Literatura académica sobre el tema "Neurones humains"
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Artículos de revistas sobre el tema "Neurones humains"
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Bohler, Sébastien. "Des neurones humains à sens unique". Cerveau & Psycho N° 166, n.º 6 (14 de mayo de 2024): 11. http://dx.doi.org/10.3917/cerpsy.166.0011.
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Barbotin, Anne-Laure, Vincent Prévot y Paolo Giacobini. "Développement des neurones à GnRH dans le cerveau d’embryons humains". médecine/sciences 33, n.º 4 (abril de 2017): 376–79. http://dx.doi.org/10.1051/medsci/20173304003.
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Scordel, Chloé y Muriel Coulpier. "La phosphoprotéine P du virus de la maladie de Borna altère le développement des neurones GABAergiques humains". médecine/sciences 31, n.º 12 (diciembre de 2015): 1060–63. http://dx.doi.org/10.1051/medsci/20153112003.
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Mallet, L. "∑njeux de la πsychiatrie ℂomputationnelle". European Psychiatry 30, S2 (noviembre de 2015): S50—S51. http://dx.doi.org/10.1016/j.eurpsy.2015.09.143.
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La psychiatrie computationnelle est un champ émergent qui, dans le prolongement des évolutions récentes en neurosciences cognitives, cherche à comprendre les pathologies mentales par la modélisation des processus élémentaires de pensée et leurs dysfonctionnements. En explicitant l’implémentation neurobiologique des algorithmes utilisés par le cerveau humain pour choisir, percevoir, ou ressentir… D’une certaine façon, cette nouvelle approche de la physiopathologie psychiatrique a pour ambition de combler le « fossé explicatif » entre cerveau et esprit. L’approche computationnelle se base sur la confrontation entre des données neurophysiologiques (IRM, EEG, MEG, électrophysiologie) acquises à chaque niveau de description du cerveau (récepteurs, neurones, réseaux, aires corticales) et les variables cachées prédites par des modèles ajustés aux comportements humains observables. Ce point de vue permet une approche transnosographique des symptômes psychiatriques qui peuvent être reconsidérés et caractérisés en termes de traitements pathologiques de l’information. Ces principes seront illustrés pour montrer :– comment cette approche permet de mieux comprendre l’émergence des processus élémentaires de pensée à partir de réseaux neuraux distribués, à contre-pied des approches néophrénologiques ;– illustrer comment ce type d’approche permet l’étude de l’architecture neurobiologique des processus de prise de décision chez l’homme ;– montrer l’intérêt des modèles bayésiens pour comprendre l’émergence des idées délirantes dans la schizophrénie.
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Epstein, Alberto L. "Maladie d’Alzheimer, neuro-inflammation et virus herpétiques". médecine/sciences 36, n.º 5 (mayo de 2020): 479–86. http://dx.doi.org/10.1051/medsci/2020090.
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L’infection du cerveau par divers types d’agents pathogènes, et les réponses inflammatoires qui s’en suivent, occupent une place grandissante dans notre compréhension de l’étiologie de la maladie d’Alzheimer (MA). Le fait que, parmi la vingtaine de gènes identifiés comme étant des facteurs à risque, plusieurs soient impliqués dans la modulation de la réponse immunitaire, ainsi que la diversité même des agents infectieux identifiés comme étant des acteurs possibles dans l’évolution de cette maladie, plaident en faveur de l’hypothèse neuro-inflammatoire, tout comme la prise de conscience que la protéine Aβ, l’un des marqueurs les plus importants de la MA, peut agir comme un système de défense antimicrobienne, capable de neutraliser des bactéries et des virus. Différent types de pathogènes, incluant des bactéries, des champignons, des protozoaires et des virus, ont été identifiés dans le cerveau malade, souvent près des lésions caractéristiques de la MA. Parmi eux, les virus herpétiques (surtout, mais pas seulement, HSV-1), qui se caractérisent par l’établissement d’infections latentes dans les neurones, ponctuées par des épisodes de réactivation suite à des stress ou des immunodépressions, apparaissent comme des candidats très solides à un rôle étiologique, ne serait-ce qu’en tant que cofacteurs, de la MA. La présence de génomes HSV-1 latents dans le cerveau, et donc le risque de réactivation, augmentent significativement avec l’âge. Des résultats récents montrent que, dans des neurones humains et de rat, l’infection par HSV-1 augmente l’expression de la β-sécrétase et de la nicastrine, deux enzymes impliquées dans la formation des Aβ selon la voie amyloïdogénique, ainsi que de celle de GSK3β et PKA, deux kinases impliquées dans la phosphorylation des protéines Tau, un autre marqueur essentiel de la MA. Les preuves croissantes obtenues, selon lesquelles les infections chroniques et les mécanismes de défense suscités, y compris les processus inflammatoires, sont au cœur de la MA, justifient de revoir les médicaments antiviraux tels que l’acyclovir, et peut-être aussi la vaccination, comme des voies potentielles de lutte contre la MA.
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Deydier, N., N. Lebonvallet, M. Talagas, L. Misery y C. Le Gall-Ianotto. "Étude de la neuroprotection dans un modèle de co-culture 2D de keratinocytes primaires humains avec des neurones sensoriels de rat soumis à un stress inflammatoire mimant la dermatite atopique". Annales de Dermatologie et de Vénéréologie - FMC 3, n.º 8 (diciembre de 2023): A104. http://dx.doi.org/10.1016/j.fander.2023.09.113.
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Sienkiewicz, W., A. Chrószcz, A. Dudek, M. Janeczek y J. Kaleczyc. "Caudal mesenteric ganglion in the sheep – macroanatomical and immunohistochemical study". Polish Journal of Veterinary Sciences 18, n.º 2 (1 de junio de 2015): 379–89. http://dx.doi.org/10.1515/pjvs-2015-0049.
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Abstract The caudal mesenteric ganglion (CaMG) is a prevetrebral ganglion which provides innervation to a number of organs in the abdominal and pelvic cavity. The morphology of CaMG and the chemical coding of neurones in this ganglion have been described in humans and many animal species, but data on this topic in the sheep are entirely lacking. This prompted us to undertake a study to determine the localization and morphology of sheep CaMG as well as immunohistochemical properties of its neurons. The study was carried out on 8 adult sheep, weighing from 40 to 60 kg each. The sheep were deeply anaesthetised and transcardially perfused with 4% paraformaldehyde. CaMG-s were exposed and their location was determined. Macroanatomical observations have revealed that the ovine CaMG is located at the level of last two lumbar (L5 or L6) and the first sacral (S1) vertebrae. The ganglion represents an unpaired structure composed of several, sequentially arranged aggregates of neurons. Immunohistochemical investigations revealed that nearly all (99.5%) the neurons were DβH-IR and were richly supplied by VACHT-IR nerve terminals forming „basket-like” structures around the perikarya. VACHT-IR neurones were not determined. Many neurons (55%) contained immunoreactivity to NPY, some of them (10%) stained for Met-ENK and solitary nerve cells were GAL-positive. CGRP-IR nerve fibres were numerous and a large number of them simultaneously expressed immunoreactivity to SP. Single, weakly stained neurones were SP-IR and only very few nerve cells weakly stained for VIP.
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Verkhratsky, Alexei y Arthur Butt. "The History of the Decline and Fall of the Glial Numbers Legend". Neuroglia 1, n.º 1 (17 de julio de 2018): 188–92. http://dx.doi.org/10.3390/neuroglia1010013.
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In the field of neuroscience and, more specifically glial cell biology, one of the most fundamentally intriguing and enduring questions has been “how many neuronal cells—neurones and glia—are there in the human brain?”. From the outset, the driving force behind this question was undoubtedly the scientific quest for knowledge of why humans are more intelligent than even our nearest relatives; the ‘neuronal doctrine’ dictated we must have more neurones than other animals. The early histological studies indicated a vast space between neurones that was filled by ‘nervenkitt’, later identified as neuroglia; arguably, this was the origin of the myth that glia massively outnumber neurones in the human brain. The myth eventually became embedded in ideology when later studies seemed to confirm that glia outnumber neurones in the human cortex—the seat of humanity—and that there was an inevitable rise in the glia-to-neurone ratio (GNR) as we climbed the evolutionary tree. This could be described as the ‘glial doctrine’—that the rise of intelligence and the rise of glia go hand-in-hand. In many ways, the GNR became a mantra for working on glial cells at a time when the neuronal doctrine ruled the world. However, the work of Suzana Herculano-Houzel which she reviews in this first volume of Neuroglia has led the way in demonstrating that neurones and glia are almost equal in number in the human cortex and there is no inexorable phylogenetic rise in the GNR. In this commentary we chart the fall and decline of the mythology of the GNR.
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Curran, William y Catherine Lynn. "Monkey and humans exhibit similar motion-processing mechanisms". Biology Letters 5, n.º 6 (22 de julio de 2009): 743–45. http://dx.doi.org/10.1098/rsbl.2009.0407.
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Single cell recording studies have resulted in a detailed understanding of motion-sensitive neurons in non-human primate visual cortex. However, it is not known to what extent response properties of motion-sensitive neurons in the non-human primate brain mirror response characteristics of motion-sensitive neurons in the human brain. Using a motion adaptation paradigm, the direction aftereffect, we show that changes in the activity of human motion-sensitive neurons to moving dot patterns that differ in dot density bear a strong resemblance to data from macaque monkey. We also show a division-like inhibition between neural populations tuned to opposite directions, which also mirrors neural-inhibitory behaviour in macaque. These findings strongly suggest that motion-sensitive neurons in human and non-human primates share common response and inhibitory characteristics.
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Zee, D. S., E. J. Fitzgibbon y L. M. Optican. "Saccade-vergence interactions in humans". Journal of Neurophysiology 68, n.º 5 (1 de noviembre de 1992): 1624–41. http://dx.doi.org/10.1152/jn.1992.68.5.1624.
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1. We recorded eye movements in four normal human subjects during refixations between targets calling for various combinations of saccades and vergence. We confirmed and extended prior observations of 1) transient changes in horizontal ocular alignment during both pure horizontal saccades (relative divergence followed by relative convergence) and pure vertical saccades (usually divergence for upward and convergence for downward saccades); 2) occasional, high-frequency (20-25 Hz), conjugate oscillations along the axis orthogonal to the main saccade; and 3) the speeding up of horizontal vergence by both horizontal and vertical saccades. 2. To interpret these findings, we developed a hypothesis for the generation of vergence to step changes in target depth, both with and without associated saccades. The essential features of this hypothesis are 1) the transient changes in horizontal ocular alignment during pure horizontal saccades reflect asymmetries in the mechanical properties of the lateral and medial rectus muscles causing adduction to lag abduction; 2) pure vergence movements in response to step changes in target depth are generated by a neural network that uses a desired change in vergence position as its input command and instantaneous vergence motor error (the difference between the desired change and the actual change in vergence) to drive vergence premoter neurons; and 3) the facilitation of horizontal vergence by saccades arises from nonlinear interactions in central premotor circuits. 3. The hypothetical network for generating pure vergence to step changes in target depth is analogous in structure to the local feedback model for the generation of saccades and has the same conceptual appeal. With the assumption of a single nonlinearity describing the relationship between a vergence motor error signal and the output of the neurons that generate promoter vergence velocity commands, this model generates pure vergence movements with peak velocity-amplitude relationships and trajectories that closely match those of experimental data. 4. Several types of models are proposed for the central, nonlinear interaction that occurs when saccades and vergence are combined. Common to all models is the idea that omnidirectional pause neurons (OPN), which are thought to gate activity for saccade burst neurons, also gate activity for saccade-related vergence. In one model we hypothesize the existence of a separate class of saccade-related vergence burst neurons, which generate premotor horizontal vergence commands but only during saccades. In a second model we hypothesize separate right eye and left eye saccadic burst neurons that receive not only conjugate, but also equal but oppositely directed vergence error signals.(ABSTRACT TRUNCATED AT 400 WORDS)
Tesis sobre el tema "Neurones humains"
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Creyssels, Sophie. "Comprendre les mécanismes cellulaires déficients dans la MPS VII par l'utilisation de neurones humains dérivés d'iPSC". Thesis, Montpellier, 2015. http://www.theses.fr/2015MONTT009.
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Les processus moléculaires mis en jeu lors de maladies de surcharge lysosomale (MSL) et qui conduisent à des dysfonctions neuronales sont peu connus. Afin de mieux comprendre comment s’opèrent ces dysfonctions neuronales associées à la mucopolysaccharidose de type VII (MPS VII), une MSL causée par la déficience en l’activité enzymatique de la ß-glucuronidase, nous avons généré des neurones humains MPS VII à partir cellules souches pluripotentes induites (iPSC). Grâce à la reprogrammation des fibroblastes de patients MPS VII, nous avons généré et caractérisé des neuroprécurseurs dérivés d’iPSC (NSC) et des neurones. Les iPSC MPS VII ont été positives pour les tests de pluripotence (activité de la phosphatase alcaline, expression des marqueurs de pluripotence SSEA3, TRA-2-49 et Nanog par immunofluorescence et expression des gènes de pluripotence SOX2, Oct4 et Lin28 par qRT-PCR, formation des corps embryonnaires et génération de cellules dérivées des trois feuillets embryonnaires in vivo par la formation de tératomes) et présentaient un caryotype normal. Les NSC dérivés d’iPSC exprimaient les marqueurs Nestin et SOX2, et ont été utilisés pour générer des neurones. Les neurones MPS VII exprimaient des marqueurs neuronaux comme MAP2, formaient des synapses et présentaient une activité calcium-dépendante.Afin d’identifier les dysfonctions moléculaires présentes dans la MPS VII, nous avons comparé les NSC et les neurones, avec ou sans milieu conditionné contenant l’enzyme recombinante humaine de la ß-glucuronidase (rhGUS), enzyme actuellement utilisée en phase 1/2, de chez Ultragenyx. Cette enzyme est internalisée par les cellules, rejoint leurs lysosomes et corrige les dysfonctions lysosomales de la MPS VII, restaurant ainsi un phénotype cellulaire physiologique (phénomène aussi appelé ‘enzyme replacement therapy’ (ERT)). Ces diverses conditions nous permettent d’éviter la variabilité clonale des iPSC, et de mieux identifier les déficiences neuronales, corrigées par l’ERT, qui sont associées à la MPS VIIThe molecular pathways linking lysosomal storage diseases (LSD) to neuronal dysfunction are poorly understood. To better understand neuronal dysfunction associated with mucopolysaccharidosis type VII (MPS VII), a LSD due to deficiency in ß-glucuronidase activity, we generated human MPS VII neurons from induced pluripotent stem cells (iPSC). Starting from MPS VII patient fibroblasts, iPSC-derived neural stem cells (NSC) and neurons were generated and characterized. MPS VII iPSC were positive for pluripotency tests (alkaline phosphatase activity, expression of pluripotency markers SSEA3, TRA-2-49 and Nanog by immunostaining and pluripotency gene SOX2, Oct4 and Lin28 expression by qRT-PCR, embryonic bodies formation and generation of cells derivated from the three germ layers in vivo by teratoma formation) and had a normal karyotype. IPSC-derived NSC expressed the markers Nestin and SOX2, and were used to generate neurons. MPS VII neurons expressed mature neuronal markers as MAP2, formed synapses and displayed a calcium-dependent activity. To identify molecular defects in MPS VII, we compared NSC and neurons, with or without conditioned medium containing a recombinant human ß-glucuronidase (rhGUS), enzyme currently used in phase 1/2, from Ultragenyx. This enzyme is taken up by cells, reaches their lysosoms and corrects MPS VII lysosoms dysfunctions, restoring cells to healthy phenotype (phenomena also called enzyme replacement therapy (ERT)). Our assays allow us to circumvent clonal variability associated with iPSC, and to better identify neuronal defects, corrected by ERT, which are associated with MPS VII disease
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Asfogo, Noemi. "Intéraction entre synucléinopathie et dysfonctionnement mitochondrial dans des modèles neuronaux de la maladie de Parkinson". Electronic Thesis or Diss., Sorbonne université, 2023. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2023SORUS732.pdf.
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La maladie de Parkinson (MP) est une maladie neurodégénérative fréquente, caractérisée par la perte progressive des neurones dopaminergiques de la substance noire pars compacta (SNpc) et la présence d’inclusions nommées Corps de Lewy (CLs), contenant la protéine présynaptique alpha-synucléine (αSyn) comme composant majeur. Un certain nombre d’arguments, soutenus par les avancées dans le domaine de la génétique, plaident en faveur d’un rôle de l’altération de l’homéostasie de l’αSyn et du dysfonctionnement mitochondrial dans la MP. Des espèces d’αSyn qui se forment au cours de son accumulation pathologique pourraient en effet impacter la fonction mitochondriale. Cependant, nous manquons d’une vision consensuelle et intégrée des conséquences de ces formes d’αSyn sur la physiologie mitochondriale au cours du temps, ainsi que des mécanismes mis en jeu. Ce projet de thèse s’est inscrit dans le contexte de l’étude détaillée de la dysfonction mitochondriale engendrée par l’αSyn dans des modèles neuronaux et in vivo, dans le cadre du projet européen IMI2/PD-MitoQUANT. La thèse a porté sur la mise en jeu de modèles neuronaux d’agrégation pathologique de l’αSyn, induite par l’apport de fibrilles d’αSyn produites in vitro (PFFs), pour étudier l’impact de ce processus sur des aspects relatifs au contrôle de la qualité mitochondriale. Dans un premier temps, nous avons reproduit et validé au laboratoire un modèle de synucléinopathie basé sur l’exposition aux PFFs, dans des neurones primaires corticaux de souris. Après deux semaines d’exposition, nous avons observé la présence de dépôts riches en αSyn phopshorylée (pS129) dans ces neurones, ainsi qu’une forte colocalisation de cette protéine avec la mitochondrie. Ensuite, nous avons évalué l’impact des PFFs et de la synucléinopathie sur la mitophagie, à l’aide du rapporteur fluorescent MitoRosella. Nous avons démontré une hausse de ce processus suite à l’exposition aiguë des neurones aux PFFs, qui n’était pas retrouvée dans les neurones déficients en Parkine (PRKN(-/-)). Cela suggère que les PFFs endommagent les mitochondries, activant un programme de clairance mitochondriale régulé par la Parkine. Une hausse similaire de la mitophagie était retrouvée dans les neurones exposés chroniquement aux PFFs, cette fois-ci également dans un contexte PRKN(-/-), et indépendamment de la présence de dépôts de pS129 dans les cellules. En parallèle, nous avons suivi l’impact des PFFs sur la biogénèse mitochondriale, en étudiant la synthèse de novo de l’ADNmt par une approche basée sur l’incorporation de l’analogue de nucléoside EdU et sa visualisation par imagerie. Nous avons observé une hausse de la synthèse de l’ADNmt suite à une exposition courte aux PFFs, qui était absente dans les neurones PRKN(-/-). Dans un contexte d’exposition chronique, au contraire, nous avons observé une diminution progressive de la synthèse de novo de l’ADNmt qui était similaire en présence et absence de Parkine. Au cours de la dernière partie de ma thèse, j’ai cherché à confirmer une partie de ces résultats dans un modèle neuronal humain, et j’ai débuté l’exploration des mécanismes responsables de la hausse de mitophagie engendrée par la progression de la synucléinopathie. L’ensemble de ces résultats démontre une perte de l’homéostasie mitochondriale dans le contexte de synucléinopathie, avec d’une part une augmentation de la dégradation des mitochondries par la voie de mitophagie et, d’autre part, une absence de compensation par la biogénèse mitochondriale. A terme, ces altérations pourraient conduire à une dysfonction mitochondriale, comme le montrent des résultats complémentaires obtenus in vitro et in vivo dans le contexte plus global du projet PD-MitoQUANT. Des études complémentaires seront nécessaires pour identifier les mécanismes responsables des altérations observées et déterminer dans quelle mesure ils prennent part à la vulnérabilité neuronale qui conduira à leur dégénérescence dans la MPParkinson's disease (PD) is a common neurodegenerative disorder characterized by the progressive loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc) and the presence of inclusions called Lewy bodies (LBs), containing the presynaptic protein alpha-synuclein (αSyn) as a major component. A number of arguments, supported by advances in genetics, point to a role for altered αSyn homeostasis and mitochondrial dysfunction in PD. The αSyn species formed during its pathological accumulation are indeed suspected to affect the function of the mitochondria. However, we lack a consensual and integrated view of the consequences of these forms of αSyn on mitochondrial physiology over time, as well as the mechanisms involved. This thesis project was part of a detailed study aimed at exploring the contribution of αSyn-to mitochondrial dysfunction in neuronal and in vivo models, as part of the European IMI2/PD-MitoQUANT project. The thesis focused on the use of neuronal models of pathological αSyn aggregation, induced by exposure to Syn fibrils preformed in vitro (PFFs), to study the impact of this process on various aspects related to mitochondrial quality control. We first reproduced and validated in our laboratory a model of synucleinopathy based on exposure of primary mouse cortical neurons to PFFs. After two weeks of exposure, we observed the presence of deposits rich in phosphorylated αSyn (pS129) in these neurons, as well as a strong colocalization of pS129with mitochondria. We then assessed the impact of PFFs and synucleinopathy on mitophagy, using the fluorescent reporter MitoRosella. We demonstrated an increase in mitophagy following acute exposure of neurons to PFFs, which was not found in Parkin-deficient neurons (PRKN(-/-)). This suggests that PFFs damage mitochondria, activating a Parkin-dependent mitochondrial clearance program. A similar increase in mitophagy was found in neurons chronically exposed to PFFs in both wild type and PRKN(-/-) context, irrespective of the presence of pS129 deposits in the cells. In parallel, we monitored the impact of PFFs on mitochondrial biogenesis, studying de novo mitochondrial DNA (mtDNA) synthesis using an approach based on incorporation of the nucleoside analogue EdU and its visualization by imaging. We observed an increase in mtDNA synthesis following acute exposure to PFFs, which again did not occur in PRKN(-/-) neurons. In a context of chronic exposure, on the contrary, we observed a progressive decrease in de novo mtDNA synthesis, which was similar in the presence and absence of Parkin. In the last part of my thesis, I sought to confirm some of these key observations in a human neuronal model, and began exploring the mechanisms responsible for mitophagy activation in the synucleinopathy model. Taken together, these results demonstrate that progression of PFFs-induced Syn pathology is associated with imbalanced mitochondrial turnover, with on one hand enhanced mitochondrial degradation via mitophagy, and on the other hand lack of compensation via mitochondrial biogenesis. Ultimately, these alterations could lead to mitochondrial dysfunction, as shown by complementary results obtained in vitro and in vivo in the broader context of the PD-MitoQUANT project. Further studies are required to identify the mechanisms responsible for the observed alterations and determine to what extent they contribute to the neuronal vulnerability underlying neurodegeneration in PD
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Petite, Didier. "Cryopréservation de neurones embryonnaires humains et animaux dans une perspective de transplantation". Paris, EPHE, 2000. http://www.theses.fr/2000EPHE3016.
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Après mise au point de la technique de cryopréservation de tissus nerveux qui comprend la congélation sous forme de fragments, suivie d'une simple dissociation mécanique, et un taux plus élevé de sérum et de glucose dans les différents milieux, nous avons montré que les neurones et les cellules gliales humaines et animales cryopréservés sont, après culture in vitro et marquage immunocytochimique, semblabes à leurs homologues frais. Une analyse morphométrique a permis de distinguer deux types de neurones GABA-IR (à petit et à grand champ neuritique ) dans le cortex cérébral et le mésencéphale de rat embryonnaire qu'ils soient frais ou cryopréservés. De même, nous avons montré un champ dendritique plus grand dans les cellules DA-IR cryopreservées du mésencéphale et un champ axonal plus grand pour les cellules 5HT-IR cryopréservées du rhombencéphale. Des tests de toxicité chronique et aigue ont permis de mettre en évidence une neuroprotection, par la TCP pour les cellules corticales,et par la BTCP pour les cellules mésencéphaliques au même titre que les cellules fraîches. Les essais de transplantation des cellules cryopréservées du rhombencéphale embryonnaire dans des moelles de rat sectionnées totalement, ont permis de constater une réinnervation plus importante et des tests de locomotion fictive plus performants surtout après greffe d'un mélange à part égale de cellules DA- et 5HT-IR. La technique de cryopréservation décrite dans ce travail et les améliorations qu'elle a permis tant sur le plan de la morphologie des cellules que sur celui des transplantations, représente un moyen sûr et fiable de conserver des échantillons biologiques en vue de stockage et de greffe. Cette technique pourrait permettre des expérimentations, en particulier génétiques, pouvant aboutir à une meilleure connaissance des processus dégénératifs, ainsi qu'à la réparation après un traumatisme ou dans le cas d'une anomalie génétique.
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Désormeaux, Cléo. "Signalisation des "protease-activated receptors" dans les neurones sensitifs humains : implication dans le syndrome de l'intestin irritable". Thesis, Toulouse 3, 2017. http://www.theses.fr/2017TOU30198.
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Le Syndrome de l'Intestin Irritable (SII) est caractérisé par des douleurs abdominales chroniques, des diarrhées, des constipations ou l'alternance des deux. Les neurones sensitifs des patients seraient surexcitables et ainsi à l'origine de l'hypersensibilité viscérale ressentie. Parmi les médiateurs impliqués dans le SII, les protéases ont un rôle prépondérant notamment car il a été observé une augmentation de leur activité dans des surnageants de biopsies coliques de patients atteints du SII. Ces protéases sont capables d'activer les " Protease-Activated Receptors " (PARs) dans les neurones sensitifs de souris. L'activation des neurones sensitifs murins peut être déclenchée selon un mécanisme dépendant de PAR2 et générant une hypersensibilité viscérale, mais inhibée par un mécanisme dépendant de PAR4. Dans certaines cellules (plaquettes), les PARs ont des rôles très différents entre la souris et l'homme. L'expression et la signalisation des PARs dans les neurones sensitifs humains étant jusqu'alors inconnues, cette thèse a eu pour objectif général d'étudier la signalisation des PARs et d'identifier les effets de médiateurs présents dans les tissus de patients atteints du SII, sur leur capacité à activer des neurones sensitifs humains. Le but ultime était d'identifier de potentielles cibles thérapeutiques pour le traitement de la douleur viscérale associée au SII chez l'homme. Le premier objectif a été de mettre au point la culture de neurones humains des ganglions spinaux dorsaux (GSD) thoraciques, contenant des projections coliques de neurones sensitifs. Une culture de neurones sensitifs d'une pureté de 90% a été obtenue, ces neurones étaient viables et fonctionnels, mobilisant du calcium intracellulaire en réponse à différents agonistes pro-nociceptifs. L'expression des PARs a été étudiée dans ces cultures et comparée à celle dans des tissus de GSD frais. PAR1, PAR2 et PAR4 de même que d'autres récepteurs canaux de la famille des " Transcient Receptors Potential " (TRPs) étaient exprimés de façon comparable dans les GSD fraichement isolés et dans les cultures de neurones, validant ainsi le phénotype physiologique des neurones en culture. L'effet des agonistes des PARs a ensuite été étudié sur la signalisation calcique dans ces cultures de neurones sensitifs humains. De tous les agonistes peptidiques des PARs utilisés, seul le peptide activateur de PAR1 a conduit à une augmentation du flux calcique dans les neurones sensitifs humains, tandis que le peptide agoniste de PAR4 l'a réduite. Comme le peptide activateur de PAR1, la thrombine, une protéase capable d'activer à la fois PAR1 et PAR4 a induit une augmentation du flux calcique dans les neurones sensitifs humains. La mobilisation calcique induite par la thrombine a été inhibée par un antagoniste de PAR1 et potentialisée par un antagoniste de PAR4. La thrombine exerce donc un double effet contradictoire sur les neurones sensitifs humains, induisant un signal calcique par l'activation de PAR1 et l'inhibant par l'activation de PAR4. Les surnageants de biopsies coliques de patients atteints du SII mais pas ceux de contrôles sains, ont provoqué un flux calcique dans les neurones sensitifs humains par un mécanisme dépendant de l'activation de PAR1. Nos résultats mettent en évidence l'importance de réduire la sensibilisation des neurones sensitifs humains dépendante de l'activation de PAR1 dans le SII. Notre technique de culture de GSD humains offre de nouvelles applications en neurosciences et nos résultats permettent d'envisager de nouvelles perspectives thérapeutiques quant à l'utilisation d'un antagoniste de PAR1 pour le traitement de la douleur viscérale associée au SIIIrritable Bowel Syndrome (IBS) is characterized by chronic abdominal pain, diarrhea and/or constipation. Sensory neurons from IBS patients are considered to be over-activated, being thereby responsible of the experienced visceral pain. Among mediators involved in IBS, proteases seem to have a prominent role. First, proteolytic activity is increased in the supernatants of colonic biopsies from IBS patients. Second, these proteases activate " Proteases-Activated Receptors " (PARs) in rodent sensory neurons. Rodent primary afferent activation can be induced by a PAR2-dependent mechanism, which generates visceral hypersensitivity. This mechanism can be inhibited by a PAR4-dependent mechanism. In some cell types such as platelets, PARs may have very different functions in rodent versus human. The expression and the signalization of PARs in human sensory neurons have never been explored. The general aim of this thesis was to study the signalization of PARs and to identify the effect of mediators present in tissues from IBS patients, on their ability to activate human sensory neurons. The final objective was to identify new possible therapeutic targets to treat visceral pain associated with IBS. The first objective was to establish a protocol for culturing human sensory neurons isolated from thoracic dorsal root ganglia (DRG). Thoracic DRG contain the stroma of sensory neurons projecting from the colon. The culture of human sensory neurons was 90% pure with viable and functional neurons, which were able to induce calcium flux in response to different pro-nociceptive agonists. PAR expression was studied in cultures and compared to fresh DRG tissues. PAR1, PAR2 and PAR4 as well as others receptors from the " Transcient Receptors Potential " (TRPs) channel family were similarly expressed in neurons from fresh DRG tissues and in cultured sensory neurons, thereby validating the physiological phenotype of human DRG neurons in culture. The effect of PAR agonists was studied by imaging calcium mobilization in human sensory neuron cultures. From all PAR agonist peptides used, only PAR1 agonist peptide was able to increase calcium signaling in human sensory neurons, while PAR4 agonist peptide was able to decrease this calcium signaling. Similar to PAR1 agonist peptide, thrombin a protease capable of activating both PAR1 and PAR4, induced an increase of calcium flux in human sensory neurons. Thrombin-induced calcium mobilization was inhibited by a PAR1 antagonist and was potentiated by a PAR4 antagonist. Thus, thrombin has a contradictory double effect on human sensory neurons, inducing calcium signaling through PAR1 activation and inhibiting calcium signaling through PAR4 activation. In addition, supernatants of colonic biopsies from IBS patients but not from healthy controls, provoked an increased calcium signaling in human sensory neurons. This effect was dependent on the activation of PAR1. In the context of IBS, our results highlight the importance of targeting PAR1-induced sensitization in human sensory neurons. The DRG culture technique we have established offers important and new applications in the domain of neurosciences. All together, these data point to new therapeutic possibilities for the use of PAR1 antagonist in the treatment of visceral pain associated with IBS
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Gouder, Laura. "Etude de l'effet de mutations du gène SHANK3 dans les TSA à partir de neurones corticaux humains dérivés de cellules souches pluripotentes induites". Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCB089/document.
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Les Troubles du Spectre Autistique (TSA) affectent un individu sur 100 en France et sont caractérisés par des déficits de la communication et des interactions sociales ainsi que par la présence d’intérêts restreints et de comportements répétitifs. Le laboratoire a démontré l’implication de protéines synaptiques dans le développement des TSA et en particulier celle des protéines SHANK. Ces protéines sont des protéines d’échafaudage présentes au niveau de la densité post-synaptique (PSD) des neurones glutamatergiques et interagissant avec différents partenaires. Dans le cadre de mon projet de thèse, nous nous sommes particulièrement intéressés à la protéine SHANK3. Des mutations au sein du gène SHANK3 ont été détectées chez environ 1 à 2% des patients, selon le degré de sévérité du retard mental. Un déficit de SHANK3 altère le fonctionnement synaptique. En effet, des analyses sur modèles de souris invalidées pour le gène SHANK3 ont montré une diminution de la densité des épines dendritiques, de la taille de la densité post-synaptique et de l’expression des partenaires protéiques de SHANK3. Mon modèle principal d’analyse a consisté en la reprogrammation de fibroblastes en cellules pluripotentes induites (iPSC « induced pluripotent stem cells »). Les iPSCs ont ensuite été sélectivement dérivées en neurones corticaux. Nos études se sont focalisées sur l’analyse des conséquences fonctionnelles de mutations de novo du gène SHANK3 retrouvées chez 4 patients à l’état hétérozygote et présentes au sein de l’exon 21. Ces mutations conduisent à un codon stop prématuré. En parallèle, nous avons obtenu des cellules de 4 individus témoins ne présentant aucun trouble psychiatrique identifié. L’analyse a porté d’une part sur des aspects morphologiques et d’autre part sur des aspects fonctionnels. Nous avons étudié l’effet des mutations sur la maturation et les caractéristiques morphologiques des épines dendritiques. Nous avons établi un protocole permettant une analyse détaillée de la morphologie en 3D des épines dendritiques et suivi leur maturation. Un résultat majeur est l’observation d’une diminution de la densité des épines sur les dendrites des neurones pyramidaux issus des patients par rapport aux témoins. Comme attendu, la maturation des épines n’est pas complètement achevée mais varie peu dans son évolution d’un individu à l’autre (témoins vs. patients). Nous avons poursuivi ces études par deux approches fonctionnelles : l’imagerie calcique et des études d’électrophysiologie. Les données électrophysiologiques sont en cours d’analyse. En conclusion, nous avons pu obtenir des cultures de neurones corticaux glutamatergiques et les maintenir en culture durant 40 jours pour effectuer différentes analyses à un stade de maturation suffisant pour la mise en évidence de phénotypes morphologiques et fonctionnels. Nous avons principalement observé une diminution de des densités synaptiques et de maturation des épines dendritiques au sein des neurones issus de patients liée à des altérations d’oscillations calciques spontanéesAutism Spectrum Disorders (ASD) is a neurodevelopmental disorder affecting 1% of population ; characterised by impairments in social interaction and reciprocal communication as well as repetitive and stereotyped behaviors. The work of the laboratory lead to the identification of several genes associated with ASD, among which genes of the synaptic pathway such as SHANK. The SHANK proteins are scaffolding proteins of the post-synaptic density (PSD) of glutamatergic neurons and interact with several partners. In my thesis project, we were particularly interested in SHANK3 mutations. First, Shank3 mutations represent up to 2.12% of ASD cases with moderate to high ID. A SHANK3 deficit leads to the alteration of the synaptic functioning. Indeed, studies of mice KO for SHANK3 gene showed a decrease of the dendritic spines density, of the PSD size and of the expression of SHANK3 partners. My principal model of analysis consisted in the reprogrammation of fibroblasts into induced pluripotent stem cells (iPSCs). Then, the iPSCs were selectively derived into cortical neurons. Our studies were focus on the analysis of functional consequences of SHANK3 de novo mutations found within 4 patients. These mutations are heterozygous and within the exon 21. They result in a premature stop codon. In parallel, we obtained cells from 4 healthy individuals. The work was about the morphological and functional aspects. We analysed the mutations effects on the maturation and morphological caracteristics of the dendritic spines. We finalized a protocol that enabled a detailed analysis of the spine dendritic 3D morphology and their maturation follow-up. A important result was the observation of a decrease of the spine density on pyramidal neurons dendrites from patients compared to those from controls. Moreover, spines maturation was not fully accomplished but was not much different in its evolution between individuals (controls vs patients). Then, we used two functional skills : calcium imaging and electrophysiological experiments. The electrophysiological data are in progress. To conclude, we succeeded in the obtention of glutamatergic cortical neurons and to maintain them in culture during 40 days in order to realize some analysis at a sufficient maturation stage to observe morphological and functional phenotypes. We mainly observed a decrease of the dendritic spines density and maturation for the neurons from patients, with alterations of the spontaneous calcium oscillations
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Antipov, Grigory. "Apprentissage profond pour la description sémantique des traits visuels humains". Thesis, Paris, ENST, 2017. http://www.theses.fr/2017ENST0071/document.
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Les progrès récents des réseaux de neurones artificiels (plus connus sous le nom d'apprentissage profond) ont permis d'améliorer l’état de l’art dans plusieurs domaines de la vision par ordinateur. Dans cette thèse, nous étudions des techniques d'apprentissage profond dans le cadre de l’analyse du genre et de l’âge à partir du visage humain. En particulier, deux problèmes complémentaires sont considérés : (1) la prédiction du genre et de l’âge, et (2) la synthèse et l’édition du genre et de l’âge.D’abord, nous effectuons une étude détaillée qui permet d’établir une liste de principes pour la conception et l’apprentissage des réseaux de neurones convolutifs (CNNs) pour la classification du genre et l’estimation de l’âge. Ainsi, nous obtenons les CNNs les plus performants de l’état de l’art. De plus, ces modèles nous ont permis de remporter une compétition internationale sur l’estimation de l’âge apparent. Nos meilleurs CNNs obtiennent une précision moyenne de 98.7% pour la classification du genre et une erreur moyenne de 4.26 ans pour l’estimation de l’âge sur un corpus interne particulièrement difficile.Ensuite, afin d’adresser le problème de la synthèse et de l’édition d’images de visages, nous concevons un modèle nommé GA-cGAN : le premier réseau de neurones génératif adversaire (GAN) qui produit des visages synthétiques réalistes avec le genre et l’âge souhaités. Enfin, nous proposons une nouvelle méthode permettant d’employer GA-cGAN pour le changement du genre et de l’âge tout en préservant l’identité dans les images synthétiques. Cette méthode permet d'améliorer la précision d’un logiciel sur étagère de vérification faciale en présence d’écarts d’âges importantsThe recent progress in artificial neural networks (rebranded as deep learning) has significantly boosted the state-of-the-art in numerous domains of computer vision. In this PhD study, we explore how deep learning techniques can help in the analysis of gender and age from a human face. In particular, two complementary problem settings are considered: (1) gender/age prediction from given face images, and (2) synthesis and editing of human faces with the required gender/age attributes.Firstly, we conduct a comprehensive study which results in an empirical formulation of a set of principles for optimal design and training of gender recognition and age estimation Convolutional Neural Networks (CNNs). As a result, we obtain the state-of-the-art CNNs for gender/age prediction according to the three most popular benchmarks, and win an international competition on apparent age estimation. On a very challenging internal dataset, our best models reach 98.7% of gender classification accuracy and an average age estimation error of 4.26 years.In order to address the problem of synthesis and editing of human faces, we design and train GA-cGAN, the first Generative Adversarial Network (GAN) which can generate synthetic faces of high visual fidelity within required gender and age categories. Moreover, we propose a novel method which allows employing GA-cGAN for gender swapping and aging/rejuvenation without losing the original identity in synthetic faces. Finally, in order to show the practical interest of the designed face editing method, we apply it to improve the accuracy of an off-the-shelf face verification software in a cross-age evaluation scenario
7
Antipov, Grigory. "Apprentissage profond pour la description sémantique des traits visuels humains". Electronic Thesis or Diss., Paris, ENST, 2017. http://www.theses.fr/2017ENST0071.
Texto completoResumen
Les progrès récents des réseaux de neurones artificiels (plus connus sous le nom d'apprentissage profond) ont permis d'améliorer l’état de l’art dans plusieurs domaines de la vision par ordinateur. Dans cette thèse, nous étudions des techniques d'apprentissage profond dans le cadre de l’analyse du genre et de l’âge à partir du visage humain. En particulier, deux problèmes complémentaires sont considérés : (1) la prédiction du genre et de l’âge, et (2) la synthèse et l’édition du genre et de l’âge.D’abord, nous effectuons une étude détaillée qui permet d’établir une liste de principes pour la conception et l’apprentissage des réseaux de neurones convolutifs (CNNs) pour la classification du genre et l’estimation de l’âge. Ainsi, nous obtenons les CNNs les plus performants de l’état de l’art. De plus, ces modèles nous ont permis de remporter une compétition internationale sur l’estimation de l’âge apparent. Nos meilleurs CNNs obtiennent une précision moyenne de 98.7% pour la classification du genre et une erreur moyenne de 4.26 ans pour l’estimation de l’âge sur un corpus interne particulièrement difficile.Ensuite, afin d’adresser le problème de la synthèse et de l’édition d’images de visages, nous concevons un modèle nommé GA-cGAN : le premier réseau de neurones génératif adversaire (GAN) qui produit des visages synthétiques réalistes avec le genre et l’âge souhaités. Enfin, nous proposons une nouvelle méthode permettant d’employer GA-cGAN pour le changement du genre et de l’âge tout en préservant l’identité dans les images synthétiques. Cette méthode permet d'améliorer la précision d’un logiciel sur étagère de vérification faciale en présence d’écarts d’âges importantsThe recent progress in artificial neural networks (rebranded as deep learning) has significantly boosted the state-of-the-art in numerous domains of computer vision. In this PhD study, we explore how deep learning techniques can help in the analysis of gender and age from a human face. In particular, two complementary problem settings are considered: (1) gender/age prediction from given face images, and (2) synthesis and editing of human faces with the required gender/age attributes.Firstly, we conduct a comprehensive study which results in an empirical formulation of a set of principles for optimal design and training of gender recognition and age estimation Convolutional Neural Networks (CNNs). As a result, we obtain the state-of-the-art CNNs for gender/age prediction according to the three most popular benchmarks, and win an international competition on apparent age estimation. On a very challenging internal dataset, our best models reach 98.7% of gender classification accuracy and an average age estimation error of 4.26 years.In order to address the problem of synthesis and editing of human faces, we design and train GA-cGAN, the first Generative Adversarial Network (GAN) which can generate synthetic faces of high visual fidelity within required gender and age categories. Moreover, we propose a novel method which allows employing GA-cGAN for gender swapping and aging/rejuvenation without losing the original identity in synthetic faces. Finally, in order to show the practical interest of the designed face editing method, we apply it to improve the accuracy of an off-the-shelf face verification software in a cross-age evaluation scenario
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Melo, de Farias Ana Raquel. "Probing the Alzheimer’s disease risk gene PTK2B using human-derived induced neurons". Electronic Thesis or Diss., Université de Lille (2022-....), 2023. http://www.theses.fr/2023ULILS062.
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La maladie d'Alzheimer (MA) est le principal type de démence et représente un défi majeur pour la santé publique mondiale. Elle se caractérise par un déclin progressif de la cognition, de la mémoire et des fonctions comportementales et touche plus de 55 millions de personnes dans le monde. Au niveau moléculaire, la MA se définit par la présence d'enchevêtrements neurofibrillaires agrégés dans les neurones et par l'accumulation de plaques d'amyloïde-β (Aβ) dans le cerveau. Ces caractéristiques pathologiques sont associées à des altérations de l'activité neuronale, à la perte de synapses, à la gliose et à la neuroinflammation, conduisant à une neurodégénérescence irréversible. L'étiologie et la physiopathologie de la MA impliquent une interaction complexe entre des facteurs génétiques et environnementaux. Les études d'association à l'échelle du génome ont permis d'identifier plusieurs loci porteurs de polymorphismes de nucléotides simples (SNP) associés au risque de maladie d'Alzheimer. Parmi ces loci, celui qui héberge la Protéine Tyrosine Kinase 2β (PTK2B) est mis en évidence dans le présent travail. Ce gène code pour une protéine tyrosine kinase qui est impliquée dans la régulation des canaux ioniques induite par le calcium et dans l'activation de nombreuses voies de signalisation, telles que la MAP kinase. Des variations génétiques non synonymes dans le locus PTK2B ont été associées à un risque accru de maladie d'Alzheimer et on pense qu'elles régulent l'expression de PTK2B. Cependant, les rôles physiologiques et physiopathologiques de la PTK2B ne sont pas entièrement compris. Dans le cerveau humain, l'expression de la PTK2B est principalement observée dans les neurones glutamatergiques. Au cours de la progression de la maladie d'Alzheimer, son expression diminue et peut contribuer aux dysfonctionnements neuronaux observés, tels que l'augmentation de l'excitabilité électrique et les altérations synaptiques. Par conséquent, la compréhension du rôle de la PTK2B dans les neurones humains peut contribuer à révéler les mécanismes des dysfonctionnements neuronaux dans la MA. Dans cette optique, les objectifs de cette thèse sont de découvrir les processus cellulaires et les voies moléculaires régulés par la PTK2B dans les neurones humains. Pour ce faire, nous avons utilisé des cellules souches pluripotentes induites humaines (hiPSC) isogéniques pour générer des neurones exprimant différents niveaux de PTK2B. Ensuite, nous avons utilisé des tests fonctionnels et moléculaires pour étudier les conséquences de l'altération de l'expression de la PTK2B dans un contexte physiologique et dans un contexte similaire à celui de la MA. Nous montrons qu'une réduction de l'expression de PTK2B entraîne une augmentation de la phosphorylation de TAU à divers épitopes associés à la pathologie de la MA, ce qui suggère un rôle central de PTK2B dans la régulation de l'agrégation de TAU. En utilisant la transcriptomique à noyau unique, nous montrons également que l'expression réduite de la PTK2B entraîne des altérations transcriptionnelles spécifiques liées à l'activité électrique neuronale et à la transmission synaptique, principalement dans les neurones glutamatergiques. Les expériences d'imagerie calcique indiquent que la réduction de l'expression de PTK2B contribue à augmenter la fréquence des pointes de calcium sans affecter la synchronisation, ce qui indique une activité électrique neuronale élevée. En outre, les résultats des enregistrements électrophysiologiques effectués à partir de réseaux multi-électrodes (MEA) montrent une activité électrique accrue et des schémas d'éclatement perturbés dans les neurones mutants PTK2B. Dans l'ensemble, ces travaux mettent en lumière l'implication de PTK2B dans les processus cellulaires liés à la maladie d'Alzheimer, en donnant un aperçu des mécanismes moléculaires et des altérations fonctionnelles associés à la dysrégulation de PTK2B dans les cellules neuronales humaines dérivées des iPSCsAlzheimer's disease (AD) is the main type of dementia and poses a significant global public health challenge. It is characterized by a progressive decline in cognition, memory, and behavioral functions and affects more than 55 million people worldwide. At the molecular level, AD is defined by the presence of aggregated neurofibrillary tangles within neurons and the accumulation of amyloid-β (Aβ) plaques in the brain. These pathological features are associated with alterations in neuronal activity, synapse loss, gliosis, and neuroinflammation, leading to irreversible neurodegeneration. AD etiology and pathophysiology involves a complex interplay between genetic and environmental factors. Genome-Wide Association Studies have identified several loci carrying single nucleotide polymorphisms (SNPs) associated with AD risk. Among these loci, the one harboring the Protein Tyrosine Kinase 2β (PTK2B) is highlighted in the present work. This gene encodes a protein tyrosine kinase that is involved in calcium-induced regulation of ion channels and activation of numerous signaling pathways, such as MAP kinase. Non-synonimous genetic variations in the PTK2B locus have been associated with an increased risk of AD and are thought to regulate PTK2B expression. However, both the physiological and pathophysiological roles of PTK2B are not fully understood. In the human brain, PTK2B expression is mainly observed in glutamatergic neurons. Its expression declines during AD progression and may contribute to neuronal dysfunctions observed in the disease, such as increased electrical excitability and synaptic alterations. Therefore, understanding the role of PTK2B in human neurons may contribute to reveal the mechanisms of neuronal dysfunctions in AD. Considering that, the aims of this thesis are to uncover the cellular processes and molecular pathways regulated by PTK2B in human neurons. To that, we took advantage of isogenic human induced-pluripotent stem cells (hiPSCs) to generate neurons expressing different levels of PTK2B. Next, we employed functional and molecular assays to probe the consequences of altered PTK2B expression both in a physiological and in an AD-like context. We show that reduced PTK2B expression leads to increased TAU phosphorylation at various epitopes associated with AD pathology, suggesting a central role of PTK2B in regulating TAU aggregation. Using single-cell transcriptomics, we also show that reduced PTK2B expression leads to specific transcriptional alterations related to neuronal electrical activity and synaptic transmission mainly in glutamatergic neurons. Calcium imaging experiments indicate that PTK2B downregulation contributes to increased calcium spikes frequency without affecting synchronization, indicating an elevated neuronal electrical activity. Additionally, results from electrophysiological recordings from multi-electrode array (MEA) show increased electrical activity and disrupted bursting patterns in PTK2B mutant neurons. Overall, this work sheds light on the involvement of PTK2B in AD-related cellular processes, providing insights into the molecular mechanisms and functional alterations associated with PTK2B dysregulation in human iPSC-derived neural cells
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Ferreira, Stéphanie. "Etude de l'apolipoprotéine E dans un modèle cellulaire de neurones humains : synthèses et toxicité de l'apolipoprotéine E au cours de la différenciation neuronale". Lille 2, 2002. http://www.theses.fr/2002LIL2MT20.
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Guedjou, Hakim. "Influence des traits sociaux des humains sur l'apprentissage développemental d'un robot". Electronic Thesis or Diss., Sorbonne université, 2019. http://www.theses.fr/2019SORUS126.
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Dans cette thèse nous utilisons des modèles en mesure de traiter et d'apprendre une tâche donnée (jeu d’imitation de posture et de gestes) dans une interaction humain robot. Pendant cet apprentissage nous analysons la dimension sociale de l’interaction (détection de personnalité, rôle, états sociaux émotionnels, ... etc). Les modèles utilisés dans cette thèse sont des architectures neuronales permettant un apprentissage interactif autonome. Ces architectures ont pour but de faciliter la compréhension du développement des compétences cognitives. L'existence d’un apprentissage des traits sociaux de l’humain de manière implicite par le robot ouvrirait la porte à différents champs, que ce soit la possibilité d’avoir un modèle comportemental pour la détection des traits sociaux ou de personnalité ou encore l'éventualité de l’émergence des mêmes traits sociaux que l’humain dans le comportement du robot. Concrètement dans cette thèse nous abordons cette question en analysant des situations d’apprentissage qui impliquent des partenaires de populations différentes. Nous lions ensuite les performances des algorithmes du robot (trajectoire d’apprentissage, convergence, score de reconnaissance...) aux caractéristiques de ses partenaires. Nous avons réalisé plusieurs expériences liées à la fois à la pathologie (Autisme) ou aux traits de personnalité (dépression et anxiété) et nous avons remarqué l'émergence de pattern lié aux spécificités des individus interagissant avec le robotIn this thesis we use robotic learning models to learn tasks (game of imitation of posture and gestures) through a human-robot interaction. These models are integrated in the analysis of the social dimension of the interaction (detection of personality, role, emotional social states,... etc.). The models used in this thesis are neural architectures for autonomous interactive learning. The purpose of these architectures is to facilitate understanding of the development of cognitive skills. The existence of an implicit learning of the social traits of the human by the robot would open the door. Concretely, in this thesis we address this issue by analysing learning situations that involve partners from different populations. We then link the performance of the robot algorithms (learning trajectory, convergence, recognition score...) to the characteristics of its partners. We carried out several experiments related to both pathology (Autism) and personality traits (depression and anxiety) and we noticed the emergence of pattern related to the specificities of individuals interacting with the robot
Libros sobre el tema "Neurones humains"
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National Institute for Occupational Safety and Health. Division of Safety Research, ed. Performing motor and sensory neuronal conduction studies in adult humans. [Cincinnati, Ohio?]: U.S. Dept. of Health and Human Services, Public Health Service, Centers for Disease Control, National Institute for Occupational Safety and Health, Division of Safety Research, 1990.
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Wolff, Francis. Notre humanité: D'Aristote à l'homme neuronal. [Paris]: Fayard, 2010.
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Neurosis and human growth: The struggle toward self-realization. New York: Norton, 1991.
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I of the vortex: From neurons to self. Cambridge, Mass: MIT Press, 2001.
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1951-, Miles Richard, ed. Neuronal networks of the hippocampus. Cambridge: Cambridge University Press, 1991.
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Entretiens de Lyon (2nd 1990 Ecole normale supérieure de Lyon). Neural networks: Biological computers or electronic brains = Les réseaux de neurones : ordinateurs biologiques ou cerveaux électroniques. Paris: Springer-Verlag, 1990.
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Braitenberg, Valentino. Cortex: Statistics and geometry of neuronal connectivity. 2a ed. Berlin: Springer, 1998.
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Krajina, Ladislav. Jsme lepší než zvířata?: Přirozenost člověka a jeho naděje na přežití. Olomouc: Votobia, 1999.
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Kjell, Fuxe y Wenner-Grenska samfundet, eds. Trophic regulation of the basal ganglia: Focus on dopamine neurons. Oxford, OX, UK: Pergamon, 1994.
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H, Bush Brian M., Clarac François y Society for Experimental Biology (Great Britain). Neurobiology Group., eds. Coordination of motor behaviour. Cambridge [Cambridgeshire]: Cambridge University Press, 1985.
Buscar texto completoCapítulos de libros sobre el tema "Neurones humains"
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Graham, Stuart L. y Alexander Klistorner. "The Visual Evoked Potential in Humans". En Stimulation and Inhibition of Neurons, 287–99. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-233-9_17.
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Makarov, Sergey N., Jyrki Ahveninen, Matti Hämäläinen, Yoshio Okada, Gregory M. Noetscher y Aapo Nummenmaa. "Multiscale Modeling of EEG/MEG Response of a Compact Cluster of Tightly Spaced Pyramidal Neocortical Neurons". En Brain and Human Body Modeling 2020, 195–211. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-45623-8_11.
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AbstractIn this study, the boundary element fast multipole method or BEM-FMM is applied to model compact clusters of tightly spaced pyramidal neocortical neurons firing simultaneously and coupled with a high-resolution macroscopic head model. The algorithm is capable of processing a very large number of surface-based unknowns along with a virtually unlimited number of elementary microscopic current dipole sources distributed within the neuronal arbor.The realistic cluster size may be as large as 10,000 individual neurons, while the overall computation times do not exceed several minutes on a standard server. Using this approach, we attempt to establish how well the conventional lumped-dipole model used in electroencephalography/magnetoencephalography (EEG/MEG) analysis approximates a compact cluster of realistic neurons situated either in a gyrus (EEG response dominance) or in a sulcus (MEG response dominance).
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Park, Kwang Suk. "Neurons at Rest". En Humans and Electricity, 53–73. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-20784-6_3.
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Rizzolatti, Giacomo, Laila Craighero y Luciano Fadiga. "The mirror system in humans". En Mirror Neurons and the Evolution of Brain and Language, 37–59. Amsterdam: John Benjamins Publishing Company, 2002. http://dx.doi.org/10.1075/aicr.42.04riz.
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Ohye, Chihiro, Tohru Shibazaki, Masaru Matsumura, Yasuhiro Kawashima y Masafumi Hirato. "Activity of the Caudate Neurons in Humans". En Advances in Behavioral Biology, 483–88. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5347-8_35.
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Peigneux, Philippe. "Neuroimaging Studies of Sleep and Memory in Humans". En Sleep, Neuronal Plasticity and Brain Function, 239–68. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/7854_2014_326.
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Halata, Zdenek. "Sensory Innervation of the Hairless and Hairy Skin in Mammals including Humans". En The Primary Afferent Neuron, 19–34. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4613-0579-8_2.
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Pietrowsky, R., J. Born, W. Kern y H. L. Fehm. "Functional evidence for a transmission of peptides along the olfactory systems into the brain in healthy humans". En The Peptidergic Neuron, 291–96. Basel: Birkhäuser Basel, 1996. http://dx.doi.org/10.1007/978-3-0348-9010-6_32.
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Proverbio, Alice Mado y Alberto Zani. "Mirror Neurons in Action: ERPs and Neuroimaging Evidence". En Social and Affective Neuroscience of Everyday Human Interaction, 65–84. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-08651-9_5.
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Abstract According to V.S. Ramachandran (inaugural ‘Decade of the Brain’ lecture at Society for Neuroscience meeting), ‘mirror neurons are to neuroscience what DNA was to biology’. Their discovery (by Rizzolatti’s group) led to the understanding of how hominids rapidly evolved through imitation and cultural transmission in the last 100,000 years. In this chapter, we will review the role of human mirror neuron system (MNS) in several mental and brain functions including: interacting with the environment, grasping objects, empathy and compassion for others, empathizing, emulation and emotional contagion, observing and imitating, learning sports, motor skills and dance, motor rule understanding, understanding the intentions of others, understanding gestures and body language, lip reading, recognizing actions by their sounds, learning to play a musical instrument. The chapter is enriched with a discussion of possible criticalities and caveats.
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Strominger, Norman L., Robert J. Demarest y Lois B. Laemle. "Neurons and Associated Cells". En Noback's Human Nervous System, Seventh Edition, 11–38. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-779-8_2.
Texto completoActas de conferencias sobre el tema "Neurones humains"
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Pitta, Marina Galdino da Rocha, Jordy Silva de Carvalho, Luzilene Pereira de Lima y Ivan da Rocha Pitta. "iPSC therapies applied to rehabilitation in parkinson’s disease". En XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.022.
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Background: Parkinson’s disease (PD) is a neurological disorder that affects movement, mainly due to damage and degeneration of the nigrostriatal dopaminergic pathway. The diagnosis is made through a clinical neurological analysis where motor characteristics are considered. There is still no cure, and treatment strategies are focused on symptoms control. Cell replacement therapies emerge as an alternative. Objective: This review focused on current techniques of induced pluripotent stem cells (iPSCs). Methods: The search terms used were: “Parkinson’s Disease”, “Stem cells” and “iPSC”. Open articles written in English, from 2016-21 were selected in the Pubmed database, 10 publications were identified. Results: With the modernization of iPSC, it was possible to reprogram pluripotent human somatic cells and generate dopaminergic neurons and individual-specific glial cells. To understand the molecular basis, cell and animal models of neurons and organelles are currently being employed. Organoids are derived from stem cells in a three-dimensional matrix, such as matrigel or hydrogels derived from animals. The neuronal models are: α-synuclein (SNCA), leucine-rich repeat kinase2 (LRRK2), PARK2, putative kinase1 induced by phosphatase and tensin homolog (PINK1), DJ-1. Both models offer opportunities to investigate pathogenic mechanisms of PD and test compounds on human neurons. Conclusions: Cell replacement therapy is promising and has great capacity for the treatment of neurodegenerative diseases. Studies using iPSC neuron and PD organoid modeling is highly valuable in elucidating relevants neuronal pathways and therapeutic targets, moreover providing important models for testing future therapies.
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Schmieder, F., R. Habibey, V. Busskamp, J. W. Czarske y L. Büttner. "Adaptive Holographic Optogenetic Illumination for Human Neural Network Analysis". En Digital Holography and Three-Dimensional Imaging. Washington, D.C.: Optica Publishing Group, 2022. http://dx.doi.org/10.1364/dh.2022.w4a.7.
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A two-wavelength optogenetic stimulation platform with high spatiotemporal resolution and inherent aberration correction is presented. By stimulating single neurons, we investigated the temporal evolution of connectivity in human induced pluripotent stem cell-derived neuronal networks in-vitro.
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Vingrys, Algis J. y Shaban Demirel. "Temporal modulation thresholds isolate mechanisms with different adaptational and spatial properties". En Vision Science and its Applications. Washington, D.C.: Optica Publishing Group, 1998. http://dx.doi.org/10.1364/vsia.1998.sab.2.
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Temporaland spatial properties of a stimulus visual can be used to isolate different visual pathways (sustained and transient) which are thought to be mediated by different neuronal sub-populations (M- and P-cells) in humans. Temporal modulation has been used to detect early visual dysfunction by way of flicker modulation thresholds or frequency doubling (Casson et al., 1993: Johnson & Samuels, 1997). In these cases it has been assumed that flicker detects losses by targeting sub-populations of neurones.
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Prince, Akimul y Biswanath Samanta. "Control of Autonomous Robots Using the Principles of Neuromodulation". En ASME 2013 Dynamic Systems and Control Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/dscc2013-4107.
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The paper presents a control approach based on vertebrate neuromodulation and its implementation on an autonomous robot platform. A simple neural network is used to model the neuromodulatory function for generating context based behavioral responses to sensory signals. The neural network incorporates three types of neurons — cholinergic and noradrenergic (ACh/NE) neurons for attention focusing and action selection, dopaminergic (DA) neurons for curiosity-seeking, and serotonergic (5-HT) neurons for risk aversion behavior. The implementation of the neuronal model on a relatively simple autonomous robot illustrates its interesting behavior adapting to changes in the environment. The integration of neuromodulation based robots in the study of human-robot interaction would be worth considering in future.
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Mahmoudi, Mehrak, Piroz Zamankhan y William Polashenski. "Simulations of Synaptic Transmission Using Lattice Boltzmann Methods". En ASME 2002 International Mechanical Engineering Congress and Exposition. ASMEDC, 2002. http://dx.doi.org/10.1115/imece2002-32812.
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The nervous system remains one of the least understood biological structures due in large part to the enormous complexity of this organ. A theoretical model for the transfer of nerve impulses would be valuable for the analysis of various phenomena in the nervous system, which are difficult to study by experiments. The central nervous system is composed of more than 100 billion neurons, through which information is transmitted via nerve impulses. Nerve impulses are not immediately apparent since each impulse may be blocked during transmission, changed from a single impulse into repetitive impulse, or integrated with impulses from other neurons to form highly intricate patterns. In the human central nervous system, a neuron secretes a chemical substance called a neurotransmitter at the synapse, and this transmitter in turn acts on another neuron to cause excitation, inhibition, or some other modification of its sensitivity.
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Wang, Xin, Zifei Pei, Aasma Hossain, Tania T. Barnatan, Yuting Bai y Gong Chen. "Abstract 5224: Conversion of human glioblastoma cells into neurons by neuronal transcription factors". En Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-5224.
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Wang, Xin, Zifei Pei, Aasma Hossain, Tania T. Barnatan, Yuting Bai y Gong Chen. "Abstract 5224: Conversion of human glioblastoma cells into neurons by neuronal transcription factors". En Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-5224.
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Lusardi, Theresa A., John Wolf, Douglas H. Smith y David F. Meaney. "Strain and Strain Rate Dependent Changes in Cytosolic Calcium of Cultured Neurons Subjected to Mechanical Stretch". En ASME 1998 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1998. http://dx.doi.org/10.1115/imece1998-0795.
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Abstract In this study, we examined the response of cultured neurons to mechanical stretch, varying the rate and magnitude of mechanical stretch to encompass both physiological and non-physiological levels. Fully differentiated NTera2 cells, a human-derived neuronal cell line, were cultured on a flexible substrate and a uniaxial strain was applied to the neurons at a specified magnitude and rate. Using rates representing non-physiologic (rapid onset time of 20ms and intermediate onset time of 85 ms), and physiologic levels (slow onset time of 1.5sec), we measured the intracellular calcium transient using the calcium indicator dye Fura-2. Immediately following the stretch, intracellular calcium concentration increased, then decreased as the cells attempted to restore pre-stretch cytosolic calcium levels. Statistical analysis using ANOVA showed that normalized peak [Ca+2]i immediately following stretch, average [Ca+2]i following the stimulation, and the final [Ca+2]i value at 4 minutes post-stretch had a significant (p < .0005) dependence on the rate and magnitude at which stretch was applied. At the physiologic rate cell response was minimal, while cell response was maximal at the severe onset rate. Unexpectedly, we observed an attenuation in the response in high stretch, high rate group. At the highest stretch rate studied, these data provide insight into the response of neurons to deformations associated with mechanical trauma. Since calcium is an important cation for processes that can remodel the cytoarchitecture, affect cell signaling, and influence gene expression, the changes associated with the high rates provide at least one pathway for influencing both acute and chronic changes in neuronal behavior following traumatic injury.
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Ferreira, João, Manuel de Sousa Ribeiro, Ricardo Gonçalves y João Leite. "Looking Inside the Black-Box: Logic-based Explanations for Neural Networks". En 19th International Conference on Principles of Knowledge Representation and Reasoning {KR-2022}. California: International Joint Conferences on Artificial Intelligence Organization, 2022. http://dx.doi.org/10.24963/kr.2022/45.
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Deep neural network-based methods have recently enjoyed great popularity due to their effectiveness in solving difficult tasks. Requiring minimal human effort, they have turned into an almost ubiquitous solution in multiple domains. However, due to the size and complexity of typical neural network models' architectures, as well as the sub-symbolical nature of the representations generated by their neuronal activations, neural networks are essentially opaque, making it nearly impossible to explain to humans the reasoning behind their decisions. We address this issue by developing a procedure to induce human-understandable logic-based theories that attempt to represent the classification process of a given neural network model, based on the idea of establishing mappings from the values of the activations produced by the neurons of that model to human-defined concepts to be used in the induced logic-based theory. Exploring the setting of a synthetic image classification task, we provide empirical results to assess the quality of the developed theories for different neural network models, compare them to existing theories on that task, and give evidence that the theories developed through our method are faithful to the representations learned by the neural networks that they are built to describe.
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Das, Payel, Brian Quanz, Pin-Yu Chen, Jae-wook Ahn y Dhruv Shah. "Toward a neuro-inspired creative decoder". En Twenty-Ninth International Joint Conference on Artificial Intelligence and Seventeenth Pacific Rim International Conference on Artificial Intelligence {IJCAI-PRICAI-20}. California: International Joint Conferences on Artificial Intelligence Organization, 2020. http://dx.doi.org/10.24963/ijcai.2020/381.
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Creativity, a process that generates novel and meaningful ideas, involves increased association between task-positive (control) and task-negative (default) networks in the human brain. Inspired by this seminal finding, in this study we propose a creative decoder within a deep generative framework, which involves direct modulation of the neuronal activation pattern after sampling from the learned latent space. The proposed approach is fully unsupervised and can be used off- the-shelf. Several novelty metrics and human evaluation were used to evaluate the creative capacity of the deep decoder. Our experiments on different image datasets (MNIST, FMNIST, MNIST+FMNIST, WikiArt and CelebA) reveal that atypical co-activation of highly activated and weakly activated neurons in a deep decoder promotes generation of novel and meaningful artifacts.
Informes sobre el tema "Neurones humains"
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Takeda, Mamoru. Neurophysiological Mechanisms Underlying the Attenuation of Nociceptive and Pathological Pain by Phytochemicals: Clinical Application as Therapeutic Agents. Progress in Neurobiology, abril de 2024. http://dx.doi.org/10.60124/j.pneuro.2024.10.02.
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Although phytochemicals are plant-derived toxins that are primarily produced by plants as a form of defense against insects or microbes, several lines of studies have demonstrated that phytochemicals (e.g., polyphenols, carotenoids, and amino acids) have several beneficial biological actions for human health, such as anti-oxidative, anti-inflammatory, and cardioprotective effects. Recent studies have demonstrated that phytochemicals can modulate neuronal excitability in the nervous system, including nociceptive sensory transmission, so it is possible that phytochemicals could be complementary alternative medicine candidates; specifically, therapeutic agents against pain. The focus of this review is to elucidate the mechanisms underlying the modulatory effects of phytochemicals on neuronal electrical signals, such as generator potentials, action potentials, and postsynaptic potentials, in the nociceptive pathway neurons resulting in potential local anesthetic effects, intravenous anesthesia and analgesic effects, and inflammatory pain relief effects. In addition, we discuss the contribution of phytochemicals to the relief of nociceptive and/or pathological pain and their potential clinical application on the basis of our recent studies in vivo.
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Werning, Marius. Testing Synaptic Properties of Human Neurons Derived from Fragile-X Patients. Fort Belvoir, VA: Defense Technical Information Center, septiembre de 2012. http://dx.doi.org/10.21236/ada573368.
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Jones, Howland D. T., Edward V. Thomas, Jason C. Harper, Andrew R. Mayer, Arvind Caprihan, Charles Gasparovic, Krastan B. Blagoev y David M. Haaland. Detectability of Neuronal Currents in Human Brain with Magnetic Resonance Spectroscopy. Office of Scientific and Technical Information (OSTI), septiembre de 2012. http://dx.doi.org/10.2172/1113876.
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Yu, Mei, Pengyu Wang, Binbin Li, Qiaoling Ruan, Jingzi ZhangBao, Lei Wu, Xiaoshuang Zhang, Zhaolin Liu y Fang Huang. NRSF Negatively Regulates Microglial Pro-Inflammatory Activation. Progress in Neurobiology, mayo de 2024. http://dx.doi.org/10.60124/j.pneuro.2024.20.02.
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Microglial activation contributes to neurological disorders like Parkinson’s disease (PD), and modulating this activation is a potential therapeutic approach. The neuron-restrictive silencer factor (NRSF) functions as a negative regulator of gene transcription through epigenetic modifications. While previous research has primarily examined the role of NRSF in neuronal differentiation and injury, emerging evidence indicates that NRSF also plays a significant role in maintaining the phenotype of glial cells. In this study, we explored the role and underlying mechanisms of NRSF in lipopolysaccharide (LPS)-induced pro-inflammatory or interleukin-4 (IL4)-induced anti-inflammatory phenotype of microglial activation. Following LPS stimulation, the nuclear localization of NRSF increased in BV2 microglial cells, primary mouse microglia, and microglia within the substantia nigra of PD mice. Knockdown of NRSF enhanced the expression of inflammation-related factors induced by LPS via the mitogen-activated protein kinase-extracellular signal-regulated kinase (MAPK-ERK) and nuclear factor-κB (NF-κB) p65 signalling pathways in BV2 cells. Moreover, the culture medium from LPS-treated NRSF knockdown BV2 cells exerted greater toxic effects on human neuroblastoma SH-SY5Y cells compared to the control. However, NRSF knockdown exerted inconsistent effects on the expression of anti-inflammatory-related genes in IL4-treated BV2 cells. Our findings suggest that NRSF knockdown promotes microglial pro-inflammatory activation.
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Morphett, Jane, Alexandra Whittaker, Amy Reichelt y Mark Hutchinson. Perineuronal net structure as a non-cellular mechanism of affective state, a scoping review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, agosto de 2021. http://dx.doi.org/10.37766/inplasy2021.8.0075.
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Is the perineuronal net structure within emotional processing brain regions associated with changes in affective state? The objective of this scoping review is to bring together the literature on human and animal studies which have measured perineuronal net structure in brain regions associated with emotional processing (such as but not limited to amygdala, hippocampus and prefrontal cortex). Perineuronal nets are a specialised form of condensed extracellular matrix that enwrap and protect neurons (Suttkus et al., 2016), regulate synaptic plasticity (Celio and Blumcke, 1994) and ion homeostasis (Morawski et al., 2015). Perineuronal nets are dynamic structures that are influenced by external and internal environmental shifts – for example, increasing in intensity and number in response to stressors (Blanco and Conant, 2021) and pharmacological agents (Riga et al., 2017). This review’s objective is to generate a compilation of existing knowledge regarding the structural changes of perineuronal nets in experimental studies that manipulate affective state, including those that alter environmental stressors. The outcomes will inform future research directions by elucidating non-cellular central nervous system mechanisms that underpin positive and negative emotional states. These methods may also be targets for manipulation to manage conditions of depression or promote wellbeing. Population: human and animal Condition: affective state as determined through validated behavioural assessment methods or established biomarkers. This includes both positive and negative affective states. Context: PNN structure, measuringPNNs.
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Agrela, Fabiano de Abreu. TEA: O cérebro e a infância de uma pessoa com autismo. CPAH REDAÇÃO, junio de 2023. http://dx.doi.org/10.56238/cpahciencia-011.
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O TEA - Transtornos do Espectro Autista - ainda é um campo onde há muito a ser descoberto, apesar dos grandes e significativos avanços da ciência na compreensão da condição, existem detalhes que não são totalmente entendidos, um dos principais é a sua evolução durante a vida adulta. Não há apenas uma causa para o desenvolvimento de autismo, ele é multifatorial e pode sofrer influência de inúmeras variáveis, como fatores genéticos, condições neurológicas e mentais pré-existentes, fatores ambientais, entre vários outros, no entanto, entende-se que essa vasta gama de influências converge para prejudicar a comunicação entre os dois hemisférios cerebrais. A hipoconectividade entre os hemisférios é uma das mais marcantes características do autismo, uma espécie de assimetria entre as funções de cada parte do cérebro, o que gera, principalmente, dificuldade em realizar tarefas que demandem a interação e integração entre os dois hemisférios, como as habilidades sociais. As dobras presentes no cérebro, conhecidas como giros ou sulcos, possuem uma função primordial para o melhor funcionamento cerebral, elas possibilitam o aumento da área da superfície encefálica, permitindo o aumento do processamento de informações, ou seja, quanto mais dobras um cérebro possuir, maior a sua capacidade de processar informações e estímulos. No cérebro humano, os lobos frontal, parietal, occipital e temporal desempenham papéis fundamentais em uma variedade de funções, desde o movimento até o pensamento, localizado no topo desses lobos está o córtex cerebral, conhecido como massa cinzenta, onde ocorre o processamento das informações, a presença de dobras no cérebro aumenta a área de superfície do córtex cerebral, permitindo o processamento de mais informações.O que se nota no cérebro de uma pessoa com autismo é uma maior incidência das dobras em determinadas regiões cerebrais, como os lobos parietais e temporais esquerdo e lobos frontais e temporais direitos,o que altera a forma como ocorre a conectividade neuronal. Também é importante notar que indivíduos com autismo geralmente apresentam um padrão de crescimento acelerado em certas áreas do cérebro, especialmente durante o segundo ano de vida, no entanto, na idade adulta, ocorre um encolhimento, assim como em indivíduos não autistas, embora de forma precoce, geralmente antes dos 20 anos, entretanto, este tipo de redução não implica necessariamente que o cérebro ficará menor em relação ao período de expansão, podendo até mesmo ser maior que a média da população e variando consideravelmente dependendo do nível de severidade do autismo. Ainda durante a infância pode-se notar uma característica em comum, as altas concentrações de líquido cefalorraquidiano em comparação com os pares não-autistas, esse excesso surge a partir dos 6 meses de idade e vai aproximadamente até os 3 anos. Alguns sintomas mais tradicionalmente encontrados são dificuldades em usar concomitantemente a linguagem corporal, expressões faciais e manter contato visual, dificuldade em se expressar, não compreender totalmente as “regras sociais”, apresentar reações inesperadas a estímulos visuais, auditivos e táteis, comportamentos repetitivos, não responder ao próprio nome aos 12 meses, entre outros aspectos. O autismo é um distúrbio multigênico, envolvendo muitos genes, principalmente agindo em conjunto uns com os outros, assim, não existe uma associação direta e linear entre genes e autismo, mas isso não significa que não haja uma base genética para o autismo ou que o distúrbio não seja hereditário. Também deve ser analisado que há casos de pessoas com predisposição genética alta para o autismo e não apresentar os sintomas, então é importante não apenas analisar probabilidades genéticas, como também uma anamnese para os sintomas. Além disso, pode-se notar, de acordo com algumas pesquisas, uma relação próxima entre o autismo e QI, estudos indicam que mais da metade de todos os indivíduos autistas possuem um QI acima da média e 16%, um superior a 130. Um conjunto de estudos relatou correlações genéticas positivas entre o risco de autismo e as medidas de capacidade mental, há, pelo menos da minha parte, por enquanto, uma suspeita de predisposição alta para o autismo em relatório genético de pessoas de alto QI. Mesmo que o indivíduo não apresente todos os sintomas de autismo, mas sim, algumas singularidades comuns, também deve-se determinar se é uma forma mais leve como Síndrome de Asperger, ou intermediário como Transtorno Invasivo do Desenvolvimento ou o Autismo em si, denominado TEA. Por isso, a complexidade do autismo ainda é uma das características que dificultam a sua total compreensão, mas com a complementação de conhecimentos de diversas áreas, como neurociência, genética, biologia, psicologia, entre outras, possibilita um conhecimento mais amplo acerca da multifatoriedade e complexidade do TEA.
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Performing motor and sensory neuronal conduction studies in adult humans. U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control, National Institute for Occupational Safety and Health, septiembre de 1990. http://dx.doi.org/10.26616/nioshpub90113.
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