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Schulz, Simon R. "Information encoding in the mammalian cerebral cortex." Thesis, University of Oxford, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.284455.
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Rabiei, Hamed. "Spectral analysis of the cerebral cortex complexity." Thesis, Aix-Marseille, 2017. http://www.theses.fr/2017AIXM0289/document.
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La complexité de la forme de la surface est une caractéristique morphologique des surfaces pliées. Dans cette thèse, nous visons à développer des méthodes spectrales pour quantifier cette caractéristique du cortex cérébral humain reconstruit à partir d'images MR structurales. Tout d'abord, nous suggérons certaines propriétés qu'une mesure standard de la complexité de surface devrait posséder. Ensuite, nous proposons deux définitions claires de la complexité de la surface en fonction des propriétés de flexion de surface. Pour quantifier ces définitions, nous avons étendu la transformée de Fourier à fenêtres illustrée récemment pour transformer en maillage des surfaces. Grâce à certaines expériences sur les surfaces synthétiques, nous montrons que nos mesures basées sur la courbure permettent de surmonter les surfaces classiques basées sur la surface, ce qui ne distingue pas les plis profonds des oscillants ayant une surface égale. La méthode proposée est appliquée à une base de données de 124 sujets adultes en bonne santé. Nous définissons également la complexité de la surface par la régularité de Hölder des mouvements browniens fractionnés définis sur les collecteurs. Ensuite, pour la première fois, nous développons un algorithme de régression spectrale pour quantifier la régularité de Hölder d'une surface brownienne fractionnée donnée en estimant son paramètre Hurst H. La méthode proposée est évaluée sur un ensemble de sphères browniennes fractionnées simulées. En outre, en supposant que le cortex cérébral est une surface brownienne fractionnée, l'algorithme proposé est appliqué pour estimer les paramètres Hurst d'un ensemble de 14 corticus cérébraux fœtauxSurface shape complexity is a morphological characteristic of folded surfaces. In this thesis, we aim at developing some spectral methods to quantify this feature of the human cerebral cortex reconstructed from structural MR images. First, we suggest some properties that a standard measure of surface complexity should possess. Then, we propose two clear definitions of surface complexity based on surface bending properties. To quantify these definitions, we extended the recently introduced graph windowed Fourier transform to mesh model of surfaces. Through some experiments on synthetic surfaces, we show that our curvature-based measurements overcome the classic surface area-based ones which may not distinguish deep folds from oscillating ones with equal area. The proposed method is applied to a database of 124 healthy adult subjects. We also define the surface complexity by the Hölder regularity of fractional Brownian motions defined on manifolds. Then, for the first time, we develop a spectral-regression algorithm to quantify the Hölder regularity of a given fractional Brownian surface by estimating its Hurst parameter H. The proposed method is evaluated on a set of simulated fractional Brownian spheres. Moreover, assuming the cerebral cortex is a fractional Brownian surface, the proposed algorithm is applied to estimate the Hurst parameters of a set of 14 fetal cerebral cortices
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NEIDECKER, GUILLEMETTE. "Atrophies cerebrales corticales focalisees primaires : a propos d'une observation d'atrophie corticale posterieure." Lyon 1, 1993. http://www.theses.fr/1993LYO1M186.
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Striegel, Deborah A. "Modeling the folding pattern of the cerebral cortex." Tallahassee, Florida : Florida State University, 2009. http://etd.lib.fsu.edu/theses/available/etd-11092009-184905/.
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Thesis (Ph. D.)--Florida State University, 2009.Advisor: Monica K. Hurdal, Florida State University, College of Arts and Sciences, Dept. of Mathematics. Title and description from dissertation home page (viewed on May 12, 2010). Document formatted into pages; contains xii, 114 pages. Includes bibliographical references.
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Scannell, Jack. "The connectional organization of the cat cerebral cortex." Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.260175.
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Goldman, Jennifer Sarah. "Netrin-1 regulates early development of cerebral cortex." Thesis, McGill University, 2014. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=122967.
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Netrin-1 is a ~75kDa secreted molecule as old as bilateral symmetry in animals, whose existence was initially postulated more than a century ago by Ramon y Cajal. Since the initial discovery of netrin-1 as a determinant of spinal commissural neuron axon guidance, netrin-1 has been attributed manifold roles in the histogenesis of embryonic tissues, functioning both cell and non-cell autonomously, at short and long ranges from the source of its secretion. During mammalian embryonic development, a laminated pallium - the cerebral cortex - blooms out of the neural tube. Cortical neurons born along the lateral ventricles establish polarized processes which connect into synaptic circuits capable of encoding, predicting, remembering, and even comprehending the complex statistics of the environment. Developmental defects in the formation of these circuits are associated with developmental cognitive disorders and the disintegration of cortical circuits leads to the devastating cognitive pathologies of dementia. In this thesis I present evidence that netrin-1 directs the development of cortex both during the proliferation of cortical neurons and later during the establishment of excitatory cortical synapses. These findings identify netrin-1 as a novel regulator of the development of excitatory circuits of the cerebral cortex during the generation of neurons and their connection into synaptic circuits.Nétrine-1 est une molécule sécrétée de ~75kDa qui existe depuis le développement de la symétrie bilatérale chez les animaux, et dont l'existence a été postulé il'ya plus d'un siècle par Ramon y Cajal. Depuis la découverte initiale de la nétrine-1 comme un déterminant dans la guidance des axones commissure dans la moelle neurone, la nétrine-1 a été attribué à multiples rôles dans l'histogenèse des tissus embryonnaires, fonctionnant à la fois autonome cellulaire et non cellulaire, et à des distances courtes et longues de la source de sa sécrétion. Les neurones corticaux nées le long des ventricules latéraux mettent en place des processus polarisés qui relient des circuits synaptiques capables de codage, prévision, mémoire, et même la compréhensions des statistiques complexes de l'environnement. Des défauts de développement dans la formation de ces circuits sont associés à des troubles du développement cognitif et la désintégration des circuits corticaux conduisant à des pathologies cognitives dévastateurs de la démence. Dans cette thèse, je présente des preuves que la nétrine-1 dirige le développement du cortex à la fois au cours de la prolifération des neurones corticaux, et plus tard, lors de la mise en place des synapses corticales excitateurs. Ces résultats permettent d'identifier la nétrine-1 comme un nouveau régulateur dans le développement des circuits corticaux au cours de la génération de neurones corticaux et leur connexion à des circuits synaptiques.
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Gariel, Marie-Alice. "Connectivity and Processing in the Macaque Cerebral Cortex." Thesis, Lyon, 2017. http://www.theses.fr/2017LYSE1005/document.
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Pour comprendre comment le cortex cérébral extrait du sens et produit des actions à partir des informations sensorielles, il est nécessaire de comprendre à la fois son architecture et ses états dynamiques. Dans la présente thèse nous avons abordé cette relation structure-fonction au niveau des aires cérébrales, leurs connections et leurs interactions au sein du réseau cortical. Les aires sont connectées entre elles par deux grands types de projections axonales. D'une part, les connections « feedforward » (littéralement « antéroactives ») transmettent l'information des aires sensorielles aux aires de plus haut niveau dans la hiérarchie corticale et dont l'activité sous-tend des représentations plus abstraites. À l'inverse, les connections feedback (rétroactives) relient des aires dans la direction descendante de la hiérarchie corticale, vers les aires sensorielles primaires. Pour explorer les rôles respectifs des connections feedforward et feedback nous avons utilisé une triple approche. Premièrement, nous avons mis en évidence une asymétrie fonctionnelle très nette entre propagation feedforward et feedback grâce à des enregistrements et de la microstimulation électrique dans les aires V1 et V4 de macaques en comportement. D'autre part, nous avons étudié les propriétés globales du réseau cortical grâce à une riche base de données de connectivité basée sur des injections de traceurs fluorescents, et décrit une propriété générale et fondamentale de l'organisation corticale. Enfin, nous avons combiné des propriétés anatomiques des aires corticales et les données de connectivité dans un modèle dynamique à grande échelle du cortexTo understand how the cerebral cortex does what it does, it is necessary to elucidate both how its dynamic states are correlated with the functions it performs, and how it is organised. Many functional and anatomical gradients have been described that reflect the hierarchical abstraction at the heart of cortical computation. It was showed that two flavours of cortical connections exist, and that in the visual cortex they happen to transport information in opposite directions along this gradient. It was also hypothesised that other modalities exhibit the same type of gradient in their respective domains. However, studying requires knowledge of the architecture at different levels (such as the cortical column) and a causal understanding of the functional properties of these types of connections. First, we have studied the dynamics of both feedforward and feedback propagation in the visual system of awake, behaving macaque monkeys. Using the causal method of electrical microstimulation and recording, we have found a dynamic signature of each type of projections and an asymmetry in the way each type of input interacts with ongoing activity in a given visual area. Secondly, thanks to a rich and systematic data set in the macaque, we have found a fundamental organisational principle of the embedded and weighted cortical network that holds also in the more detailed level of neuronal connections inside an area. Finally, we have combined known anatomical gradients with actual inter-areal connectivity into a dynamic model, and here we show how it relates to both the ordering of areas along a hierarchical gradient and the wiring diagram of the cortical network
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Wells, Jason Eric. "Epileptiform bursting in the disinhibited neonatal cerebral cortex." Morgantown, W. Va. : [West Virginia University Libraries], 2003. http://etd.wvu.edu/templates/showETD.cfm?recnum=3005.
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Thesis (Ph. D.)--West Virginia University, 2003.Title from document title page. Document formatted into pages; contains xii, 231 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references.
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Popesco, Magdalena Cristina. "Gene expression in the mouse cerebellar cortex." Columbus, Ohio Ohio State University, 2003. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1072885001.
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Thesis (Ph. D.)--Ohio State University, 2003.Title from first page of PDF file. Document formatted into pages; contains xiii, 184 p.; also includes graphics (some col.). Includes abstract and vita. Advisor: Andrej Rotter, Dept. of Biochemistry. Includes bibliographical references (p. 158-184).
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SUN, Xue-Zhi, Sentaro TAKAHASHI, Chun GUI, Rui ZHANG, Kazuo KOGA, Minoru NOUYE, and Yoshiharu MURATA. "Neuronal Migration and Neuronal Migration Disorder in Cerebral Cortex." Research Institute of Environmental Medicine, Nagoya University, 2002. http://hdl.handle.net/2237/2773.
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Cushion, Thomas David. "Tubulin genes in human disorders of cerebral cortex development." Thesis, Swansea University, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.678290.
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AL, Saidi Waleed Hamdan Khalfan. "Theoretical Investigation of NMDA Effect on the Cerebral Cortex." The University of Waikato, 2008. http://hdl.handle.net/10289/2465.
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This thesis examines the dynamical behaviour of incorporating NMDA (an excitatory neurotransmitter) for the electrodynamic model of the cerebral cortex. The model used is the mean-field model developed by Steyn-Ross et al. (2005) which describes the behaviour of the cortex in terms of parameters averaged over spatially localised populations. The behaviour of the model is determined by the four control parameters: inhibitory effect li, subcortical drive s, and NMDA neurotransmitter e ect set by an excitatory factor le and the magnesium concentration C. Adopting this model could give a better understanding of the cortex functionality and the anaesthetic mechanism. The model predicts that there are either one or three stationary states available to the cortex. We identify two of these with highly activated state and a quiescent state and focus on the transition between the two. Theoretical stability predictions (eigenvalue analysis) verified by a numerical simulation show that the system is unstable between the two Hopf bifurcations. In addition, in the stable region the steady states remains stable under a small perturbation, while in the unstable region either a transition between states or a limit cycle (oscillation) occurs depending on the position of the steady state.
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Evans, Stephen Mark. "Stereological investigation of the ageing of human cerebral cortex." Thesis, University of Liverpool, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.257130.
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Arslan, Salim. "Connectivity-driven parcellation methods for the human cerebral cortex." Thesis, Imperial College London, 2017. http://hdl.handle.net/10044/1/54760.
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The macro connectome elucidates the pathways through which brain regions are structurally connected or functionally coupled to perform cognitive functions. It embodies the notion of representing, analysing, and understanding all connections within the brain as a network, while the subdivision of the brain into interacting cortical units is inherent in its architecture. As a result, the definition of network nodes is one of the most critical steps in connectivity network analysis. Parcellations derived from anatomical brain atlases or random parcellations are traditionally used for node identification, however these approaches do not always fully reflect the functional/structural organisation of the brain. Connectivity-driven methods have arisen only recently, aiming to delineate parcellations that are more faithful to the underlying connectivity. Such parcellation methods face several challenges, including but not limited to poor signal-to-noise ratio, the curse of dimensionality, and functional/structural variations inherent in individual brains, which are only limitedly addressed by the current state of the art. In this thesis, we present robust and fully-automated methods for the subdivision of the entire human cerebral cortex based on connectivity information. Our contributions are four-fold: First, we propose a clustering approach to delineate a cortical parcellation that provides a reliable abstraction of the brain's functional organisation. Second, we cast the parcellation problem as a feature reduction problem and make use of manifold learning and image segmentation techniques to identify cortical regions with distinct structural connectivity patterns. Third, we present a multi-layer graphical model that combines within- and between-subject connectivity, which is then decomposed into a cortical parcellation that can represent the whole population, while accounting for the variability across subjects. Finally, we conduct a large-scale, systematic comparison of existing parcellation methods, with a focus on providing some insight into the reliability of brain parcellations in terms of reflecting the underlying connectivity, as well as, revealing their impact on network analysis. We evaluate the proposed parcellation methods on publicly available data from the Human Connectome Project and a plethora of quantitative and qualitative evaluation techniques investigated in the literature. Experiments across multiple resolutions demonstrate the accuracy of the presented methods at both subject and group levels with regards to reproducibility and fidelity to the data. The neuro-biological interpretation of the proposed parcellations is also investigated by comparing parcel boundaries with well-structured properties of the cerebral cortex. Results show the advantage of connectivity-driven parcellations over traditional approaches in terms of better fitting the underlying connectivity. However, the benefit of using connectivity to parcellate the brain is not always as clear regarding the agreement with other modalities and simple network analysis tasks carried out across healthy subjects. Nonetheless, we believe the proposed methods, along with the systematic evaluation of existing techniques, offer an important contribution to the field of brain parcellation, advancing our understanding of how the human cerebral cortex is organised at the macroscale.
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Royackkers, Nicolas. "Modelisation et reconnaissance des sillons du cortex cerebral humain." Caen, 1997. http://www.theses.fr/1997CAEN2058.
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Un grand nombre d'etudes menees sur le cerveau humain utilisent l'anatomie de celui-ci comme referentiel spatial pour localiser ses fonctions. Mais l'anatomie cerebrale s'avere extremement variable d'un individu a l'autre, en particulier au niveau des sillons corticaux. Des outils denommes atlas sont destines a faciliter l'interpretation des images anatomiques cerebrales, et peuvent egalement etre utilises en applications cliniques. Nos travaux visent d'abord a specifier et a realiser un atlas numerique des sillons corticaux a partir d'images irm 3d, puis a concevoir et a implanter une methode realisant l'identification automatique des sillons dans un nouvel examen a partir de cet atlas. Le systeme developpe s'appuie sur une base de donnees contenant des images irm de cerveaux sains dont la partie debouchante des sillons est representee sous la forme de courbes 3d etiquetees. Cette base permet la construction d'un atlas statistique de la topographie corticale d'une irm cerebrale particuliere sous forme d'un modele a priori. L'atlas est completement individualise et adapte a la reconnaissance des sillons du patient observe. Il s'agit d'un graphe dont les nuds representent les sillons, et les arcs les relations qui les unissent. C'est aussi une representation statistique qui decrit la variabilite de la geometrie et de la topologie des sillons corticaux. Reconnaitre les sillons consiste a rechercher les courbes decrivant la topographie corticale la plus proche possible du modele moyen attendu. Il s'avere que la partie surfacique des sillons les plus stables peut etre reconnue automatiquement de maniere efficace et robuste. Les taux de reconnaissance sont plus variables pour d'autres sillons majeurs, mais restent en moyenne tres acceptables. Les informations generees pourront etre utilisees dans un systeme d'aide a l'interpretation d'images anatomiques plus complet.
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Régis, Jean. "Anatomie sulcale profonde et cartographie fonctionnelle du cortex cerebral." Aix-Marseille 2, 1994. http://www.theses.fr/1994AIX20716.
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Ganepola, Tharindu. "Parcellation of the human cerebral cortex using diffusion MRI." Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10044170/.
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Histological methods have long been used to segment the cerebral cortex into structurally distinct cortical areas that have served as a basis for research into brain structure and function and remain in use today. There is great interest in adapting and extending these methods to be able to use non-invasive imaging, so that tighter structure-function relationships can be measured in living subjects. Whilst diffusion neuroimaging methods have been widely applied to white matter, the reduced anisotropy in the thin, complexly folded grey matter of the cortex has so far limited its study. In vivo parcellation pipelines have instead focussed on T1 and T2 weighted MRI. Recent advances in imaging hardware have reignited interest in grey matter diffusion MRI as a viable candidate for characterising architectonic domains. This Thesis explores the capabilities of dMRI as a measure of cortical microstructure using in vivo datasets from healthy adult participants. A cortical parcellation pipeline was developed in which both unsupervised and supervised algorithms were explored. Results were presented at both the group level and single subject level across the entire cortical sheet. The diffusion-based feature space characterised the known variation in cellular composition and fibre density relative to the local cortical surface normal. Thus they remain invariant to the confounding orientation changes associated with cortical folding, which usually inhibit studies of cortical microstructure. The features were compared to the alternative T1w/T2w myelin mapping methods to demonstrate that the diffusion MRI signal provides a complementary mode of contrast. A series of classification experiments were used to determine the most effective methods for utilising diffusion in grey matter applications. Several additional methods from the dMRI literature were compared to highlight the benefit of higher-order tissue representations. Similarly, classification tasks were used to corroborate the benefits of sampling multiple b-values in cortical studies. The experimental chapters provide strong evidence in favour of the future use of diffusion MRI as a measure of the varying microstructure that defines cortical areas.
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Naumann, Robert Konrad. "Comparative areal and modular architecture of the cerebral cortex." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2015. http://dx.doi.org/10.18452/17206.
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Die Neurone der Hirnrinde sind in Mikroschaltkreisen, Modulen und Arealen organisiert. In dieser Doktorarbeit habe ich die Neurobiologie und Hirnrindenstruktur der Etruskerspitzmaus - ein neues Modelltier für neurobiologische Forschung - und die modulare Struktur des entorhinalen Kortex der Ratte untersucht. Die geringe Größe des Gehirns der Etruskerspitzmaus bietet besondere Vorteile für das Verständnis kortikaler Aktivität von Zellgruppen. Die entorhinale Kortex enthält sowohl gut definierte funktionelle als auch anatomische Module und bietet daher eine einzigartige Gelegenheit für das Studium ihrer Wechselbeziehungen. Die Organisation der Hirnrinde der Etruskerspitzmaus reflektiert die Spezialisierung als schnelle, auf taktile Reize spezialisierte Jäger. Mehrere kortikale Regionen, die ein Drittel des kortikalen Volumens ausmachen, reagieren auf taktile Reize. Eine kortikale Hemisphäre enthält nur etwa eine Million Neuronen. Basierend auf der Zellarchitektur und histochemischen Färbungen haben wir 13 kortikale Regionen definiert - eine große Zahl angesichts der geringen Größe des Spitzmausgehirns. Pyramidenzellnester in Schicht 2 des medialen entorhinalen Kortex sind einfach zu identifizieren und eignen sich als Bezugssystem für die verschiedenen modulären Strukturen dieser Hirnregion. Diese Pyramidenzellen bündeln ihre Dendriten hin zu einem Punkt, der sich mit erhöhten Konzentrationen von präsynaptischen cholinergen Markern überschneidet. Cholinerge Transmission ist ein wichtiger Bestandteil des Theta-Rhythmus und unsere Ergebnisse zeigen, daß Pyramidenzellen im Vergleich zu Sternzellen doppelt so stark Theta-moduliert sind. Da fast alle Gitterzellen stark Theta-moduliert sind, ist anzunehmen dass Pyramidenzellen eine wichtige Rolle für die räumliche Navigation spielen. In dieser Arbeit wurden an der Hirnrinde der Etruskerspitzmaus sowie der entorhinalen Hirnrinde der Ratte modellhaft Struktur-Funktions-Beziehungen in der Großhirnrinde aufgeklärt.Neurons of the cerebral cortex are collectively organized into microcircuits, modules and cortical areas. Here, I study the neurobiology and cortical structure of the Etruscan shrew - a new model animal for neurobiological research - and the modular structure of the entorhinal cortex of the rat. The small size of the Etruscan shrew''s brain offers particular advantages for understanding cortical activity at the multi-cell level, due to its small number of cortical neurons and its intrinsic advantages for optical imaging approaches. The entorhinal cortex contains well-defined functional and anatomical modules and provides a unique opportunity for studying their interrelation. The organization of the cerebral cortex of the Etruscan shrew reflects their behavioral specialization as fast touch-and-kill hunters. Several cortical areas comprising a third of the cortical volume respond to vibrissal touch. One cortical hemisphere contains only about 1 million neurons. Cytoarchitecture and histochemical staining revealed 13 cortical regions - a large number considering the small size of the shrew''s brain. Pyramidal cell clusters in layer 2 of medial entorhinal are reliably identifiable and thus provide common anatomical framework for entorhinal cortex modularity. These cells form geometrically arranged clusters and bundle their dendrites towards a common point overlapping with presynaptic markers of cholinergic inputs. Cholinergic drive is an important component of theta-rhythmicity which we found to be two-fold stronger in pyramidal than in stellate neurons. Since nearly all grid cells are strongly theta modulated, we suggest that pyramidal cells may play an important role in microcircuits for spatial navigation. In this work, we studied the areal architecture of the Etruscan shrew cortex and the modular architecture of the rat medial entorhinal cortex as contributions towards understanding structure-function relations in the cerebral cortex.
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Camassa, Alessandra. "Spatiotemporal dynamics of the cerebral cortex: from unconscious brain states towards consciousness." Doctoral thesis, Universitat de Barcelona, 2021. http://hdl.handle.net/10803/672946.
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Understanding the dynamics of the brain that gives rise to conscious experience and that underscore the transition through different brain states is one of the central problems of today’s neuroscience. The cerebral cortex as a structured network is capable to spontaneously express different types of dynamics that are continuously changing over time according to the ongoing brain state. Transitions across physiological or pharmacologically induced brain states are correlated with changes in network excitability and functional connectivity, giving rise to a wide repertoire of spatiotemporal patterns of neuronal activity. In this context, the pharmacologically induced brain states transitions provide a good model to understand the interplay of mechanisms that give rise to conscious behavior, where more gradual changes can be induced in order to disentangle the transitions dynamics. In this Thesis, we developed a set of new analytical tools to provide a thorough analysis of the cortical spatiotemporal dynamics under highly synchronized, unconscious brain states characterized by slow wave activity, and during the transitions towards consciousness. We reveal the mechanisms related to such activity at multiple scales, in vivo, in vitro and in silico, and their relationship with the disruption of causal interactions that causes the drop of cortical complexity typical of unconscious brain states.Comprender la dinámica del cerebro que da lugar a la experiencia consciente y que caracteriza las transiciones a través de diferentes estados cerebrales es uno de los problemas centrales de la neurociencia actual. La corteza cerebral es una red estructurada capaz de expresar de forma espontánea diferentes tipos de dinámicas que cambian continuamente de acuerdo con el estado cerebral. Las transiciones a través de estados cerebrales fisiológicos (e.g. sueño, vigilia) o inducidos farmacológicamente (e.g. anestesia) se correlacionan con cambios en la excitabilidad de la red y la conectividad funcional que dan lugar a un amplio repertorio de patrones espacio-temporales de actividad neuronal. En consecuencia, especulamos que mediante el estudio de la dinámica espaciotemporal de la corteza cerebral y su complejidad es posible estimar el nivel de conciencia relacionado con cada estado cerebral. En este contexto, nuestro objetivo es explorar y cuantificar cómo varía la dinámica cortical dentro de un mismo estado cerebral, y durante las transiciones de estado del cerebro. Para ello, desarrollamos aquí nuevos métodos analíticos para el estudio de la propagación de ondas lentas, la sincronización de la red y su complejidad. Aplicamos dichas medidas tanto a la actividad espontánea en estados de alta sincronización asociados a falta de consciencia, como a la actividad evocada de la corteza cerebral a múltiples escalas in vivo, in vitro e in silico. Nuestros resultados demuestran que es posible modular la actividad de ondas lentas típica de los estados de inconsciencia a través de manipulaciones experimentales químicas y eléctricas, obteniendo sub-estados, cada uno caracterizado por distintas propiedades dinámicas que reflejan los estados cerebrales de la corteza en las transiciones hacia estados en los que la consciencia emerge. Además, revelamos aquí los mecanismos relacionados con la actividad cortical sincrónica que se asocia a estados de falta de consciencia, y su relación con la disrupción de interacciones causales que provoca la caída de la complejidad cortical típica de dichos estados cerebrales.
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LHULLIER, CHANTAL. "Evaluation de l'attention dans les lesions aigues du cortex posterieur." Lille 2, 1994. http://www.theses.fr/1994LIL2M279.
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McGuire, Philip K. "The distribution of Cat-301 immunoreactivity in the cerebral cortex." Thesis, University of Edinburgh, 1992. http://hdl.handle.net/1842/28581.
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The distribution of the monoclonal antibody Cat-301 was examined in the cerebral cortex of macaque monkeys. Throughout the cerebral cortex, Cat-301 labelled the soma and proximal dendrites of a restricted population of neurones. The distribution was uniform within cytoarchitecturally defined areas (or subareas) but varied between them, with respect to the density of labelled neurones, the intensity of their immunoreactivity, their morphology, and their laminar distribution. Large numbers of intensely immunoreactive neurones were evident in motor related areas of the frontal lobe, somatosensory areas in the pareital lobe, and areas specialised for the analysis of visual motion in the parietal and occipital lobes. The heavily labelled areas are known to be interconnected, and the Cat-301 positive neurones within them were concentrated in the laminae from which their cortico-cortical connections arise. Given the critical role of somatosensory and visuospatial information in the execution of somatic and ocular movements, the heavily labelled areas may be regarded as sharing a broadly motor function. The timing of the expression of the antigen recognised by Cat-301 during development, its peri-synaptic location, and its biochemical characteristics suggest that it may play a role in the stabilisation of synaptic connections. Cat-301 may label networks of areas with a similar functional specialisation because the antigen plays such a role in relation to the specific interconnections that exist between them.
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Michel, Anton D. "α-adrenoceptor subtypes in rat cerebral cortex and vas deferens." Thesis, Heriot-Watt University, 1985. http://hdl.handle.net/10399/1618.
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Chan, Chun-Hun. "Development of the cerebral cortex : emx genes and interneuron migration." Thesis, University College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.368096.
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Alsiö, Jessica Martina. "Functions of Ikaros family transcription factors in cerebral cortex development." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610061.
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Wang, Peter Pei. "Progenitor Cell Diversity and Function in the Developing Cerebral Cortex." Thesis, Harvard University, 2015. http://nrs.harvard.edu/urn-3:HUL.InstRepos:17467353.
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The human cerebral cortex, the largest structure of our brain, is the seat of our most highly developed cognitive functions. Its normal development, proper function, and ultimate size depend on a precisely controlled balance between self-renewal and differentiation of neural progenitor cells that reside in distinct germinal zones during development. Compared to other species, human cortical progenitor cells are exceptionally diverse in both cellular morphology and gene expression profile.
In particular, previous work has identified specialized progenitors, called outer radial glia (ORG), that are especially common in humans yet virtually absent in rodents and other species with relatively smaller brains. This has led to the suggestion that ORG may represent targets of developmental mechanisms underlying the rapid evolutionary expansion of the human cortex. However, these cells have not been sufficiently profiled at the transcriptional level. To address this question, we combined cell type-specific sorting of cortical progenitor cells with transcriptome-wide RNA-sequencing (RNA-seq) to identify genes enriched in human ORG, which included several targets of the transcription factor Neurogenin as well as a surprising number of previously unknown, evolutionarily dynamic long noncoding RNAs (lncRNAs). We showed that activating the Neurogenin pathway in cortical progenitors of the ferret, a species with abundant ORG, promotes delamination and outward migration. We then used single-cell transcriptional profiling to compare patterns in human, ferret, and mouse progenitors, and found that a larger proportion of human RGC co-express proneural Neurogenin targets, suggesting greater self-renewal of neuronal lineage-committed progenitors in humans. Finally, comparative genomic analysis of several novel, human ORG-enriched long noncoding RNA genes indicated that many of these loci, while potentially present in the common ancestor of human, ferret, and mouse, show highly distinct patterns of ORG expression accompanied by greater genomic sequence divergence in rodents.
Taken together, we find that the expansion of the ORG subpopulation and increased cortical size in humans is paralleled by increased transcriptional diversity of human RGC. Furthermore, we identify coding and noncoding genes that may be involved in human cortical progenitor identity, function, and evolution.Medical Sciences
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Pinto, Luisa. "Molecular mechanisms regulating neurogenesis in the developing mouse cerebral cortex." Diss., kostenfrei, 2008. http://edoc.ub.uni-muenchen.de/9379/.
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Rakic, Sonja. "The role of p35/Cdk5 in the developing cerebral cortex." Thesis, University College London (University of London), 2005. http://discovery.ucl.ac.uk/1445810/.
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This thesis has focussed on the role of cyclin-dependent kinase 5 (Cdk5) and its activator, p35, in controlling the proper formation of the cerebral cortex. First, cortical layer formation in p35 mutants was re-examined. Interestingly, the prenatal layer I (LI) seems wider, more cellular, and without a clear border with the cortical plate (CP) in these animals. Second, interneuron arrangement in p35 and Cdk5 mutants was studied. Molecules, such as neuregulins (NRGs), which can bind to ErbB receptors and potentially signal through the p35/Cdk5 pathway, were also examined. Cortical interneurons express Cdk5, but Cdk5 is not active in developing forebrain in p35 mutants. It appears that migration of cortical interneurons from the ganglionic eminence (GE) is a Cdk5-independent process. However, my results have suggested that: (i) radial inward migration of interneurons, from LI into the CP, might be a Cdk5-dependent mechanism (ii) prenatal cortical interneurons and projection neurons do not communicate directly. Intriguingly, ErbB4 is highly expressed on the surface of migrating cortical interneurons. Two intracellular isoforms of the rat ErbB4 exist, with one having a unique tyrosine residue for binding PI3-kinase. I have shown that, although ErbB4 signalling is necessary for migration of cortical interneurons from the GE, this process could occur through a PI3K-independent mechanism. The hypothesis that the ErbB4 receptor signals via the Cdk5 pathway was also tested. I found that: (i) Roscovitine, a Cdk5 specific inhibitor, impairs the neuronal chemotactic response to NRGlp (ii) Cdk5 phosphorylates ErbB4 threonine (1152) in vitro. Third, splitting of the preplate layer (PPL) in p35 mutants was studied. In these animals the PPL splits incompletely, which results in misplaced subplate neurons and reeler-Uke positioning of thalamocortical axons. In summary, my experiments have provided novel information about some signalling molecules, and their receptors, that are involved in the migration of cortical neurons.
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Pinho, Diana Vanessa Arcanjo. "Modulação purinérgica da transmissão noradrenérgica no córtex cerebral." Master's thesis, Universidade de Aveiro, 2010. http://hdl.handle.net/10773/3852.
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Mestrado em Bioquímica - Métodos BiomolecularesNo córtex cerebral de rato, a libertação de noradrenalina (NA) pode ser desencadeada por activação de neurónios que se projectam a partir do locus coeruleus ou então por activação local dos receptores NMDA do glutamato. Ambos os processos são regulados por nucleótidos como o ATP, através da activação de receptores P2Y, embora os subtipos de receptores P2Y envolvidos ainda não tenham sido identificados. O ATP desempenha igualmente um papel importante na captação de NA pelos astrócitos e na comunicação neurónio-astrócito em sinapses noradrenérgicas e uma desregulação na transmissão noradrenérgica pode contribuir para várias patologias como as perturbações do humor (depressão, doença bipolar, mania, ansiedade) e as doenças neurodegenerativas. O objectivo deste estudo consistiu na caracterização dos receptores P2Y envolvidos na regulação da transmissão noradrenérgica no córtex cerebral de Rato, através do estudo do efeito de vários agonistas purinérgicos e da sua interacção com antagonistas selectivos, na modulação da libertação de NA induzida por estimulação eléctrica (100 pulsos a 5 Hz) em fatias de córtex, e na captação de NA em culturas primárias de astrócitos. Os nucleótidos ATP, ADP, ADPβS, UTP, UDP inibiram a libertação de NA até 58% com a seguinte ordem de potência: ADP ≥ ATP> ADPβS > UTP≥ UDP. O efeito inibitório do ADP (0,3 mM) e do ADPβS (0,3 mM) foram ambos bloqueados pelos antagonistas selectivos dos receptores A1 e P2Y1, DPCPX (0,1 μM) e MRS 2500 (1 M), respectivamente. Os efeitos inibitórios do UTP (1 mM) e UDP (1 mM) foram ambos antagonizados pelo MRS 2578 (1 M) que é um antagonista selectivo para os receptores P2Y6. Ao contrário do ADP (0,3 mM), o efeito do ADPβS (0,3 mM) não foi modificado pela desaminase da adenosina (ADA, 2U/ml), excluindo um papel da adenosina nos efeitos antagonizados pelo DPCPX (0,1 μM). No entanto o efeito do ADPβS foi abolido pela combinação de DPCPX (0,1 μM) e MRS 2500 (1 μM), sugerindo parte do efeito inibitório deste agonista na libertação de NA poderá ser mediada por heterodímeros A1/P2Y1. Nas culturas de astrócitos, os agonistas ADP S (0,1 mM), UDP (1 mM) e CGS 21680 (0,1 μM) aumentaram captação de NA até 117 %. O efeito do ADPβS (0,1 mM) foi antagonizado pelo MRS 2500 (0.1 μM) e pelo antagonista selectivo dos receptores P2Y12 AR-C66096 (10 μM). O efeito do UDP (1 mM) foi atenuado pelo MRS2578 (1 μM) e o efeito facilitatório do CGS 21680 (0,1 μM) na captação de NA foi atenuado pelo antagonista selectivo dos receptores A2A SCH58261 (30 nM). Em conclusão, os nucleótidos inibem a libertação de NA por activação de receptores P2Y1, P2Y6, A1 e possivelmente heterodímeros A1/P2Y1. Também aumentam a captação de NA pelos astrócitos através da activação de receptores P2Y1, P2Y12,P2Y6 e A2A, em ambos os casos conduzindo a uma inibição da transmissão noradrenérgica no córtex cerebral.
In the rat cerebral cortex, release of noradrenaline (NE) can be triggered by activation of neurons projecting from locus coeruleus and by locally released glutamate through activation of NMDA receptors. Both mechanisms are regulated by nucleotides such as ATP, which acts through activation of P2Y receptors; however the subtypes involved have not yet been identified. ATP plays an equally important role in the uptake of NE by astrocytes and in the neuron-astrocyte communication at noradrenergic synapses, with a deregulation of noradrenergic transmission being associated to the pathogenesis of several mood disorders and neurodegenerative diseases. The aim of this thesis was to identify, in the rat barin cortex, the P2Y receptors involved in the regulation of noradrenergic transmission by testing the effect of several purinergic agonists and its interaction with selective antagonists in NE release, evoked by electrical field stimulation (100 pulses at 5 Hz) of cortical brain slices, and in NE uptake by primary cultures of cortical astrocytes. The nucleotides ATP, ADP, ADPβS, UTP and UDP caused an inhibition of NE release up to 58% with the following order of potency: ADP≥ATP> ADPβS>UTP≥UDP. The inhibitory effect of ADP (0,3 mM) and ADPβS (0,3 mM) were both attenuated by the selective antagonists of A1 and P2Y1 receptors, DPCPX (0,1 μM) and MRS 2500 (1 M), respectively. The inhibitory effects of UTP (1 mM) and UDP (1 mM) were antagonized by MRS 2578 (1 M) which is a selective P2Y6 receptor antagonist. Unlike the effect of ADP (0,3 mM), the effect of ADPβS (0,3 mM) was not changed by the adenosine deaminase, excluding the participation of adenosina on the effects antagonized by DPCPX (0,1 μM). However, the effect of ADPβS was abolished by DPCPX (0,1 μM) in combination with MRS 2500 (1 μM), suggesting that a component of the inhibitory effect of this agonist in the NA release could be mediated by A1/P2Y1heterodímers. In primary astrocyte cultures, the agonists ADP S (0,1 mM), UDP (1 mM) and CGS 21680 (0,1 μM) all increased NE uptake up to 117 %. The effect of ADPβS (0,1 mM) was almost abolished by MRS 2500 (0.1 μM) and was also attenuated by the P2Y12 antagonist AR-C66096 (10 μM) whereas the effect of UDP (1 mM) was attenuated by MRS 2578 (1 μM) and the facilitatory effect of CGS 21680 (0,1 μM) on NE uptake was reduced by the selective antagonist of A2A receptors SCH 58261 (30 nM). In conclusion, the nucleotides tested inhibited NE release evoked by electrical stimulation through activation of P2Y1, P2Y6, A1 receptors and eventually A1/P2Y1 heterodímers. Additionally, they increased NA uptake by astrocytes upon activation of P2Y1, P2Y12 ,P2Y6 e A2A receptors, in both cases leading to an inhibition of the noradrenergic transmission in the rat brain cortex.
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Bozicovich, Thais Freitas Marques [UNESP]. "Efeito do enriquecimento ambiental sobre a ansiedade e morfologia neuronal de coelhos (Oryctolagus cuniculus)." Universidade Estadual Paulista (UNESP), 2015. http://hdl.handle.net/11449/138525.
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000860125.pdf: 2144441 bytes, checksum: ecb35b63c1ad4deb4ecb1a021fcb8317 (MD5)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
O estudo foi realizado com 56 coelhos do grupo genético Botucatu desmamados com 35 dias de idade e acompanhados até atingirem 79 dias. O objetivo foi avaliar a ansiedade de coelhos em crescimento frente a dois tipos de enriquecimento: o ambiental e o social. Os animais foram distribuídos em um delineamento inteiramente casualizado, com arranjo fatorial de 2 x 2 (com ou sem enriquecimento físico e com ou sem enriquecimento social), com 4 repetições. Os animais com enriquecimento social foram alojados em oito gaiolas coletivas, seis por gaiola; já os animais privados do contato social foram alojados em oito gaiolas individuais. Chapas galvanizadas foram instaladas nas paredes laterais destas gaiolas para evitar o contato visual entre os animais. Metade das gaiolas (individuais e coletivas), definidas ao acaso, foi enriquecida com pedaços de eucalipto dependurados no teto da gaiola. A avaliação da ansiedade foi realizada com o uso do labirinto em cruz elevado, por meio dos comportamentos de locomoção e os relacionados à ansiedade (imobilização). Realizou-se a observação do tempo de latência até mover-se para um dos braços, bem como o número de entradas e o tempo gasto em cada um dos braços abertos e fechados. Duas observações foram realizadas, cada uma com duração de 5 minutos: a primeira aos 49 e a segunda aos 77 dias de idade. Houve avaliação do desempenho de crescimento dos animais (ganho de peso, consumo e conversão alimentar). Os coelhos alojados sem enriquecimento social permaneceram mais tempo tanto nos braços abertos quanto nos braços fechados, que os animais em grupo. Contudo os animais com enriquecimento social demoraram menos tempo para entrar nos braços abertos, bem como para chegar até o final dos mesmos, além de apresentarem maior número de mergulhos. Nos animais alojados em grupo, os mais velhos fizeram mais tentativas de entrar nos braços abertos que os mais...
The study was carried out with 56 rabbits from the Botucatu genetic group weaned at 35 days of age and followed up to 79 days of age. The objective was to evaluate the anxiety of growing rabbits using two types of enrichment: physical and social. The animals were assigned to a completely randomized design with a 2 x 2 factorial arrangement (with or without physical enrichment and with or without social enrichment), with four replicates. The animals with social enrichment were allocated six per cage in eight wire cages whereas the animals deprived of social contact were housed in eight individual wire cages. Galvanized sheets were adapted to the lateral parts of these cages to avoid the visual contact with other animals. Half the cages, randomly chosen, were enriched with eucalyptus sticks hung to the cage ceiling. The evaluation of anxiety was conducted using the elevated plus maze, through the locomotor activity and immobilization behaviors. The latency time to enter one of the arms, as well as the number of entries into and the time spent in each of the arms (open and closed) were recorded. Two observations were made, with the duration of 5 minutes each: the first at 49 and the second at 77 days of age. Growth performance was also assessed (average daily gain, feed consumption and feed conversion). The rabbits housed without social enrichment stayed longer both in the open and closed arms than the animals housed in groups. However, the later showed shorter latency to enter the open arms as well as to reach the end of the open arm, besides presenting a higher number of head dipping. Group-housed animals made more entries into the open arms when they were older than when they were younger. Isolated animals, on the other hand, showed the opposite response: a higher number of entries into the open arms when they were younger than when they were older. The rabbits in physically enriched environment show ...
FAPESP: 12/17157-7
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Berlin, Heather. "Impulsivity, the orbitofrontal cortex and borderline personality disorder." Thesis, University of Oxford, 2003. http://ora.ox.ac.uk/objects/uuid:df454308-aea1-448a-9237-83735452947f.
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Damage to the orbitofrontal cortex (OFC) has been associated with disinhibited or socially inappropriate behaviour and emotional irregularities in both humans and monkeys. Prominent characteristics of several personality disorder syndromes, in particular Borderline Personality Disorder (BPD), are impulsivity and affective instability. This investigation aimed to determine if certain aspects of the Borderline Personality syndrome, in particular impulsivity, are associated with OFC dysfunction. Basic questionnaires of personality, emotion, and impulsivity together with tasks sensitive to frontal lobe dysfunction that assess possible factors related to impulsivity, including time perception, sensitivity to reinforcers, and spatial working memory (SWM), were administered to OFC lesion, BPD, non-OFC prefrontal cortex lesion control, and normal control participants. OFC and BPD patients performed similarly, in that they were more impulsive, reported more inappropriate behaviours, BPD traits, anger, and less happiness than both control groups. They were also less open to experience and had a faster perception of time (in terms of time production) than normal controls. They performed differently on other tasks: BPD patients were less extraverted and conscientious and more neurotic and emotional than all other groups. OFC patients had more severe deficits in reversing stimulus-reinforcer associations compared to all other groups and had a faster perception of time (in terms of time estimation) than normal controls. Both OFC and non-OFC lesion patients had mixed lesions that included dorsolateral prefrontal cortex (DLFC) damage. Accordingly, they both had SWM deficits, a task used to control for DLFC damage, compared to normal and BPD participants. Since BPD participants were not impaired on this task and non-OFC patients did not perform poorly on the same tests that OFC patients did, the neuropsychological deficits of BPD and OFC patients could not be attributed to SWM deficits or DLFC dysfunction. The findings suggest that some of the cognitive/behavioural deficits commonly found in BPD patients are related to OFC dysfunction while others are unrelated and are perhaps related to other brain systems. The possibility of amygdala dysfunction is discussed. The similarities and dissociations found between BPD and OFC patients on certain tasks may lead to a better understanding of the aetiology of BPD and the functions of the OFC. Theoretical and therapeutic implications of the findings are discussed.
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Jercog, Daniel Alejandro. "Dynamics of spontaneous activity in the cerebral cortex across brain states." Doctoral thesis, Universitat de Barcelona, 2013. http://hdl.handle.net/10803/134500.
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Spontaneous activity in the cerebral cortex changes in different brain states. During desynchronized brain states (e.g. wakefulness, REM sleep), populations of neurons in the cerebral cortex fire action potentials in a stochastic and uncorrelated manner. In contrast, during synchronized states (e.g. slowwave sleep, anesthesia) cortical neurons display the alternation between quiescent periods (DOWN) and periods of spiking activity (UP) coherently across cortical layers. In recent years, the view has emerged that brain states are not defined in discrete categories, but rather form a continuum of possible states.
In this thesis, we address three main questions regarding this phenomenon: How is the oscillatory activity at high frequencies (10-100 Hz) distributed across the cortical laminae during UP states? What are the mechanisms underlying UP and DOWN dynamics in neocortex in vivo? How do brain states shape the statistics of cortical spontaneous activity?
First, we analyzed laminar local field potential recordings of spontaneous activity in the visual cortex in vivo and characterized the laminar profile of fast oscillatory activity present during UP states, which showed overall similar spectral properties across layers but were generated independently in two different compartments determined by superficial and deep cortical layers. In order to explore whether this laminar profile of fast oscillatory activity was generated intrinsically by cortical circuitry or by external inputs, we performed simultaneous local field potential recordings in spontaneously active cortical slices in vitro. By manipulating the slices pharmacologically, we concluded that neural excitability can control inter-laminar couplings and oscillatory dynamics in cortical circuits.
Second, we made a quantitative analysis of UP and DOWN dynamics in vivo by analyzing multiple single-unit cortical recordings during synchronized states. The classic view about what causes cortical UP and DOWN dynamics during synchronized states implicates a "fatigue" or adaptation process (such as spike frequency adaptation or synaptic depression), but our results were inconsistent with a dominant role for this mechanism. Using a low dimensional modeling approach, we proposed a rate model that displays UP and DOWN dynamics, in which bistability can be obtained at arbitrarily low rates. With this model we explored the role and interplay of adaptation and external fluctuations in shaping the statistics of UP and DOWN state dynamics, and determined that a regime of weak adaptation and strong fluctuations is necessary to qualitatively reproduce the statistical features of the experimental data.
Finally, we studied the impact of brain states in cortical dynamics. Under urethane anesthesia, spontaneous transitions between synchronized states (with UP and DOWN state dynamics) and desynchronized states (with sporadic or absent DOWN states) are observable, and these transitions resemble those observed from slow-wave to REM sleep states. Investigating multiple single-unit recordings during these transitions, we found that the statistics of UP and DOWN states are largely determined by the brain state in a continuous manner, consistently across experiments and cortical areas. This constrains the possible cortical mechanisms modulated during transitions between desynchronized and synchronized states, as revealed in a low-dimensional firing rate network model.La actividad espontánea en la corteza cerebral cambia en diferentes estados cerebrales. Durante estados desincronizados (e.g. estado de vigilia, sueño MOR), las poblaciones de neuronas en los potenciales de acción en una manera aparentemente estocástica y no correlacionada. Por el contrario, durante estados sincronizados (e.g. sueño de ondas lentas, anestesia) las neuronas corticales muestran la alternancia entre periodos de reposo (DOWN) y los períodos de actividad (UP) de manera coherente a través de las capas corticales. En los últimos años, ha emergido la visión de que los estados cerebrales no están definidos en categorías discretas, sino que forman un continuo de estados posibles. En esta tesis, nos dirigimos a tres preguntas principales con respecto a este fenómeno: ¿Cómo es la actividad oscilatoria a altas frecuencias (10-100 Hz) distribuída a través de las capas de la neocorteza durante los períodos UP? ¿Cuáles son los mecanismos que subyacen a la dinámica UP y DOWN en el neocórtex in vivo? ¿Cómo se determinan los estados cerebrales estadísticas de actividad espontánea cortical? En primer lugar, analizamos registros de potencial de campo local en la corteza visual in vivo y caracterizamos el perfil laminar de actividad oscilatoria rápida durante los estados UP, que mostraron en general propiedades espectrales similares a través de las distintas capas, pero generadas de forma independiente en dos compartimentos distintos determinados por capas corticales superficiales y profundas. Con el fin de explorar si este perfil laminar de la actividad oscilatoria rápida es generada intrínsecamente por los circuitos corticales o por inputs externos, se realizaron registros de potencial de campo local en rebanadas corticales espontáneamente activas in vitro. Mediante la manipulación farmacológica in vitro, se concluyó que la excitabilidad neuronal puede controlar los acoplamientos entre capas y dinámica oscilatoria en los circuitos corticales. En segundo lugar, realizamos un análisis cuantitativo de la dinámica UP y DOWN in vivo mediante el análisis de registros corticales múltiples de una sola unidad durante estados sincronizados. El punto de vista clásico sobre las causas de esta dinámica durante los estados sincronizados implica un mecanismo de "fatiga" o proceso de adaptación (e.g. adaptación de frecuencia disparo o depresión sináptica), pero los resultados que observamos resultan inconsistentes con un papel dominante de este mecanismo. Utilizando un enfoque de modelado de baja dimensión, propusimos un modelo que muestra dinámica UP y DOWN, en la que biestabilidad se puede conseguir a tasas de descarga arbitrariamente bajas. Con este modelo hemos explorado el papel y la interacción de la adaptación y las fluctuaciones externas en la conformación de las estadísticas de la dinámica del estado UP y DOWN, y determinamos un régimen de adaptación débil pero con fluctuaciones fuertes es necesario para reproducir cualitativamente la estadística de los datos experimentales. Por último, transiciones espontáneas entre estados sincronizados (con la dinámica del estado UP y DOWN) y estados desincronizados (con los períodos DOWN esporádicos o ausentes) son observables bajo la influencia del anestésico uretano, y estas transiciones se asemejan a las observadas a partir de ondas lentas de los estados de sueño REM. Investigando registros múltiples de una sola unidad durante estas transiciones, encontramos que la estadísticas de la dinámica UP y DOWN está determinada en gran medida por el estado del cerebro de forma continua, de manera consistente a través de experimentos y áreas corticales. Esto limita los posibles mecanismos corticales modulados durante las transiciones entre estados desincronizados y sincronizados, tal como lo revela el uso de un modelo de baja dimensión.
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Van, Den Ameele Jelle. "Identification of new genes that control neurogenesis in the cerebral cortex." Doctoral thesis, Universite Libre de Bruxelles, 2014. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/209298.
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The cerebral cortex is one of the most complex and divergent of all biological structures and is composed of hundreds of different types of highly interconnected neurons. This complexity underlies its ability to perform exceedingly complex neural processes. One of the most important questions in developmental neurobiology is how such a vast degree of diversity and specificity is achieved during embryogenesis. Furthermore, understanding the cellular and genetic basis of cortical development may yield insights into the mechanisms underlying human disorders such as mental retardation, autism, epilepsies and brain tumors. During this Phd-project, we set out to identify novel transcription factors involved in cortical neurogenesis. Therefore, we initially took advantage of a model of in vitro embryonic stem cell (ESC)-derived corticogenesis that was previously established in the lab (Gaspard et al. 2008) and from several previously generated ESC lines that allow overexpression of specific transcription factors potentially involved in corticogenesis (van den Ameele et al. 2012).
Among the genes tested, Bcl6, a B-cell lymphoma oncogene known to be expressed during cortical development but without well-characterized function in this context, displayed a strong proneurogenic activity and thus became the main focus of this thesis.
During neurogenesis, neural stem/progenitor cells (NPCs) undergo an irreversible fate transition to become neurons. The Notch pathway is well known to be important for this process, and repression of Notch-dependent Hes genes is essential for triggering differentiation. However, Notch signalling often remains active throughout neuronal differentiation, implying a change in the transcriptional responsiveness to Notch during the neurogenic transition.
We showed that Bcl6 starts to be expressed specifically during the transition from progenitors to postmitotic neurons and is required for proper neurogenesis of the mouse cerebral cortex. Bcl6 promotes this neurogenic conversion by switching the composition of Notch-dependent transcriptional complexes at the Hes5 promoter. Bcl6 triggers exclusion of the co-activator Mastermind-like 1 and recruitment of the NAD+-dependent deacetylase Sirt1, which we showed to be required for Bcl6-dependent neurogenesis in vitro. The resulting epigenetic silencing of Hes5 leads to neuronal differentiation despite active Notch signalling. These findings thus suggest a role for Bcl6 as a novel proneurogenic factor and uncover Notch-Bcl6-Sirt1 interactions that may affect other aspects of physiology and disease (Tiberi et al. 2012a).
A subsequent yet unpublished part of this Phd-project focused on unraveling roles for Bcl6 in regionalization of the cerebral cortex. In all mammals, the three major areas of the neocortex are the motor, somatosensory and visual areas, each subdivided in secondary domains and complemented with species-specific additional areas. All these domains comprise of neurons with different functionality, molecular profiles, electrical activity and connectivity. Spatial patterning of the cortex is mainly under the control of diffusible molecules produced by organizing centers, but is also regulated by intrinsic, cell-autonomous programs (Tiberi et al. 2012b).
Since Bcl6 expression is confined to frontal and parietal regions of the developing cerebral cortex and remains high in postmitotic neurons, also after completion of neurogenesis, we hypothesized it would be involved in acquisition of motor and somatosensory identity. As expected from the neurogenesis defect in these regions, we observed a trend towards a reduced size of the frontal areas in the Bcl6 mutant cortex. Preliminary data from cDNA microarray profiling after gain- and loss-of-function of Bcl6 and from in situ hybridization on mouse cortex however do not show dramatic changes in molecular markers of different cortical areas. Similarly, the coarse-grained pattern of thalamocortical and efferent projections of motor and somatosensory neurons appears to be spared. These preliminary findings thus suggest that Bcl6 is not strictly required for proper acquisition of motor and somatosensory areal identity.
Doctorat en Sciences médicales
info:eu-repo/semantics/nonPublished
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Adams, Julian David. "Excitotoxin-induced changes in gene expression in the rat cerebral cortex." Thesis, Imperial College London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.339139.
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Su, Shen-Wei. "Modelling blood flow and oxygen transport in the human cerebral cortex." Thesis, University of Oxford, 2012. http://ora.ox.ac.uk/objects/uuid:cee70abb-8c36-4244-920c-71305cf97bd0.
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Dementia, a stepwise deterioration of cognitive function, affects over 700,000 people in the UK, resulting in over 60,000 deaths and a cost of over £1.7 billion each year. It is believed to have a combination of vascular and degenerative origins and to have correlations with localised lesions, or infarctions, in the brains of affected patients. Mini-strokes are one of the causes for this disease as the presence of ischemia is highly related to the risk factors for dysfunction of the neurovascular unit. The underlying interacting mechanisms are, however, often very complex and they remain largely poorly understood. The cerebral microvascular bed is highly irregular and localised variations in its structure are large. To capture these variations, statistical algorithms are required, rather than large volumes of expensive experimental data. Therefore, accurate modelling of blood flow and oxygen transport at the microvascular level is important in improving our understanding of the structure and function of the cerebral vasculature and hence of brain diseases. A novel algorithm is proposed here to create artificial microvascular networks that match quantitatively experimental data previously obtained in human brain tissue. Blood flow and oxygen transport in the network and the tissue are analysed through both discretised and continuum transport models. By disabling flow sources, ischemic events can be simulated. Using multiple networks, the influence of individual network structures on the response to ischemia is analysed. The relationship between the discretised and continuum formulations of the model is quantified, providing a means for scaling up the model over multi length scales. Finally, the phenomenon of microvessel collapse under ischemic conditions is examined and it is shown that this is fundamentally dependent upon the variability found at the network level, since it cannot be modelled by a continuum model. An initial infarction is also found to facilitate the occurrence of collapse events for most networks.
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Sparshott, Neil. "Role of FGF receptors (FGFRs) in neurocytogenesis within the cerebral cortex." Thesis, University of East Anglia, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.514345.
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蘇廷弼 and Ting-pat Albert So. "A computerized thermal imaging system for studying thyroid and cerebral cortex." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1994. http://hub.hku.hk/bib/B31233892.
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Al-Gadi, M. A. "Histamine receptors mediating the cyclic AMP accumulation in rabbit cerebral cortex." Thesis, University of Nottingham, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.374811.
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Pennington, Kyla. "Cellular and proteomic analysis of the human cerebral cortex in schizophrenia." Thesis, King's College London (University of London), 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.439397.
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El-Bouri, Wahbi K. "Multi-scale modelling of the microvasculature in the human cerebral cortex." Thesis, University of Oxford, 2017. http://ora.ox.ac.uk/objects/uuid:8a9409a6-6279-4f7b-a975-b70149732378.
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Cerebrovascular diseases are by far the largest causes of death in the UK, as well as one of the leading causes of adult disability. The brain's healthy function depends on a steady supply of oxygen, delivered through the microvasculature. Cerebrovascular diseases, such as stroke and dementia, can interrupt the transport of blood (and hence oxygen) rapidly, or over a prolonged period of time. An interruption in flow can lead to ischaemia, with prolonged interruptions leading to tissue death and eventual brain damage. The microvasculature plays a key role in the transport of oxygen and nutrients to brain tissue; however, its role in diseases such as dementia is poorly understood, primarily due to the inability of current clinical imaging techniques to resolve microvessels, and due to the complexity of the underlying microvasculature. Therefore, in order to understand cerebrovascular diseases, it is necessary to be able to resolve and understand the microvasculature. In particular, generating large-scale models of the human microvasculature that can be linked back to contemporary clinical imaging is important in helping plug the current imaging gap that exists. A novel statistical model is proposed here that generates such large-scale models efficiently. Homogenization theory is used to generate a porous continuum capillary bed (characterised by its permeability) that allows for the efficient scaling up of the microvasculature. A novel order-based density-filling algorithm is then developed which generates morphologically accurate penetrating arterioles and venules, also demonstrating that the topology of the vessels only has a minor influence on CBF compared to diameter. Finally, the capillary bed and penetrating vessels are coupled into a large voxel-sized model of the microvasculature from which pressure and flux variations through the voxel can be analysed. A decoupling of the pressure and flux, as well as a layering of flow, was observed within the voxel, driven by the topology of the penetrating vessels. Micro-infarctions were also simulated, demonstrating the large local effects they have on the pressure and flux, whilst only causing a minor drop in CBF within the voxel.
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Chen, Yijing. "Investigating the mechanism by which thalamocortical projections reach the cerebral cortex." Thesis, University of Edinburgh, 2012. http://hdl.handle.net/1842/6517.
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This thesis provides insights into the mechanism by which thalamocortical axons (TCAs) approach the cortex from their origin in the thalamus. Previous studies suggested that the reciprocal projections from the prethalamus and the ventral telencephalon guide TCAs to descend through the prethalamus and cross the diencephalic-telencephalic boundary (DTB), after which TCAs navigate through permissive corridor cells in the ventral telencephalon and cross the pallial-subpallial boundary (PSPB) before reaching their final targets in the cortex. The ‘Handshake Hypothesis’ proposed that pioneer axons from cortical preplate neurons guide TCAs into corresponding cortical areas. However, there is a lack of convincing evidence on whether TCAs need any guidance to cross the PSPB. In the current study, Adenomatous polyposis (Apc) gene is conditionally deleted from the cortex, by using Emx1Cre-APCloxP recombination technology. Apc is widely expressed in the nervous system including the cortical plate of the cortex and regulates axonal growth and neuronal differentiation. Deleting Apc may block neurite extension and/or affect the formation of attractive or repulsive cues in the cortex. By using DiI tracing as well as L1 immunohistochemistry techniques, I showed that in the Apc mutants cortical axons are absent and that TCAs initially navigate into the ventral telencephalon normally but fail to complete their journey into the cortex. They stop as they approach the PSPB, although the PSPB doesn’t seem to be directly affected by the mutation of Apc in the cortex. Additionally, Ig-Nrg1 (Neuregulin-1), the secreted protein that was suggested to play long-range roles in attracting TCAs towards the cortex, is present in the Apc mutant. This implies that Ig-Nrg1 is not sufficient for guiding TCAs into the cortex, and that additional guidance factors are needed. Moreover, my in vitro explant culture experiments show that the mutant cortex neither repel nor inhibit thalamic axonal outgrowth, indicating that the failure of TCAs in reaching the cortex is not due to the change of repulsive cues secreted by the mutant cortex. It rather indicates that the guidance factors for TCAs are likely to function through cell-cell contact mediated mechanisms. The Apc mutant cortex lacks these guidance factors, which might be the cortical axons. In conclusion, my data reveal a choice point for TCAs at the PSPB. Guidance factors from the cortex are needed for TCAs to cross the PSPB, which are absent in the Apc mutant. TCAs may need the direct contact with cortical axons and use them as an axonal scaffold to navigate into the cerebral cortex.
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So, Ting-pat Albert. "A computerized thermal imaging system for studying thyroid and cerebral cortex /." [Hong Kong : University of Hong Kong], 1994. http://sunzi.lib.hku.hk/hkuto/record.jsp?B13829890.
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Delfiol, Diego José Zanzarini [UNESP]. "Indução experimental de polioencefalomalacia em ovinos confinados ingerindo dieta com alto teor de enxofre." Universidade Estadual Paulista (UNESP), 2012. http://hdl.handle.net/11449/89254.
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Em ovinos o excesso de enxofre na dieta é apontado como uma das principais causas de polioencefalomalacia (PEM). Na literatura nacional relatos de PEM induzida por enxofre em ovinos são escassos. O objetivo desta dissertação foi induzir PEM em ovinos fornecendo uma dieta rica em carboidratos e com diferentes níveis de enxofre e realizar avaliações clínicas e laboratoriais. Foram utilizados 18 ovinos divididos em três grupos (G1, G2 e G3) que receberam diferentes níveis de enxofre na dieta 0,2%, 0,9% e 1,2% respectivamente. Exames clínicos (frequência cardíaca, frequência respiratória, temperatura retal e motricidade ruminal) e laboratoriais (concentração de sulfeto de hidrogênio ruminal, hemogasometria venosa, pH do fluído ruminal, concentração de cobre sérico e hepático, tomografia computadorizada, necropsia e histopatológico) foram realizados em diferentes momentos. A temperatura retal, hemogasometria venosa e pH do fluido ruminal estavam dentro dos valores de referência para a espécie. Taquicardia e taquipnéia foram observadas nos três grupos. A motricidade ruminal estava diminuída nos grupos G2 e G3 em relação ao G1. Quanto maior a ingestão de enxofre, menor foram os níveis de cobre sérico e hepático detectados nos ovinos. Elevados valores de sulfeto de hidrogênio foram detectados nos grupos G2 e G3. Nenhum animal apresentou sinais clínicos de PEM. Na tomografia computadorizada, necropsia e exame histopatológico do sistema nervoso central, nenhuma alteração compatível com PEM foi observada. É provável que algum outro fator pode estar associado ao excesso de enxofre na dieta para que os ovinos desenvolvam PEM
The excess sulfur intake in sheep is described as major cause of polioencephalomalacia (PEM). In the national literature are scarce reports of sulfur induced PEM in sheep. This work aimed to feed sheep using a rich carbohydrate diet supplemented with different levels of sulfur in order to induce PEM, and to perform clinical and laboratory tests. Eighteen sheep were divided into three groups (G1, G2, and G3) and supplemented with 0.2%, 0.9% and 1.2% sulfur in diet, respectively. Clinical evaluation (i.e., heart rate, respiratory rate, rectal temperature and rumen motility) and laboratory exams (i.e., ruminal hydrogen sulfide concentration, venous gas analysis, ruminal pH, serum and liver copper concentration, computed axial tomography, necropsy, and histopathological examination) were performed. Rectal temperature, venous gas and ruminal pH were within normal limits. Tachycardia and tachypnea were observed in the three groups. Rumen motility was decreased in groups G2 and G3 when compared with G1. The higher the sulfur intake, the lower the serum and liver levels of copper. Increased ruminal hydrogen sulfide concentration was detected in G2 and G3. None of the animals had clinical signs of PEM. Computed axial tomography, necropsy, and histopathological examination of the central nervous system showed no evidence of PEM. It is thought that other factors are associated with excessive sulfur consumption for a PEM outbreak to occur in sheep
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Delfiol, Diego José Zanzarini. "Indução experimental de polioencefalomalacia em ovinos confinados ingerindo dieta com alto teor de enxofre /." Botucatu : [s.n.], 2012. http://hdl.handle.net/11449/89254.
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Orientador: Alexandre Secorun BorgesBanca: Roberto Calderon Gonçalves
Banca: José Augusto Bastos Afonso da Silva
Resumo: Em ovinos o excesso de enxofre na dieta é apontado como uma das principais causas de polioencefalomalacia (PEM). Na literatura nacional relatos de PEM induzida por enxofre em ovinos são escassos. O objetivo desta dissertação foi induzir PEM em ovinos fornecendo uma dieta rica em carboidratos e com diferentes níveis de enxofre e realizar avaliações clínicas e laboratoriais. Foram utilizados 18 ovinos divididos em três grupos (G1, G2 e G3) que receberam diferentes níveis de enxofre na dieta 0,2%, 0,9% e 1,2% respectivamente. Exames clínicos (frequência cardíaca, frequência respiratória, temperatura retal e motricidade ruminal) e laboratoriais (concentração de sulfeto de hidrogênio ruminal, hemogasometria venosa, pH do fluído ruminal, concentração de cobre sérico e hepático, tomografia computadorizada, necropsia e histopatológico) foram realizados em diferentes momentos. A temperatura retal, hemogasometria venosa e pH do fluido ruminal estavam dentro dos valores de referência para a espécie. Taquicardia e taquipnéia foram observadas nos três grupos. A motricidade ruminal estava diminuída nos grupos G2 e G3 em relação ao G1. Quanto maior a ingestão de enxofre, menor foram os níveis de cobre sérico e hepático detectados nos ovinos. Elevados valores de sulfeto de hidrogênio foram detectados nos grupos G2 e G3. Nenhum animal apresentou sinais clínicos de PEM. Na tomografia computadorizada, necropsia e exame histopatológico do sistema nervoso central, nenhuma alteração compatível com PEM foi observada. É provável que algum outro fator pode estar associado ao excesso de enxofre na dieta para que os ovinos desenvolvam PEM
Abstract: The excess sulfur intake in sheep is described as major cause of polioencephalomalacia (PEM). In the national literature are scarce reports of sulfur induced PEM in sheep. This work aimed to feed sheep using a rich carbohydrate diet supplemented with different levels of sulfur in order to induce PEM, and to perform clinical and laboratory tests. Eighteen sheep were divided into three groups (G1, G2, and G3) and supplemented with 0.2%, 0.9% and 1.2% sulfur in diet, respectively. Clinical evaluation (i.e., heart rate, respiratory rate, rectal temperature and rumen motility) and laboratory exams (i.e., ruminal hydrogen sulfide concentration, venous gas analysis, ruminal pH, serum and liver copper concentration, computed axial tomography, necropsy, and histopathological examination) were performed. Rectal temperature, venous gas and ruminal pH were within normal limits. Tachycardia and tachypnea were observed in the three groups. Rumen motility was decreased in groups G2 and G3 when compared with G1. The higher the sulfur intake, the lower the serum and liver levels of copper. Increased ruminal hydrogen sulfide concentration was detected in G2 and G3. None of the animals had clinical signs of PEM. Computed axial tomography, necropsy, and histopathological examination of the central nervous system showed no evidence of PEM. It is thought that other factors are associated with excessive sulfur consumption for a PEM outbreak to occur in sheep
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Sargeant, Timothy John. "The effect of opiates on developing cerebral cortex : a thesis submitted to the Victoria University of Wellington in fulfilment of the requirements for the degree of Doctor of Philosophy in Cell and Molecular Bioscience /." ResearchArchive@Victoria e-Thesis, 2008. http://hdl.handle.net/10063/414.
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Adams, Niels C. "An investigation of the rat's perireticular nucleus and its possible role in the formation of corticofugal and corticopetal connections." Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.308700.
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Pinzan, Moira. "Modelling etiopathogenesis of the FOXG1-duplication-linked variant of West syndrome." Doctoral thesis, SISSA, 2016. http://hdl.handle.net/20.500.11767/4743.
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ABSTRACT
Here we describe the characterization of a novel Foxg1-GOF model we created to dissect the role of Foxg1 in postmitotic neuronal differentiation and reconstruct pathogenetic mechanisms which underlie the FOXG1 duplication-linked West syndrome. This is a devastating neurological disorder, triggered by a complex variety of pathogenic conditions. It is characterized by infantile spasms, abnormal EEG with hypsarrhytmia and seizures and dramatic cognitive impairment. For it only symptomatic treatments are presently available.
As expected, these Foxg1-GOF mice showed increased neuronal activity in baseline conditions and were more prone to limbic motor seizures upon kainic acid administration.
A preliminary developmental profiling of their cerebral cortex unveiled four major histogenetic anomalies, likely contributing to their hyperexcitability. These anomalies were: (1) an altered neocortical laminar blueprint with impaired layer VI/layer V segregation and defective activation of layer IV-II programs; (2) a substantial reduction of PV+ interneurons; (3) a patterned, area- and lamina-specific astrocyte deprivation; (4) a defective expression of the Gabra1 receptor subunit. Similar phenomena might concur to neurological anomalies of West syndrome patients harboring FOXG1 duplications.
A parallel in vitro study, run on dissociated cortico-cerebral cultures, revealed that a substantial Foxg1 upregulation occurred upon delivery of depolarizing stimuli. Neuronal, activity-linked Foxg1 elevation required the presence of astrocytes. Activity-linked Foxg1 fluctuations were inter-twinned with immediate-early genes fluctuations and depended on them, according to distinct, neuron- and astrocyte-specific patterns. In West syndrome patients with augmented FOXG1 dosage, a FOXG1-mRNA increase evoked by depolarizing stimuli might ignite a vicious circle, exacerbating neuronal hyperactivity and contributing to interictal EEG anomalies and seizures.
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Pearson, Helen Catherine. "Analysis of the roles of Pax6 in development of the cerebral cortex." Thesis, University of Edinburgh, 2000. http://hdl.handle.net/1842/25067.
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Here, cellular and molecular techniques were employed to elucidate the function of Pax6 in cortical development. It has been proposed that cell division within the VZ may be either symmetric, generating two progenitor cells, or asymmetric, generating a progenitor and a migratory neuron. An analysis of progenitor cleavage orientation revealed an increase in asymmetric division in the Sey/Sey cortex. In addition, interkinetic nuclear migration during the cell cycle is disrupted. I propose that these defects are most consistent with a role for Pax6 in regulating progression through the cell cycle. DiI labelling revealed a complete absence of innervation from thalamus to cortex in the Sey homozygote which may play a role in the cortical phenotype. To address this possibility an explant system was established to study cortical migration in vitro. The analysis showed that neurons migrating from the mutant cortex show a tendency to clump together indicative of differences in their adhesive properties. These defects are not rescued by co-culture with wildtype diencephalon, suggesting that the absence of thalamocortical innervation does not contribute to the Sey/Sey cortical phenotype in vivo. On the basis of these findings I hypothesise that loss of Pax6 function results in increased cortical proliferation and altered neuronal adhesion and that these abnormalities account for gradual accumulation of neurons in the VZ during later cortical development. In order to identify molecular differences between wildtype and Sey/Sey underlying these defects, candidate gene and differential gene expression analyses were performed. The former revealed altered expression patterns of putative cell determination molecules Numb and Prox1 and cell adhesion molecules L1 and TAG1. The latter involved construction and analysis of a subtracted cDNA library from which two molecules were identified which mediate protein interactions in transcriptional complexes. Expression of these genes is absent from the Sey/Sey cortex; they therefore represent exciting candidate genes acting downstream of Pax6.
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Huntenburg, Julia M. [Verfasser]. "A core organizing axis of the human cerebral cortex / Julia M. Huntenburg." Berlin : Freie Universität Berlin, 2018. http://d-nb.info/1150704497/34.
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Pollard, Marie. "Differential involvement of glutamate receptors in neuronal responses of the cerebral cortex." Thesis, University of Oxford, 2001. http://ora.ox.ac.uk/objects/uuid:f6c716f7-021d-4d73-8108-493fdd51e8ae.
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I studied how glutamate receptor-mediated responses, spatial arrangements, intrinsic properties and molecular specificity of cells serve cortical functions. I tested whether two somatosensory submodalities in the primary somatosensory (SI) cortex can be distinguished by glutamate receptor involvement in vivo. Low-threshold responses evoked by innocuous stimuli had a short-duration and long-duration component. The short-duration responses were mostly mediated by AMPA/kainate receptors and the long-duration responses involved the additional recruitment of NMDA receptors. High-threshold responses evoked by noxious stimuli were unimodal and mediated by both AMPA/kainate and NMDA receptors throughout the entire response. During noxious stimulus trials, an increase in baseline activity in SI cortical cells was observed. I attribute the changes in baseline activity to cells in the medial thalamic nuclei, which project to the SI cortex and are involved in the affective-motivational aspects of nociceptive signalling. To gain insight into the influence of synaptic organisation of a well-defined cortical area, I studied in vitro whether the intrinsic properties of two anatomically well-defined nonpyramidal cells in the hippocampus can provide clues into the modulation of neuronal signalling. During a depolarising current pulse, O-LM and O-Bi cells were distinguished by their accommodation of action potentials depending on the early or late part of the response. Also, during a hyperpolarising current pulse, O-LM cells displayed a prominent voltage 'sag' as compared to O-Bi cells. Both cell types contain somatostatin and I showed that O-LM cells express the metabotropic glutamate receptor type 1α. Although O-LM and O-Bi cells have a similar somatodendritic position their different axonal arbours imply that they are involved in the feedback modulation of the entorhinal and CA3 glutamatergic influences, respectively. I also found that contrary to previous reports not only somatostatin but also vasoactive intestinal polypeptide containing cells express mGluR1α, which might facilitate their oscillatory responses. To relate the action potential discharge of specific cortical cell classes to behaviourally relevant network activity, I also sought to identify hippocampal cells following in vivo recording. Novel information was provided for both the temporal and anatomical properties of cells not recorded previously. In particular, a putative interneuron targeting nonpyramidal cell and backprojection cell was recorded in relation to theta field events. A novel nonpyramidal projection cell was recorded in relation to sharp wave field events. A remarkable specificity was found in the dendritic and axonal patterns of these cells. The results show that distinct types of glutamate receptors are differentially involved in cortical function. The intrinsic properties and expression of mGluR1α in particular is highly specific in distinct nonpyramidal cell classes.
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Diaz-Arnesto, Larre Laura. "Presynaptic metabotropic glutamate receptors and neurotransmitter release in the rat cerebral cortex." Thesis, Open University, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.385195.
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