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Literatura académica sobre el tema "Substrat neuronal"

Autor: Grafiati

Publicado: 15 de marzo de 2025

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Artículos de revistas sobre el tema "Substrat neuronal"

Zarka, D., A. M. Cebolla y G. Cheron. "Neurones miroirs, substrat neuronal de la compréhension de l’action?" L'Encéphale 48, n.º 1 (febrero de 2022): 83–91. http://dx.doi.org/10.1016/j.encep.2021.06.005.

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Rutka, Roman, Anne Denis, Laurent Vercueil y Pascal Hot. "Crises psychogènes non épileptiques : état des connaissances et apports de l’évaluation des traitements émotionnels". Santé mentale au Québec 41, n.º 1 (5 de julio de 2016): 123–39. http://dx.doi.org/10.7202/1036968ar.

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Des crises psychogènes non épileptiques (CPNE) sont des manifestations transitoires d’allure neurologique pouvant évoquer, à tort, le diagnostic de crise épileptique, mais qui n’en présentent en réalité pas l’origine neurologique. Les CPNE ont rencontré ces cinq dernières années un intérêt croissant tant dans la description de la population concernée, que des origines du trouble et du substrat neuronal qui pourraient les sous-tendre. L’existence d’un profil particulier de traitements émotionnels constitue à ce jour une piste prometteuse de caractérisation de cette population qui a reçu une série de confirmations récentes. Nous présentons ici les données issues de différents domaines allant de la psychologie clinique aux neurosciences affectives et examinant les spécificités de traitements émotionnels rapportés dans les CPNE, ainsi que les pistes d’études à développer afin de mieux les caractériser.

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Friedlander, D. R., P. Milev, L. Karthikeyan, R. K. Margolis, R. U. Margolis y M. Grumet. "The neuronal chondroitin sulfate proteoglycan neurocan binds to the neural cell adhesion molecules Ng-CAM/L1/NILE and N-CAM, and inhibits neuronal adhesion and neurite outgrowth." Journal of Cell Biology 125, n.º 3 (1 de mayo de 1994): 669–80. http://dx.doi.org/10.1083/jcb.125.3.669.

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We have previously shown that aggregation of microbeads coated with N-CAM and Ng-CAM is inhibited by incubation with soluble neurocan, a chondroitin sulfate proteoglycan of brain, suggesting that neurocan binds to these cell adhesion molecules (Grumet, M., A. Flaccus, and R. U. Margolis. 1993. J. Cell Biol. 120:815). To investigate these interactions more directly, we have tested binding of soluble 125I-neurocan to microwells coated with different glycoproteins. Neurocan bound at high levels to Ng-CAM and N-CAM, but little or no binding was detected to myelin-associated glycoprotein, EGF receptor, fibronectin, laminin, and collagen IV. The binding to Ng-CAM and N-CAM was saturable and in each case Scatchard plots indicated a high affinity binding site with a dissociation constant of approximately 1 nM. Binding was significantly reduced after treatment of neurocan with chondroitinase, and free chondroitin sulfate inhibited binding of neurocan to Ng-CAM and N-CAM. These results indicate a role for chondroitin sulfate in this process, although the core glycoprotein also has binding activity. The COOH-terminal half of neurocan was shown to have binding properties essentially identical to those of the full-length proteoglycan. To study the potential biological functions of neurocan, its effects on neuronal adhesion and neurite growth were analyzed. When neurons were incubated on dishes coated with different combinations of neurocan and Ng-CAM, neuronal adhesion and neurite extension were inhibited. Experiments using anti-Ng-CAM antibodies as a substrate also indicate that neurocan has a direct inhibitory effect on neuronal adhesion and neurite growth. Immunoperoxidase staining of tissue sections showed that neurocan, Ng-CAM, and N-CAM are all present at highest concentration in the molecular layer and fiber tracts of developing cerebellum. The overlapping localization in vivo, the molecular binding studies, and the striking effects on neuronal adhesion and neurite growth support the view that neurocan may modulate neuronal adhesion and neurite growth during development by binding to neural cell adhesion molecules.

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Gruenbaum, Lore M. y Thomas J. Carew. "Growth Factor Modulation of Substrate-Specific Morphological Patterns in Aplysia Bag Cell Neurons". Learning & Memory 6, n.º 3 (1 de mayo de 1999): 292–306. http://dx.doi.org/10.1101/lm.6.3.292.

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Components of the extracellular matrix (ECM) can act not only as passive substrates for neuronal attachment and outgrowth but also as active sites for signal transduction. Thus, specific ECM components may modulate effects of growth factors (GFs) that play an important role in structural changes in development and adult neuronal plasticity. In this study we examined the interaction of cultured Aplysia bag cell neurons (BCNs) with components of ECM and different GFs. Different ECM substrata induce a substrate-specific BCN morphology: BCNs grown on collagen or poly-l-lysine have larger soma diameter and more extensive neurite outgrowth than BCNs grown on laminin or fibronectin. BCNs also interact in a substrate-dependent way with GFs: BDNF treatment leads to a reduction of outgrowth on poly-l-lysine but an enhancement on fibronectin and laminin. CNTF reduces the soma diameter on collagen IV but enlarges it on laminin or fibronectin. In contrast, NGF induces a reduction of both soma diameter and outgrowth, on all substrata. Plating of BCNs in the presence of anti-β1-integrin reduces adhesion to fibronectin but does not change outgrowth. In contrast, RGD peptides block adhesion to laminin and poly-l-lysine and, additionally, reduce outgrowth on laminin. These data suggest that BCNs use different β1-integrin-dependent as well as RGD-dependent mechanisms for adhesion and outgrowth on different ECM substrata, providing possible sites of modulation by specific GFs.

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Vorhold, Verena. "The Neuronal Substrate of Risky Choice". Annals of the New York Academy of Sciences 1128, n.º 1 (abril de 2008): 41–52. http://dx.doi.org/10.1196/annals.1399.006.

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TOESCU, E. C. y J. XIONG. "Metabolic Substrates of Neuronal Aging". Annals of the New York Academy of Sciences 1019, n.º 1 (junio de 2004): 19–23. http://dx.doi.org/10.1196/annals.1297.004.

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da Cunha, A., L. E. Eiden y D. M. Rausch. "Neuronal substrates for SIV encephalopathy". Advances in Neuroimmunology 4, n.º 3 (enero de 1994): 265–71. http://dx.doi.org/10.1016/s0960-5428(06)80266-4.

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Athamneh, Ahmad I. M., Alexander X. Cartagena-Rivera, Arvind Raman y Daniel M. Suter. "Substrate Deformation Predicts Neuronal Growth Cone Advance". Biophysical Journal 109, n.º 7 (octubre de 2015): 1358–71. http://dx.doi.org/10.1016/j.bpj.2015.08.013.

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Calof, A. L. y A. D. Lander. "Relationship between neuronal migration and cell-substratum adhesion: laminin and merosin promote olfactory neuronal migration but are anti-adhesive." Journal of Cell Biology 115, n.º 3 (1 de noviembre de 1991): 779–94. http://dx.doi.org/10.1083/jcb.115.3.779.

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Regulation by the extracellular matrix (ECM) of migration, motility, and adhesion of olfactory neurons and their precursors was studied in vitro. Neuronal cells of the embryonic olfactory epithelium (OE), which undergo extensive migration in the central nervous system during normal development, were shown to be highly migratory in culture as well. Migration of OE neuronal cells was strongly dependent on substratum-bound ECM molecules, being specifically stimulated and guided by laminin (or the laminin-related molecule merosin) in preference to fibronectin, type I collagen, or type IV collagen. Motility of OE neuronal cells, examined by time-lapse video microscopy, was high on laminin-containing substrata, but negligible on fibronectin substrata. Quantitative assays of adhesion of OE neuronal cells to substrata treated with different ECM molecules demonstrated no correlation, either positive or negative, between the migratory preferences of cells and the strength of cell-substratum adhesion. Moreover, measurements of cell adhesion to substrata containing combinations of ECM proteins revealed that laminin and merosin are anti-adhesive for OE neuronal cells, i.e., cause these cells to adhere poorly to substrata that would otherwise be strongly adhesive. The evidence suggests that the anti-adhesive effect of laminin is not the result of interactions between laminin and other ECM molecules, but rather an effect of laminin on cells, which alters the way in which cells adhere. Consistent with this view, laminin was found to interfere strongly with the formation of focal contacts by OE neuronal cells.

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Lai, James C. K. "Oxidative metabolism in neuronal and non-neuronal mitochondria". Canadian Journal of Physiology and Pharmacology 70, S1 (15 de mayo de 1992): S130—S137. http://dx.doi.org/10.1139/y92-254.

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Methodological advances have allowed the isolation of two populations of synaptic (SM and SM2) and two populations of nonsynaptic (A and B) mitochondria from rat forebrain. All four populations of brain mitochondria are metabolically active and essentially free from nonmitochondrial contaminants. They (SM, SM2, A, and B) can oxidize a variety of substrates; the best substrate is pyruvate. With pyruvate as the substrate, the respiratory control ratios (i.e., state 3/state 4) in all four populations are routinely >6. Results from numerous enzyme activity measurements provide strong support for the hypothesis that brain mitochondria are very heterogeneous with respect to their enzyme contents and that the enzymatic activities in a particular population of mitochondria, be they synaptic or nonsynaptic, differ from those in another population of mitochondria derived from either the same or another brain region. The major methodological advances in brain mitochondrial isolation greatly facilitate metabolic studies. For example, we have demonstrated that the K+ stimulation of brain mitochondrial pyruvate oxidation is mediated through a K+-induced elevation of the activation state of the pyruvate dehydrogenase complex and the K+ stimulation of the flux through the pyruvate dehydrogenase complex. Our previous and ongoing studies using primary cultures of hypothalamic neurons and astrocytes are consistent with the proposal that brain cells are heterogeneous with respect to their capabilities in energy metabolism. I can envisage that in the not-so-distant future, one could adapt these preparations of cells as the starting material for the isolation of mitochondria of known cellular origin for metabolic studies.Key words: heterogeneity of brain mitochondria, regulation of intermediary metabolism.

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Más fuentes

Tesis sobre el tema "Substrat neuronal"

Vitay, Julien. "Emergence de fonctions sensorimotrices sur un substrat neuronal numérique distribué". Phd thesis, Université Henri Poincaré - Nancy I, 2006. http://tel.archives-ouvertes.fr/tel-00096818.

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Cette thèse s'inscrit dans le domaine des neurosciences
computationnelles dont le but est de modéliser des fonctions
cognitives complexes par le biais de simulations
informatiques et numériques en s'inspirant du fonctionnement
cérébral. Contrairement à une approche descendante nécessitant de
connaître une expression analytique de la fonction à simuler,
l'approche ascendante retenue permet d'observer
l'émergence d'une fonction grâce à l'interaction de populations de
neurones artificiels sans qu'elle soit connue à l'avance. Dans un
premier temps, nous présentons un modèle de réseau de neurones
particulier, les champs neuronaux, dont les propriétés
dynamiques de résistance au bruit et de continuité spatio-temporelle permettent cette émergence. Afin de guider l'émergence de transformations sensorimotrices sur ce substrat, nous présentons ensuite l'architecture des
systèmes visuel et moteur pour mettre en évidence le rôle central de l'attention visuelle dans la réalisation de ces fonctions
par le cerveau. Nous proposons ensuite un schéma
fonctionnel des transformations sensorimotrices dans lequel la
préparation d'une saccade oculaire guide l'attention vers une rÈgion
de l'espace visuel et permet la programmation du mouvement. Nous décrivons enfin un modèle computationnel de déplacement du point d'attention qui, en utilisant une mémoire de travail spatiale
dynamique, permet la recherche séquentielle d'une cible dans une scène visuelle grâce au phénomène d'inhibition de retour. Les performances de ce modèle (résistance au bruit, au mouvement des objets et à l'exécution de saccades) sont analysées en simulation et sur une plate-forme robotique.

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Mizzi, Raphaël. "Mécanismes cognitifs et substrat neuronal de la hérarchisation de la saillance et de la progression de l'attention : approche psychophysique". Thesis, Lyon, 2016. http://www.theses.fr/2016LYSE2122/document.

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Lorsque le système visuel est confronté à un nouvel environnement, un nombre trop important d’informations lui parvient en même temps. De façon précoce, avant tout mouvement oculaire, l’attention explore automatiquement la scène pour sélectionner les éléments d’intérêt. Des recherches récentes ont montré que cette exploration du champ visuel ne se faisait pas aléatoirement, mais se basait sur la saillance des éléments visuels. La saillance est une caractéristique qui émerge de la comparaison des éléments visuels entre eux, par exemple une fleur jaune dans un jardin de fleurs rouges va être considérée comme plus saillante que son voisinage. En permanence et de façon continue, une hiérarchie des éléments est établie à un niveau préattentif ; ils sont triés du plus au moins saillant, et l’attention se base sur cet organisation pour progresser dans le champ visuel. Les recherches présentées dans ce document avaient pour objectif d’investiguer les mécanismes de ce phénomène : quels sont les mécanismes cognitifs impliqués dans la progression de l’attention sur la base de la hiérarchie de la saillance ? Le présent document regroupe des articles qui cherchent à répondre à cette question grâce à des travaux en Psychologie expérimentale. Par ailleurs, de nombreux travaux de Psychologie, Neurophysiologie et Neuroimagerie se sont penchés sur le substrat neural de l’attention visuelle et ont révélé un ensemble de structures clés qui sous-tendraient les mécanismes responsables des fonctions attentionnelles. Cependant, vis-à-vis de la progression de l’attention sur la base de la saillance, seule une étude récente a pu apporter des indices quant au rôle de certaines voies visuelles. Les recherches présentées ici avaient donc également pour objectif de définir ces voies visuelles et les structures corticales et sous-corticales qui les composent, pour investiguer leurs rôles dans la hiérarchie de la saillance et la progression de l’attention. Le présent document regroupe des travaux qui ont exploré ces aspects par le biais de l’approche Psychophysique et Electroencéphalographique
When confronted to a new environment, the visual system faces too much information intake and cannot process it all at once. Before any eye movement, early automatic attention explores the visual scene in order to select relevant items.Recent research revealed that the exploration of the visual scene is not a random process, but is based on the respective saliency of the items in the field. Salience is not a characteristic of an item per se but is emerging as a result of the comparison between an item and its visual neighborhood. For instance, a yellow flower in a garden of red flowers will be considered as more salient than the others in its visual neighborhood. Thus, a hierarchical ordering of the items is continuously established in a preattentive stage, and consists in a sorting of every element from the most to the least salient. Attention, then, relies on this hierarchy to progress in the visual field. The present dissertation had for objective to investigate the cognitive mechanisms involved in this phenomenon: what mechanisms support the salience-based progression of visual attention? Several papers are reported here and explored this question with experimental Psychology.Moreover, numerous works in Psychology, Neurophysiology and Neuroimaging took interest in the neural substrate of visual attention and revealed several key-structures that would subtend the mechanisms involved in attentional functions. However, when it comes to the salience-based progression of attention, only one study could bring cues of the involvement of certain visual pathways in this phenomenon. Another objective of the present dissertation was to define the cortical and sub-cortical structures that constitute those pathways, in order to explore their roles in the salience-base progression of attention. Several papers in the present report are investigating this aspect through Psychophysics and Electroencephalography studies

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Ali, Pauline. "Exploration en IRM cérébrale des capacités de marche chez les sujets âgés à travers le spectre cognitif : Substrat neuronal du contrôle de la marche volontaire". Electronic Thesis or Diss., Angers, 2024. http://www.theses.fr/2024ANGE0043.

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Le vieillissement entraîne des modifications de l'organisme, dont un déclin des performances physiques et fonctionnelles lié à des facteurs génétiques, biologiques et environnementaux. Ce déclin peut devenir pathologique, affectant anormalement certaines fonctions. L’altération des fonctions cognitive et motrice est souvent intriquée, les sujets ayant de mauvaises capacités de marche sont plus à risque de développer une démence. Ces liens entre atteinte motrice et capacité cognitive sont sous-tendus par des altérations neurologiques potentiellement communes à ces fonctions. Cette thèse vise à explorer les liens entre capacités de marche et cognitives chez les sujets âgés, en identifiant les substrats neuronaux associés aux paramètres de marche. Elle examine également comment ces substrats varient selon le statut cognitif et leur rôle dans la progression vers la démence. L’étude analyse trois cohortes (IRMarche et GAIT du CHU d’Angers, et Gait&Brain de l’Université de Western Ontario) regroupant des sujets âgés (> 60 ans) avec différents statuts cognitifs (cognitivement sains, « Mild Cognitive Impairment » (MCI), démence). L’analyse des corrélats anatomo-cliniques en IRM cérébrale structurale explore les associations entre structure cérébrale et capacité de marche. Une analyse spectroscopique du proton dans le cortex moteur primaire complète la dernière étude, examinant les liens entre métabolites et capacité en double tâche chez les sujets MCI. Un premier travail a montré que la vitesse de marche en double tâche (dénomination d’animaux) distinguait le mieux les statuts cognitifs, soulignant son intérêt pour le dépistage. Les travaux suivants ont identifié des corrélats cérébraux (volume de substance grise) spécifiques aux capacités de marche, variant selon le statut cognitif. Enfin, le substrat neuronal associé à un haut coût de la double tâche (lors du décompte d’un en un) a contribué à expliquer pourquoi les sujets MCI ayant un haut coût de la double tâche évoluent plus vers la démence.Cette thèse apporte un éclairage sur les mécanismes cérébraux liés au déclin des capacités de marche et cognitives. Des études futures avec d’autres techniques de neuroimagerie et d’électrophysiologie seront nécessaires pour approfondir ces résultats
The process of aging is associated with a decline in physical and functional performance, which can be attributed to a multitude of factors, including genetic, biological and environmental influences. Such decline may become pathological, affecting specific functions. Cognitive and mobility impairment frequently coexist, and subjects exhibiting gait alterations are at an elevated risk of developing dementia. These associations between cognitive and mobility capacities are underscored by neurological alterations that are common to these functions. This thesis investigates the associations between gait and cognitive capacities across older adults, with the objective of identifying the neural substrate associated with gait parameters.The study analyzed three cohorts (IRMarche, GAIT from Angers University Hospital, Gait&Brain from Western Ontario University) comprising older adults (over 60 years) with varying cognitive statuses (cognitively healthy, mild cognitive impairment and people with dementia). The current study employs structural brain magnetic resonance imaging to examine the relationship between brain structure and gait capacity. Finally, a spectroscopy analysis with a voxel localized in the primary motor cortex was conducted to examine the link between neurometabolite changes and dual-task gait performance in MCI. A first study demonstrates that dual-task gait speed (while naming animals) is a more effective method for distinguishing cognitive statuses, making it a promising approach for screening tests. The remaining articles identified specific brain regions associated with gait parameters, with these varying according to the cognitive status of the subjects. Furthermore, the neural substrate of high dual-task cost (DTC, while counting backwards by ones) provide insight into why individuals with MCI with higher DTC progress to dementia. This thesis offers novel insights into the cerebral mechanisms associated with cognitive and gait decline. Additional studies employing other neuroimaging techniques are necessary to fully elucidate these findings

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Amejdki-Chab, Nassira. "Effets des ions sur le transport neuronal de la dopamine et sur la liaison des inhibiteurs et des substrats au transporteur, étudiée à l'aide d'un marqueur spécifique, le [3H] GBR 12783". Rouen, 1991. http://www.theses.fr/1991ROUES042.

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Nous avons effectué une étude comparative du transport de la [3H] DA et de la liaison spécifique de [3H] GBR 12783 au transporteur, en utilisant des préparations obtenues à partir de striatum de rat. La dépendance des constantes cinétiques du processus de capture vis-à-vis de la concentration des ions Cl est compatible avec un cotransport DA-Cl. La dépendance de la liaison des substrats au site marque par le [3H] GBR 127833 vis-à-vis du Cl est d'autant plus importante que le substrat a une affinité marquée pour le transporteur. Comme pour la liaison de [3H] GBR 12783 aucun cation n'est capable de substituer des ions Na+ sans provoquer par lui-même une inhibition de la capture de [3H] DA. Les profils comparés de Na+ dépendance de la capture neuronale de [3H] DA et de la liaison spécifique de [3H] GBR 12783révèlent l'effet inhibiteur de certains cations (K+, Ca++, Mg++) sur les deux processus et indiquent que ce pouvoir est d'autant plus important que la concentration de Na+ est faible. La liaison des substrats nécessiterait qu'une faible concentration de Na+ (3 ) 5 mM). La liaison spécifique de [3H] GBR 12783 et la capture spécifique de [3H] DA présentent la même sensibilité vis-à-vis des ions métalliques tels que (Hg++, Cd++, Cu++), suggérant l'implication des groupements -SH dans ces deux processus. Les groupements -SH qui lient le Zn++ joueraient un rôle important dans la translocation de la DA

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Corera, Amadou Tidjane. "Effets des ions sur la capture de [3H]dopamine et sur la liaison des substrats et des inhibiteurs au transporteur neuronal de la dopamine marqué avec le [3H]WIN 35428 ou le [3H]Mazindol". Rouen, 2000. http://www.theses.fr/2000ROUES008.

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En vue de comprendre les rapports étroits qui existent entre les gradients électrochimiques transmembranaires et le processus de capture, nous avons étudié le rôle du KC1 dans la NA +-dépendance de la capture de la [3H]dopamine (DA) réalisée par des synaptosomes issus du striatum de rat. Nous avons ainsi montré que la capture est optimale lorsque les concentrations de Na + et de K + physiologiques extracellulaires sont reproduites. Leurs modifications provoquent un blocage de la capture de [3H]DA résultant de la perturbation de l'activité de l'ATPase Na +-K +-dépendante qui ne peut plus assurer le maintien des gradients ioniques transmembranaires. Nous avons ensuite tenté de caractériser la nature des interactions entre les ions (Na +, K +, Ca 2 +,) et la liaison au transporteur neuronal de la DA (TDA) d'un analogue de la cocaïne, le [3H]WIN 35428. Les résultats révèlent l'existence au sein du TDA de 2 sites par lesquels les ions régulent la liaison du [3H]WIN 35428 : un site externe et un site interne situés respectivement à l'extérieur et à l'intérieur du domaine de liaison du radioligand. Les sites externe et interne seraient liés par des interactions allostériques négatives alors que le site externe nous avons comparé l'effet des ions sur les liaisons d'inhibiteurs et de substrats au TDA marqué avec le [3H]Mazindol. Les résultats obtenus permettent de proposer un modèle du TDA qui comporterait des sites de liaison différents mais qui se recouvriraient partiellement. En extrapolant ces données à la capture de la DA, nous avons émis un modèle de fonctionnement du TDA dans le processus de capture dans les conditions physiologiques.

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Bugnicourt, Ghislain. "Adhésion, croissance et polarisation de neurones sur substrats micro-et nano-structurés". Phd thesis, Université de Grenoble, 2011. http://tel.archives-ouvertes.fr/tel-00665074.

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Cette thèse s'intéresse au développement neuronal in vitro dans le but ultime d'enregistrer l'activité de réseaux de neurones à géométrie et connectivité contrôlées. Le développement neuronal est régi par un ensemble de régulations, intrinsèques mais également sous contrôle de facteurs extérieurs, qui permettent à la cellule d'adhérer à un substrat, de croître, et de se polariser. Une partie de ce travail de thèse explore deux types de contraintes physiques de l'environnement que sont la géométrie d'adhésion et la rugosité de surface. La première révèle l'implication des forces dans les stades précoces de développement neuronal régis par un phénomène de compétition neuritique, et permet in fine de contrôler la direction d'émission de l'axone, notamment par une inhibition de sa différenciation sur lignes ondulées. La seconde montre que la distribution des points d'adhésion peut accélérer la croissance jusqu'à favoriser la polarisation axonale. L'autre partie de ce travail s'attache à résoudre le problème technologique majeur qu'est le remplissage des sites d'adhésion par le biais d'une attraction magnétique, et démontre la possibilité de faire croître des réseaux neuronaux modèles sur nanotransistors.

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Leh-Seal, Sandra E. "Neuronal substrates of blindsight in hemispherectomized subjects". Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=95645.

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The goal of my Ph.D. project was the investigation of the neuronal correlate underlying blindsight. Blindsight is a visual phenomenon whereby hemianopic patients are able to unconsciously process visual information in their blind visual field. Previous research demonstrating its existence in hemianopic patients has been criticized for the nature of the paradigms used, for the presence of methodological artifacts, and for the possibility that spared islands of visual cortex may have sustained the phenomenon. In the behavioural part of my Ph.D. project, I modified a paradigm in which the simultaneous presentation of an unseen stimulus can alter the mean reaction time to a seen stimulus (Spatial Summation Effect). The aim was to test the processing abilities of separate visual pathways that may be involved in blindsight by using the achromatic properties of collicular cells, which receive no input from S-cones (color-blind to blue/yellow stimuli). I validated this paradigm in healthy subjects and recruited hemispherectomized patients in whom a whole cerebral hemisphere has been removed or disconnected from the rest of the brain. These patients offer a unique opportunity to establish the existence of blindsight and to investigate its underlying neuronal mechanisms because spared islands of visual cortex cannot be evoked to explain the presence of visual abilities in the blind field. Hemispherectomized subjects with and without blindsight were tested with the modified paradigm under strict control of potential methodological artifacts such as light scatter, fixation, criterion etTects, and macular sparing. The results of this study demonstrated that blindsight in hemisphercctomized subjects is color-blind to blue/yellow stimuli, suggesting a collicular involvement in the phenomenon. In the • neuroimaging part of my study, I utilized an innovative imaging technique, Diffusion Tensor Imaging tractography \vhich enables reconstruction of white matter tracts in vivo . t
Le but de mes études doctorales est d’identifier les mécanismes neuronaux qUi soustendent la vision aveugle (‘inconscient visuel’ ou ‘blindsight’). La vision aveugle est un phénomène visuel par lequel le patient hémianopique est eapable de détecter, sans en être conscient, des informations visuelles dans son champ aveugle. Les recherches dans ce domaine démontrant l’existence de la vision aveugle chez des patients hémianopiques ont été remises en question à cause du genre de paradigmes utilisés. par la présence d’artéfacts méthodologiques, ainsi que par la possibilité que des îlots de cortex visuel aient été épargnés par l’opération. Dans la partie comportementale de ce projet doctoral, j’ai démontré que les temps de réaction lors de présentations simultanées de stimuli dans les deux hémichamps de sujets hémisphérectomisés étaient plus rapides que ceux observés lors de présentations uniques dans le champs intact. Ainsi, une image invisible a pu altérer les temps de réaction à une image visible (Concept de Sommation Spatiale). Exploitant les propriétés achromatiques des colliculli supérieurs qui ne reçoivent aucune contribution des cônes S (aveugle à la couleur bleue / jaune), j’ai modifié le paradigme afin de tester les capacités des diffërcntcs voies visuelles pouvant être impliqués dans la vision aveugle. J’ai validé ce paradigme chez des sujets sains et recrutés des patients ayant subi l’ablation ou la déconnection d \m hém i sphère cérébral pour le traitement d’une épilepsie rebelle (hémisphérectomie). Ces patients offrent une opportunité unique d’établir l’existence de la vision aveugle et d’identi fier ses mécanismes neuronaux car le phénomène ne peut être expliqué par une épargne du cortex visuel. Les sujets hémisphéreetomisés avee et sans vision aveugle ont été testés avec le paradigme modifié sous contrôle ngoureux des autres artefacts méthodologiq

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Wilkinson, Kevin Anthony. "A Screen for Novel Neuronal SUMO Substrates". Thesis, University of Bristol, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.521095.

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O'Leary, Tracy Ann. "Allylamine plasma polymers as novel neuronal culture substrates". Thesis, University of Sheffield, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.251493.

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NIGRO, MARCO. "Cortical and subcortical neuronal substrates of social behavior". Doctoral thesis, Università degli studi di Genova, 2019. http://hdl.handle.net/11567/939848.

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Social behavior is one of the most important properties of animal life and it plays a critical role in biological adaptations. However, the neural substrates of social cognitive processing are complex and largely unknown. The “social brain” network, involving a range of cortical and subcortical regions and connective pathways, varies depending on task demands. The aim of this thesis was to clarify the implication of different brain pathways and systems in different aspects of mice social behavior. The work presented in the first two chapters of the thesis was to develop and validated a new behavioral test to assess the ability to discriminate unfamiliar conspecific based on their emotional state. The results provide significant new insights on the role of the PVN-CeA oxytocin pathway and the implication of an excitatory and inhibitory imbalance in mPFC as core behavioral dysfunctions in social cognitive deficits. The last part of the thesis was focused more on the investigation of the behavioral and physiological effects produced by pharmacological treatment (oxytocin). In particular, taking advantage of the effects oxytocin produced in a mouse model of genetic liability, we investigated the physiological mechanisms of exogenous oxytocin action in the mPFC. All the results presented in this thesis indicate mixed molecular factors for the different social and brain response in mice that may be crucial in the aetiology of the social disease.

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Libros sobre el tema "Substrat neuronal"

Petrovici, Mihai Alexandru. Form Versus Function: Theory and Models for Neuronal Substrates. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-39552-4.

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Hendrik, Gispen Willem y Routtenberg Aryeh, eds. Protein kinase C and its brain substrates: Role in neuronal growth and plasticity : proceedings of the Third International Meeting on Brain Phosphoproteins, held at Zeist (The Netherlands) 24-26 August, 1990. Amsterdam: Elsevier, 1991.

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International Meeting on Brain Phosphoproteins (3rd 1990 Zeist, Netherlands). Protein kinaseC and its brain substrates: Role in neuronal growth and plasticity : proceedings of the Third International Meeting on Brain Phosphoproteins held at Zeist (The Netherlands), 24-26 August, 1990. Amsterdam: Elsevier, 1991.

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Steriade, Mircea. Neuronal Substrates of Sleep and Epilepsy. Cambridge University Press, 2009.

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Steriade, Mircea. Neuronal Substrates of Sleep and Epilepsy. Cambridge University Press, 2005.

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Steriade, Mircea. Neuronal Substrates of Sleep and Epilepsy. Cambridge University Press, 2003.

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Steriade, Mircea. Neuronal Substrates of Sleep and Epilepsy. Cambridge University Press, 2003.

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Steriade, Mircea. Neuronal Substrates of Sleep and Epilepsy. Cambridge University Press, 2003.

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Petrovici, Mihai Alexandru. Form Versus Function: Theory and Models for Neuronal Substrates. Springer, 2018.

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Petrovici, Mihai Alexandru. Form Versus Function: Theory and Models for Neuronal Substrates. Springer International Publishing AG, 2016.

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Capítulos de libros sobre el tema "Substrat neuronal"

Smith, George M., Yingpeng Liu y Jee W. Hong. "Quantitative Assessment of Neurite Outgrowth Over Growth Promoting or Inhibitory Substrates". En Neuronal Cell Culture, 153–61. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-640-5_14.

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Smith, George M. y Yingpeng Liu. "Quantitative Assessment of Neurite Outgrowth Over Growth Promoting or Inhibitory Substrates". En Neuronal Cell Culture, 167–75. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1437-2_13.

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Petrovici, Mihai Alexandru. "Prologue". En Form Versus Function: Theory and Models for Neuronal Substrates, 1–6. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-39552-4_1.

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Petrovici, Mihai Alexandru. "Introduction: From Biological Experiments to Mathematical Models". En Form Versus Function: Theory and Models for Neuronal Substrates, 7–58. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-39552-4_2.

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Petrovici, Mihai Alexandru. "Artificial Brains: Simulation and Emulation of Neural Networks". En Form Versus Function: Theory and Models for Neuronal Substrates, 59–81. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-39552-4_3.

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Petrovici, Mihai Alexandru. "Dynamics and Statistics of Poisson-Driven LIF Neurons". En Form Versus Function: Theory and Models for Neuronal Substrates, 83–142. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-39552-4_4.

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Petrovici, Mihai Alexandru. "Cortical Models on Neuromorphic Hardware". En Form Versus Function: Theory and Models for Neuronal Substrates, 143–217. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-39552-4_5.

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Petrovici, Mihai Alexandru. "Probabilistic Inference in Neural Networks". En Form Versus Function: Theory and Models for Neuronal Substrates, 219–346. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-39552-4_6.

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Petrovici, Mihai Alexandru. "Epilogue". En Form Versus Function: Theory and Models for Neuronal Substrates, 347–49. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-39552-4_7.

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Klein, D., G. Pohlentz, G. Schwarzmann y K. Sandhoff. "Substrate Specifity of GM2 Synthase and GD3 Synthase of Golgi Vesicles Derived from Rat Liver". En Gangliosides and Modulation of Neuronal Functions, 317–18. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71932-5_26.

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Actas de conferencias sobre el tema "Substrat neuronal"

Cao, Guoxin, You Zhou, Jeong Soon Lee, Jung Yul Lim y Namas Chandra. "Mechanical Model of Neuronal Function Loss". En 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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Previtera, Michelle L., Mason Hui, Malav Desai, Devendra Verma, Rene Schloss y Noshir A. Langrana. "Neuronal Precursor Cell Proliferation on Elastic Substrates". En ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53246.

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Numerous stem cells therapies have been studied for the replacement of damaged neurons due to spinal cord injury. Our laboratory’s goal is to design an implantable platform for spinal cord neuron (SCN) proliferation and differentiation in order to replace damaged neurons in the injured spinal cord. Based on previous literature, we suspect we can promote neuronal precursor cell (NPC) proliferation and differentiation utilizing elastic matrices.

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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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Cohen, Larry, Hans-Peter Hoepp, Jian-Young Wu, Chun Xiao, Dejan Zecevic y Jill London. "Optical recording of membrane potential at the single cell level". En OSA Annual Meeting. Washington, D.C.: Optica Publishing Group, 1989. http://dx.doi.org/10.1364/oam.1989.wd2.

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Certain membrane bound dyes change their optical properties (absorption, fluorescence, birefringence) in response to changes in membrane potential. These signals are thought to arise from electrochromic effects, molecular rotation, and/or changes in aggregation state of the dyes. Several factors make a potentially sensitive optical signal interesting to neuroscientists. First is the possibility of making simultaneous measurements from multiple sites; important because many different neurons in a nervous system may be active during each behavior. In addition, optical measurements can be made with excellent time resolution and they are in some sense noninvasive. Optics was used to obtain an overview of the number and activity of neurons in the Aplysia abdominal ganglion during the gill-withdrawal reflex. Action potential activity in cell bodies was monitored via a 124 element photodiode array using the oxonol dye, NK3041 (nee RH155). In a habituated preparation, activity in 90 neurons was detected during the gill-withdrawal reflex. When this preparation was sensitized, we detected activity in 150 neurons during the reflex. The completeness of these recordings was relatively low; between 250 and 400 of the 700 or 1100 neurons present in the abdominal ganglion were actually active during the reflex. Thus the neuronal substrate of a relatively simple reflex in a relatively simple nervous system may be very complex. These experiments would be easier if the optical signals were larger.

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Hockberger, Philip E. y Anita Soekarno. "Image analysis of neuronal pathfinding on microfabricated substrates". En OE/LASE '94, editado por Joseph R. Lakowicz. SPIE, 1994. http://dx.doi.org/10.1117/12.182734.

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Van Dyke, William S., Ozan Akkus y Eric Nauman. "Murine Osteochondral Stem Cells Express Collagen Type I More Strongly on PDMS Substrates Than on Tissue Culture Plastic". En ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14272.

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The discovery of the multipotent lineage of mesenchymal stem cells has dawned a new age in tissue engineering, where an autologous cell-seeded scaffold can be implanted into different therapeutic sites. Mesenchymal stem cells have been reported to differentiate into numerous anchorage-dependent cell phenotypes, including neurons, adipocytes, myoblasts, chondrocytes, tenocytes, and osteoblasts. A seminal work detailing that mesenchymal stem cells can be directed towards differentiation of different cell types by substrate stiffness alone [1] has led to numerous studies attempting to understand how cells can sense the stiffness of their substrate [2–3] Substrate stiffness has been shown to be an inducer of stem cell differentiation. MSCs on extremely soft substrates (250 Pa), similar to the stiffness of bone marrow, became quiescent but still retained their multipotency [4]. Elastic substrates in the stiffness range of 34 kPa revealed MSCs with osteoblast morphology, and osteocalcin along with other osteoblast markers were expressed [1]. However, osteogenesis has been found to increase on much stiffer (20–80 kPa) [5–6] (400 kPa) [7] as well as much softer substrates (75 Pa) [8]. Overall, cells have increased projected cell area and proliferation on stiffer substrates, leading to higher stress fiber formation. This study seeks to understand if the stiffness of the substrate has any effect on the differentiation potential of osteochondral progenitor cells into bone cells, using an in vitro dual fluorescent mouse model.

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Chunlin Li, Jinglong Wu y Hirosi Kusahara. "Investigation of neuronal substrates for language processing, using word priming". En 2009 International Conference on Mechatronics and Automation (ICMA). IEEE, 2009. http://dx.doi.org/10.1109/icma.2009.5246099.

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Grot, Annette, Steven Lin y Demetri Psaltis. "Optoelectronic neurons using MSM detectors in GaAs". En OSA Annual Meeting. Washington, D.C.: Optica Publishing Group, 1991. http://dx.doi.org/10.1364/oam.1991.mk4.

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We present a new GaAs integrated optoelectronic neuron for use in neural networks. We have previously demonstrated that the integration of photodetectors, thresholding transistors, and a light source on a single substrate allows one to have high neuron density with acceptable power dissipation. In this paper we report a circuit in which we used a double heterostructure LED (light emitting diode) as the light source. We use an LED rather than laser diodes because LEDs can be operated with small currents, due to the lack of a threshold current. To minimize the total mesa height and maintain high LED quantum efficiency, MSM (metal–semiconductor–metal) photodetectors were used. The thresholding transistor was a MESFET (metal–semiconductor field-effect transistor). The total mesa height is less than 3 μm. Since no two devices share an epitaxial layer, each device is individually optimized. Our circuit uses two photodetectors, one to set the threshold voltage and the other to detect the signal. With this circuit, we can also build both excitatory and inhibitory neurons. Results from our experimental studies are presented.

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Cao, Guoxin, You Zhou, Jeong Soon Lee, Jung Yul Lim, Shailesh Ganpule y Namas Chandra. "Computational Simulation of the Deformation of Neuronal Cells". En ASME 2010 International Mechanical Engineering Congress and Exposition. ASMEDC, 2010. http://dx.doi.org/10.1115/imece2010-37949.

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A numerical simulation (finite element method (FEM)) is used to determine the local mechanical response of a neuron based on the real neuron geometry. The real 3D geometry of a neuron can be constructed from the 2D confocal image stack which is taken per micron along the thickness direction from the top surface of neuron to the substrate. By matching the simulated deformation of the neuron with the measured results from the confocal microscopy images, the relative strength of the neuron components can be determined based on the reverse analysis of FEM. Then, the neuron local mechanical response and the relationship between the local response and the global applied deformation can be obtained, which will be the first step of building the mechanical injury model of neuron.

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Yang, Jingjing, Xiujun Li, Qi Li, Dan Tong y Jinglong Wu. "Brain Activation Neuronal Substrates of Nonword Priming Effect: An tMRI Study". En 2018 IEEE International Conference on Mechatronics and Automation (ICMA). IEEE, 2018. http://dx.doi.org/10.1109/icma.2018.8484529.

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