI where membrane disruption was quantified and its mechanisms elucidated. Permeability marker(s) were added to neuronal cultures before the insult as indicators for increases in plasma membrane permeability. The percentage of cells containing the permeability marker was dependent on the molecular mass, as smaller molecules gained access to a higher percentage of cells than larger ones. Permeability increases were also positively correlated with the rate of insult. Membrane disruption was transient, evidenced by a robust resealing within the first minute after the insult. In addition, membrane resealing was found to be dependent on extracellular Ca2+, as chelation of the ion abolished a significant amount of resealing. We have also investigated the effects of mechanically-induced plasma membrane disruptions on neuronal network electrical activity. We have developed a multielectrode array system that allows the study of electrical activity before, during, and after a traumatic insult to neurons. Endogenous electrical activity of neuronal cultures presented a heterogeneous response following mechanical insult. Moreover, spontaneous firing dysfunction induced by injury outlasted the presence of membrane disruptions. This study provides a multi-faceted approach to elucidate the role of neuronal plasma membrane disruptions in TBI and its functional consequences.
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Farber, Steven Arthur. "Neuronal activity and membrane turnover in rat brain." Thesis, Massachusetts Institute of Technology, 1993. http://hdl.handle.net/1721.1/12673.
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Raju, Rajeswari. "Optimisation of image processing networks for neuronal membrane detection." Thesis, University of Nottingham, 2016. http://eprints.nottingham.ac.uk/33948/.
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This research dealt with the problem of neuronal membrane detection, in which the core challenge is distinguishing membranes from organelles. A simple and efficient optimisation framework is proposed based on several basic processing steps, including local contrast enhancement, denoising, thresholding, hole-filling, watershed segmentation, and morphological operations. The two main algorithms proposed Image Processing Chain Optimisation (IPCO) and Multiple IPCO (MIPCO)combine elements of Genetic Algorithms, Differential Evolution, and Rank-based uniform crossover. 91.67% is the highest recorded individual IPCO score with a speed of 280 s, and 92.11% is the highest recorded ensembles IPCO score whereas 91.80% is the highest recorded individual MIPCO score with a speed of 540 s for typically less than 500 optimisation generations and 92.63% is the highest recorded ensembles MIPCO score. Further, IPCO chains and MIPCO networks do not require specialised hardware and they are easy to use and deploy. This is the first application of this approach in the context of the Drosophila first instar larva ventral nerve cord. Both algorithms use existing image processing functions, but optimise the way in which they are configured and combined. The approach differs from related work in terms of the set of functions used, the parameterisations allowed, the optimisation methods adopted, the combination framework, and the testing and analyses conducted. Both IPCO and MIPCO are efficient and interpretable, and facilitate the generation of new insights. Systematic analyses of the statistics of optimised chains were conducted using 30 microscopy slices with corresponding ground truth. This process revealed several interesting and unconventional insights pertaining to preprocessing, classification, post-processing, and speed, and the appearance of functions in unorthodox positions in image processing chains, suggesting new sets of pipelines for image processing. One such insight revealed that, at least in the context of our membrane detection data, it is typically better to enhance, and even classify, data before denoising them.
Books on the topic "Membrane neuronale"
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Wright, William Neil. Nonlinear models of the electrical properties of neuronal membranes. National Library of Canada = Bibliothèque nationale du Canada, 1993.
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Montgomery, Erwin B. Controlling the Flow of Electrical Charges. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190259600.003.0004.
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In depolarization to effect neuronal activations,, electrical charges are delivered to the neuron to affect the electrical potential across the neuronal membrane to subsequently affect voltage-gated ionic conductance channels. The orientation of the field of electrical charges to the neuronal membrane is critical. Electrical charges flow from the negative contact to the positive contact. The negative electrostatic charge “pushes” negative charges onto the outer surface of the neuron, which results in depolarization of the neuronal membrane. Neurons near the positive contact will not have negative electrical charges deposited on the outer surface, will not be depolarized, and thus, are not activated. Likewise, neurons whose membranes are oriented parallel to the lines of electrical forces that move electrical charges will not receive the electrical charges and, consequently, will not be activated. The electronics of the DBS systems are designed to control the electrostatic forces so as to control the activations of the nervous system to generate benefit and avoid adverse effects.
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Laktionova, A. A., and O. S. Sotnikov. Membrane Fusion and Syncytial Neuronal Cytoplasmic Connection. Trans Tech Publications, Limited, 2016.
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Laktionova, A. A., and O. S. Sotnikov. Membrane Fusion and Syncytial Neuronal Cytoplasmic Connection. Trans Tech Publications, Limited, 2016.
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Slimp, Jefferson C. Neurophysiology of Multiple Sclerosis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199341016.003.0003.
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Any discussion of the pathomechanisms and treatments of MS benefits from an understanding of the physiology of the neuronal membrane and the action potential. Neurons and glia, are important for signal propagation, synaptic function, and neural development. The neuronal cell membrane, maintains different ionic environments inside and outside the cell, separating charge across the membrane and facilitating electrical excitability. Ion channels allow flow of sodium, potassium, and calcium ions across the membrane at selected times. At rest, potassium ion efflux across the membrane establishes the nerve membrane resting potential. When activated by a voltage change to threshold, sodium influx generates an action potential, or a sudden alteration in membrane potentials, that can be conducted along an axon. The myelin sheaths around an axon, increase the speed of conduction and conserve energy. The pathology of MS disrupts the myelin structures, disturbs conduction, and leads to neurodegeneration. Ion channels have been the target of investigation for both restoration of conduction and neuroprotection.
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Mason, Peggy. The Neuron at Rest. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190237493.003.0009.
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Neuronal membrane potential depends on the distribution of ions across the plasma membrane and the permeability of the membrane to those ions afforded by transmembrane proteins. Ions cannot pass through a lipid bilayer but enter or exit neurons through ion channels. When activated by voltage or a ligand, ion channels open to form a pore through which selective ions can pass. The ion channels that support a resting membrane potential are critical to setting a cell’s excitability. From the distribution of an ionic species, the Nernst potential can be used to predict the steady-state potential for that one ion. Neurons are permeable to potassium, sodium, and chloride ions at rest. The Goldman-Hodgkin-Katz equation takes into consideration the influence of multiple ionic species and can be used to predict neuronal membrane potential. Finally, how synaptic inputs affect neurons through synaptic currents and changes in membrane resistance is described.
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Orchinik, Miles. Biochemical and behavioral characterization of steroid receptors in neuronal membranes. 1992.
Find full textBook chapters on the topic "Membrane neuronale"
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De Bartolo, Loredana, and Antonietta Messina. "Neuronal Regeneration." In Encyclopedia of Membranes. Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-40872-4_410-1.
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Bear, Mark F., Barry W. Connors, and Michael A. Paradiso. "Die neuronale Membran im Ruhezustand." In Neurowissenschaften. Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-662-49933-7_3.
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Bear, Mark F., Barry W. Connors, and Michael A. Paradiso. "Die neuronale Membran im Ruhezustand." In Neurowissenschaften. Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-662-57263-4_3.
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Bear, Mark F., Barry W. Connors, and Michael A. Paradiso. "Die neuronale Membran im Ruhezustand." In Neurowissenschaften. Spektrum Akademischer Verlag, 2009. http://dx.doi.org/10.1007/978-3-8274-2228-6_3.
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Cole, Gregory J., and Richard W. Bond. "Neuronal Antigens Involved in Cell Adhesion and Cell Recognition." In Cell Membranes. Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-1915-3_3.
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Moore, J. W., and N. E. Berthier. "Purkinje Cell Activity and the Conditioned Nictitating Membrane Response." In Cerebellum and Neuronal Plasticity. Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-0965-9_22.
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Yu, Robert K., James R. Goldenring, John Y. H. Kim, and Robert J. DeLorenzo. "Gangliosides as Differential Modulators of Membrane-Bound Protein Kinase Systems." In Gangliosides and Neuronal Plasticity. Springer New York, 1986. http://dx.doi.org/10.1007/978-1-4757-5309-7_8.
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Levin, Ellis R. "Nuclear Receptor Versus Plasma Membrane Oestrogen Receptor." In Neuronal and Cognitive Effects of Oestrogens. John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/0470870818.ch5.
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Ando, Susumu, Yasukazu Tanaka, and Kazuo Kon. "Membrane Aging of the Brain Synaptosomes with Special Reference to Gangliosides." In Gangliosides and Neuronal Plasticity. Springer New York, 1986. http://dx.doi.org/10.1007/978-1-4757-5309-7_9.
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Breer, H., and M. Knipper. "Synaptosomes and Neuronal Membranes from Insects." In Springer Series in Experimental Entomology. Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70045-3_6.
Full textConference papers on the topic "Membrane neuronale"
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Cecílio, Samyra Giarola, Jéssica Naiara Lara, Camila Raianna Justiniana Rocha, and Juliana Pereira Cardoso. "EPILEPSIAS E A HOMEOSTASE DE CLORETO." In II Congresso Brasileiro de Ciências Biológicas On-line. Revista Multidisciplinar Educação e Meio Ambiente, 2021. http://dx.doi.org/10.51189/rema/1662.
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Introdução: Os íons sódio, potássio, cálcio e cloreto são os principais envolvidos na determinação do potencial de membrana das células neuronais. Uma vez que o potencial de equilíbrio do cloreto (ECl), de - 80 mV, é próximo ao potencial de repouso da membrana (- 75 mV), pequenas variações na concentração intracelular do íon interferem de modo significativo no gradiente transmembrânico e, consequentemente, na excitabilidade celular. Objetivo: A proposta do presente estudo consistiu em uma revisão da literatura sobre a influência do desequilíbrio iônico de cloreto. Método: Realizou-se levantamento bibliográfico dos últimos 20 anos (2000- 2020) por meio da busca “chloride” AND “epilepsy” Resultados: A concentração intracelular de cloreto ([Cl-]i) determina a força do sistema de inibição ativado pelos receptores GABAA. Os canais ativados por estes receptores são permeáveis ao íon cloreto. O neurotransmissor GABA possui ação predominantemente inibitória no SNC, porém, as mudanças conformacionais desencadeadas pela ligação do neurotransmissor a estes receptores permitem que haja um influxo ou efluxo de cloreto através dos canais, resposta que será variável conforme a [Cl-]i e o potencial de equilíbrio do íon. Nos neurônios imaturos, nos quais a [Cl-]i é elevada, o ECl é positivo em relação ao Vm, e com a abertura de canais iônicos ativados por GABA, ocorre o efluxo de íons cloreto e despolarização neuronal, com a geração de respostas excitatórias. Esta característica é fundamental para o desenvolvimento neuronal. Inversamente, no cérebro adulto, o cloreto intracelular é mantido a baixas concentrações nos neurônios, sendo a [Cl-]i cerca de 10 a 20 vezes menor do que a concentração extracelular. Nessas condições, ECl é negativo em relação ao Vm e, quando os receptores GABAA são ativados, há o influxo de cloreto e hiperpolarização da membrana neuronal. Durante uma crise epiléptica, a [Cl-]i pode chegar a 26 mM. A falha do sistema de inibição e a despolarização gerada pela alta concentração intracelular acentuam o disparo neuronal, bem como a probabilidade de ocorrência e gravidade das crises. Conclusão: O aumento da [Cl-]i no cérebro aumenta a excitabilidade e os disparos neuronais, favorecendo a ocorrência de crises epilépticas.
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Allen, Kathleen B., and Bradley Layton. "A Mechanical Model for Cytoskeleton and Membrane Interactions in Neuronal Growth Cones." In ASME 2007 International Mechanical Engineering Congress and Exposition. ASMEDC, 2007. http://dx.doi.org/10.1115/imece2007-42008.
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Revealing the molecular events of neuronal growth is critical to obtaining a deeper understanding of nervous system development, neural injury response, and neural tissue engineering. Central to this is the need to understand the mechanical interactions among the cytoskeleton and the cell membrane, and how these interactions affect the overall growth mechanics of neurons. Using ANSYS, the force produced by a cytoskeletal protein acting against a deformable membrane was modeled, and the deformation, stress, and strain were computed for the membrane. Parameters to represent the flexural rigidities of the well-studied actin and tubulin cytoskeletal proteins as well as the mechanical properties of neuronal growth cones were used in the simulations. Our model predicts that while a single actin filament is able to produce a force sufficient to cause membrane deformation and thus growth, it is also possible that the actin filament may cause the membrane to rupture, if a dilatational strain of more than 3–4% occurs. Additionally, neurotoxins or pharmaceuticals that alter the mechanical properties of either the cell membrane or cytoskeletal proteins could disrupt the balance of forces required for neurons to not only push out and grow correctly, but also to sustain their shapes as high-aspect-ratio structures once growth is complete. Understanding how cytoskeletal elements have coevolved mechanically with their respective cell membranes will yield insights into the events that gave rise to the sequences and quaternary structures of the major cytoskeletal elements.
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Cao, Guoxin, You Zhou, Jeong Soon Lee, Jung Yul Lim, and Namas Chandra. "Mechanical Model of Neuronal Function Loss." In ASME 2010 International Mechanical Engineering Congress and Exposition. ASMEDC, 2010. http://dx.doi.org/10.1115/imece2010-39447.
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The mechanism of mild traumatic brain injury (mTBI) is directly related to the relationship between the mechanical response of neurons and their biological/chemical functions since the neuron is the main functional component of brain.1 The hypotheses is that the external mechanical load will firstly cause the mechanical deformation of neurons, and then, when the mechanical deformation of neurons reaches to a critical point (the mechanical deformation threshold), it will initiate the chemical/biological response (e.g. neuronal function loss). Therefore, defining and measuring the mechanical deformation threshold for the neuronal cell injury is an important first step to understand the mechanism of mTBI. Typically, the mechanical response of neurons is investigated based on the deformation of in vitro model, in which the neurons are cultured on the elastic substrate (e.g. PDMS membranes). The elastic membrane is deformed by the external load, e.g. equibiaxial stretching. The substrate deformation is considered to be the deformation of neurons since the substrate is several orders stiffer than the neurons and the neurons are perfectly bonded with the substrate. The fluoresce method is typically used to test the cell injury, e.g. the cell vitality and the neuron internal ROS level.1, 2
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Roke, S. "Probing Neuronal Activity using Membrane Interfacial Water." In 2019 Conference on Lasers and Electro-Optics Europe & European Quantum Electronics Conference (CLEO/Europe-EQEC). IEEE, 2019. http://dx.doi.org/10.1109/cleoe-eqec.2019.8873282.
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Dolotova, S. M., Y. V. Bershatsky, Yu A. Zagryadskaya, et al. "OBTAINING MUTANT FORMS OF THE TRANSMEMBRANE DOMAIN OF THE RECEPTOR FOR ADVANCED GLYCATION END PRODUCTS (RAGE) FOR STRUCTURAL NMR STUDIES." In X Международная конференция молодых ученых: биоинформатиков, биотехнологов, биофизиков, вирусологов и молекулярных биологов — 2023. Novosibirsk State University, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-173.
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The membrane receptor RAGE of immunoglobulin family is involved in regulation of neuronal homeostasis and inflammatory processes in human body. To understand the molecular mechanism of signal transduction across the membrane by RAGE, we performed structural-dynamic NMR studies of recombinant transmembrane fragments of RAGE with oncogenic mutations G365R and G368E in membrane-mimicking media.
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LaPlaca, M. C., G. R. Prado, D. Kacy Cullen, and C. M. Simon. "Plasma membrane damage as a marker of neuronal injury." In 2009 Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2009. http://dx.doi.org/10.1109/iembs.2009.5334457.
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Lee, Sung Jin, Jingjing Sun, Michael King, Huikai Xie, and Malisa Sarntinoranont. "Viscoelastic Property Changes of Acute Rat Brain Tissue Slices as a Function of Cell Viability." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53909.
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Changes in mechanical properties within brain tissues after losses in cell viability have not been well investigated. Lack of oxygen and nutrient transport can induce hypoxic neuronal injury and increase cell membrane permeability, and cell membranes and matrix components can lose their structural and mechanical integrity. These physical changes may have an effect on mechanical properties of brain tissue [1]. In this study, the viscoelastic behavior of two anatomical regions (cerebral cortex and hippocampus) in acute rat brain tissue slices were measured as a function of cell viability using indentation combined with optical coherence tomography (OCT). Neuronal viability in brain tissue slices was determined by measuring Fluoro-Jade C (FJC) staining to assay neuronal death or degeneration as a function of incubation time. OCT-measured deformation depths were compared with finite element (FE) simulations to estimate the relaxation of shear modulus. Measured equilibrium shear modulus (μ∞) after 8 hrs incubation was lower than μ∞ measured after 2 hrs incubation in the cerebral cortex (μ∞, 2hrs = 225 Pa, μ∞, 8hrs = 62 Pa) and hippocampus regions (μ∞, 2hrs = 170 Pa, μ∞, 8hrs = 33 Pa). Instantaneous shear modulus (μ0) after 8 hrs incubation was also an order of magnitude lower than μ0 after 2 hrs incubation in cortex (μ0, 2hrs = 1600 Pa, μ0, 8hrs = 100 Pa) and hippocampus regions (μ0, 2hrs = 370 Pa, μ0, 8hrs = 70 Pa). The results of this study provide a timeline for measuring mechanical properties of brain tissues ex vivo and provide better understanding of changes in brain modulus after injury or cell death.
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Wallace, Ron. "Microgravity and charge transfer in the neuronal membrane - Implications for computational neurobiology." In Life Sciences and Space Medicine Conference. American Institute of Aeronautics and Astronautics, 1995. http://dx.doi.org/10.2514/6.1995-1053.
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Tkachenko, A. D. "Photosensitivity of bilirubin incorporated in neuronal membrane particles or in biological gel." In Optical Information Science and Technology, edited by Andrei L. Mikaelian. SPIE, 1998. http://dx.doi.org/10.1117/12.304985.
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Me´ndez-Rojas, Miguel A., Claudia Cravioto Guzman, and Oscar Arias-Carrion. "Synthesis and Chemical Functionalization of Ferromagnetic Nanoparticles to Manipulate Stem Cells Using External Magnetic Fields." In ASME 2007 5th International Conference on Nanochannels, Microchannels, and Minichannels. ASMEDC, 2007. http://dx.doi.org/10.1115/icnmm2007-30188.
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The human brain is able to respond to several situations that promotes neural survivance, growth and neuronal cells regeneration. The potential of stem cells from the subventricular zone to be used for neuronal cell substitution has been widely studied. However, migration of endogen or transplanted cells is random, not efficient and with a very low survivance rate. The use of ferromagnetic nanoparticles may be of interest to guide the stem cells to the desired site using external fields. In this project, we have synthesized ferromagnetic nanoparticles (magnetite) with an average diameter of 10–12 nm, and functionalized with folic acid-flourosceine (with an average yield of 60–70%) in order to induce their entry into rat neuronal precursor cells in vivo and in vitro. The efficiency of cellular incorporation was low in vitro, observing clustering of the nanoparticles at the cytoplasm membrane. During the in vivo tests, no incorporation of nanoparticles was detected. Several results and perspectives are discussed in this work.
Reports on the topic "Membrane neuronale"
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Esteban, José Antonio. Del tráfico de membrana a la comunicación neuronal (Especial Premio Nobel de Medicina 2013). Sociedad Española de Bioquímica y Biología Molecular (SEBBM), 2014. http://dx.doi.org/10.18567/sebbmdiv_anc.2014.07.1.
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