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Sherwood, James Lawrence. "Mossy fibre plasticity." Thesis, University of Bristol, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.618313.
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This study used extracellular field potential recordings (fEPSP) to investigate the role of kainate receptors (containing GLUK5) in short- and long-term potentiation (S-/L-TP) in the mossy fibre (MF) pathway. In vitro, the role of GLUK5 in synaptic plasticity is dependent on extracellular calcium concentration. So the physiological importance was investigated in vivo. In a single experiment GLUK5 selective antagonist, LY382884 (10 mg.kg-l, i.v.), attenuated STP. Notwithstanding, there is continued controversy regarding the role of GLUK5 in MF synaptic plasticity. Using GLUK5 selective antagonists, LY382884 and ACET, the method of hippocampal slice preparation is identified as deterministic. In parasagittal slices prepared in standard aCSF (PsH), STP, measured as ratio of 1st and 5th pulse (P5:P1) evoked at 25Hz, was antagonised by 10uM LY382884; NMDAR independent L TP, evoked by 100 pulses at 100Hz in 50uM AP5, was reversibly antagonised by 50nM ACET. Transverse hippocampal slices prepared in standard aCSF were not viable. In transverse slices prepared in high sucrose aCSF (TH), 10uM LY382884 had no effect on P5:P1-25Hz or P5:P1-50Hz; furthermore 100nM ACET had no effect on P5:P1-50Hz, or on the induction of NMDAR independent LTP. The depression of transmission by Group II mGluR agonists is reportedly a characteristic MF property. In PsH, DCG-IV had no effect on MF fEPSP but depressed P5:Pt-25Hz. In TH, DCG-IV and LY395756 (mGlu2 selective agonist) transiently depressed MF fEPSP. This was attenuated by a Group U competitive antagonist L Y341495. DCG-IV and LY395756 induced a concentration dependent long-term depression (LTD). While 100nM L Y341495 had no effect on OCGI-IV L TO, 300nM transiently reversed L Y395756 L TO. In conclusion, the pharmacology of synaptic plasticity in vitro is critically dependent on slice preparation; preliminary data suggest that GLUK5 receptors contribute to MF plasticity in vivo. Disparity in EC50 values for DCG-IV and L Y395756 induced depression suggests the possible involvement of mGlu3.
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Klempin, Friederike Claudia. "Adult brain plasticity." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2008. http://dx.doi.org/10.18452/15844.
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Der Hippocampus ist eine von zwei Gehirnregionen, in der zeitlebens kontinuierlich neue Nervenzellen gebildet werden. Er spielt eine wichtige Rolle bei der Gedächtniskonsolidierung und wird mit der funktionellen Entstehung neurodegenerativer Erkrankungen in Verbindung gebracht. Strukturveränderungen im erwachsenen Gehirn, die mit einer Depression einhergehen, sind laut Literatur auf einen geringen Serotoninspiegel und reduzierte hippocampale Neurogenese zurückzuführen. Selektive Serotonin-Wiederaufnahmehemmer (SSRI) erhöhen die Serotoninkonzentration im synaptischen Spalt und üben einen positiven Effekt auf die adulte Neurogenese aus. In der vorliegenden Arbeit wird untersucht, wie Veränderungen in der Serotonin (5-HT)-Neurotransmission durch einmalige oder chronische Gaben von Fluoxetin und speziellen Agonisten und Antagonisten für die Serotoninrezeptoren 5-HT1a und 5-HT2 in der erwachsenen Maus die Proliferation und Differenzierung von neugebildeten Nervenzellen im Gyrus dentatus beeinflussen. Die Ergebnisse zeigen, dass ein konträres Agieren beider Rezeptoren zu einem ausgewogenen Serotoninspiegel führt. 5-HT1a- und 5-HT2c-Rezeptoren haben einen Einfluss auf das Überleben neugebildeter Nervenzellen, wobei sie unterschiedliche Entwicklungsstadien innerhalb der adulten Neurogenese kontrollieren. Die vorliegende Arbeit bekräftigt außerdem, dass die chronische Gabe von Fluoxetin die adulte Neurogenese steigert.The hippocampus as one region with ongoing neurogenesis throughout life contributes to the formation of long-term memory and has also been implicated in the pathology of major depression. Studies suggest that depression might be due to decreased levels of serotonin and reduced neurogenesis in the adult brain and that the beneficial effects of selective serotonin reuptake inhibitors would require adult hippocampal neurogenesis. Here, I investigated how modulation of serotonergic neurotransmission by acute and chronic treatment with the antidepressant fluoxetine, and selective serotonin receptor agonists and antagonists in adult mice influences precursor cell activity during development. I focused on 5-HT1a and 5-HT2 receptors as major mediators of serotonin action. The present findings suggest that an opposed action of 5-HT1a and 5-HT2c receptor subtypes result in a balanced regulation of serotonin levels in the dentate gyrus. Both receptors differentially affect intermediate cell stages in adult hippocampal neurogenesis and play an important role in the survival of newly generated neurons. Furthermore, this study confirms that chronic fluoxetine treatment increases adult neurogenesis. In conclusion, the latency of onset of fluoxetine action can be explained by a balanced interplay of 5-HT1a and 5-HT2c receptor subtypes.
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Elramah, Sara. "Towards a Better Understanding of miRNA Function in Neuronal Plasticity : implications in Synaptic Homeostasis and Maladaptive Plasticity in Bone Cancer Pain Condition." Thesis, Bordeaux 2, 2013. http://www.theses.fr/2013BOR22073/document.
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Les micro-ARNs (miRNAs) sont de petits ARNs (20-25 nt) qui ont un rôle important dans les mécanismes d'interférence ARN. Les miRNAs sont des inhibiteurs de l'expression génique qui interviennent au niveau post-traductionnel en s'hybridant à des sites spécifiques de leurs ARNm cibles. Ce mécanisme induit la dégradation de l'ARNm ou l'inhibition de sa traduction. Puisque l'hybridation partielle du miRNA est suffisante pour induire une inhibition, chaque miRNA peut avoir des centaines de cibles. Les miRNAs sont impliqués dans de nombreuses fonctions biologiques et en particulier dans processus neuronaux. Plus de la moitié des miRNAs connus sont exprimés dans le cerveau de mammifère avec une distribution spécifique du miRNA considéré. A l'échelle sub-cellulaire il y a également une distribution hétérogène des miRNAs. De plus, il a été montré récemment une implication des miRNAs dans la régulation de la traduction locale dans les neurones. En effet, des miRNAs et des protyeines impliquées dans la biogenèse et la fonction des miRNAs ont été retrouvés dans le soma, les dendrites et les axones. Il a été montré que la dérégulation des miRNAs été impliquée dans de nombreux mécanismes pathologiques. Cette thèse a pour objectif de révéler le rôle des miRNAs dans la plasticité synaptique. Nous avons étudié l'implication des miRNAs dans les mécanismes de la plasticité synaptique homéostatique et dans la plasticité dysfonctionnelle rencontrée en condition de douleur cancéreuse.Notre hypothèse était que la régulation de la traduction locale des récepteurs AMPA dans les dendrites en condition d'homéostasie synaptique implique les miRNAs. Par bio-informatique, qRT-PCR et test luciférase, nous avons identifié le miRNA miR-92a comme régulateur de la traduction de l'ARNm de GluA1. Des immunomarquages des récepteurs AMPA et des enregistrements des courants miniatures AMPA montrent que miR-92a régule spécifiquement l'incorporation synaptique de nouveau récepteurs AMPA contenant GluA1 en réponse à un blocage de l'activité synaptique. La douleur est un symptôme très fréquemment associé au cancer et constitue un challenge pour les médecins puisque aucun traitement spécifique et efficace n'existe. C'est sans doute le résultat d'un manque de connaissances des mécanismes moléculaires responsables de la douleur cancéreuse. En combinant les screening des miRNA et des ARNm, nous avons mis en évidence une voie de régulation impliquant miR-124, un miRNA enrichi dans le système nerveux. Ainsi, dans un modèle de douleur cancéreuse chez la souris, la diminution de miR-124 est associée à une augmentation de ces cibles : calpain 1, synaptopodine et tropomyosine 4. Toutes ces protéines ont précédemment été identifiées comme des molécules clef de la fonction et de la plasticité synaptique. Des experiences in vitro ont confirmé que miR-124 exercait une inhibition multiple de calpain 1, synaptopodine et tropomyosine 4. La pertinence clinique de cette découverte a été vérifiée par le screening du liquide cérébro-spinal de patients souffrant de douleur cancéreuse qui montre également une diminution de miR-124. Ce résultat suggère un fort potentiel thérapeutique du ciblage de miR-124 dans les douleurs cancéreuses. Enfin, l'injection intrathécale de miR-124 dans des souris cancéreuses a permis de normaliser l'expression de la synaptopodine et de stopper la douleur cancéreuse lors de la phase initiale de la maladieMicroRNAs (miRNAs) are a type of small RNA molecules (21-25nt), with a central role in RNA silencing and interference. MiRNAs function as negative regulators of gene expression at the post-transcriptional level, by binding to specific sites on their targeted mRNAs. A process results in mRNA degradation or repression of productive translation. Because partial binding to target mRNA is enough to induce silencing, each miRNA has up to hundreds of targets. miRNAs have been shown to be involved in most, if not all, fundamental biological processes. Some of the most interesting examples of miRNA activity regulation are coming from neurons. Almost 50% of all identified miRNAs are expressed in the mammalian brain. Furthermore, miRNAs appear to be differentially distributed in distinct brain regions and neuron types. Importantly, miRNAs are reported to be differentially distributed at the sub-cellular level. Recently, miRNAs have been suggested to be involved in the local translation of neuronal compartments. This has been derived from the observations reporting the presence of miRNAs and the protein complexes involved in miRNA biogenesis and function in neuronal soma, dendrites, and axons. Deregulation of miRNAs has been shown to be implicated in pathological conditions. The present thesis aimed at deciphering the role of miRNA regulation in neuronal plasticity. Here we investigated the involvement of miRNA in synaptic plasticity, specifically in homeostatic synaptic plasticity mode. In addition, we investigated the involvement of miRNAs in the maladaptive nervous system state, specifically, in bone cancer pain condition.We hypothesized that local regulation of AMPA receptor translation in dendrites upon homeostatic synaptic scaling may involve miRNAs. Using bioinformatics, qRT-PCR and luciferase reporter assays, we identified several brain-specific miRNAs including miR-92a, targeting the 3’UTR of GluA1 mRNA. Immunostaining of AMPA receptors and recordings of miniature AMPA currents in primary neurons showed that miR-92a selectively regulates the synaptic incorporation of new GluA1-containing AMPA receptors during activity blockade.Pain is a very common symptom associated with cancer and is still a challenge for clinicians due to the lack of specific and effective treatments. This reflects the crucial lack of knowledge regarding the molecular mechanisms responsible for cancer-related pain. Combining miRNA and mRNA screenings we were able to identify a regulatory pathway involving the nervous system-enriched miRNA, miR-124. Thus, miR-124 downregulation was associated with an upregulation of its predicted targets, Calpain 1, Synaptopodin and Tropomyosin 4 in a cancer-pain model in mice. All these targets have been previously identified as key proteins for the synapse function and plasticity. Clinical pertinence of this finding was assessed by the screening of cerebrospinal fluid from cancer patient suffering from pain who presented also a downregulation of miR-124, strongly suggesting miR-124 as a therapeutic target. In vitro experiments confirmed that miR-124 exerts a multi-target inhibition on Calpain 1, Synaptopodin and Tropomyosin 4. In addition, intrathecal injection of miR-124 was able to normalize the Synaptopodin expression and to alleviate the initial phase of cancer pain in mice
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VanDam, Mark. "Plasticity of phonological categories." [Bloomington, Ind.] : Indiana University, 2007. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3277973.
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Thesis (Ph.D.)--Indiana University, Dept. of Linguistics, 2007.Source: Dissertation Abstracts International, Volume: 68-09, Section: A, page: 3830. Adviser: Robert F. Port. Title from dissertation t.p. (viewed May 1, 2008).
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Brookes, Jill. "The plasticity of diamond." Thesis, University of Hull, 1992. http://hydra.hull.ac.uk/resources/hull:6745.
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Aspects of the crystal structure of diamond, and its associated defects, have been considered with reference to the effect such characteristics might have on its mechanical properties. Also, established resolved shear stress models, which account for anisotropy in conventional Knoop indentation hardness of all single crystals, have been reviewed. Particular attention has been given to the role of microplasticity and the nature of crack formation in the deformed zone formed beneath the indenter. It is then shown that a similar approach can be applied to the case where a cone, made from a softer material, replaces the conventional rigid indenter. By using different materials covering a range of hardness, impressions can be formed beneath which there is a controlled density and depth of dislocations. In this work, the 'soft' indenter technique has been extended to high temperatures and applied to study the plasticity of various types of natural and synthetic diamond. Consequently, the effect of temperature on the critical resolved shear stress of synthetic type Ib, and natural type Ia and type IIa has been established. Above a critical threshold temperature for the onset of plasticity, time dependent growth of the impression volume occurs whilst the mean contact pressure is decreasing. It is shown that geometrical similarity, i.e. the ratio of the impression size to dislocated volume, is maintained whilst the critical mean pressure continues to be exceeded during this process of 'impression creep'. Activation energies of about 2.9 eV and 1.2 eV were determined, from rates of volume change, for natural (both type I and II) and synthetic type Ib respectively. Whilst no significant differences were observed between 98.9% 12C (natural abundance) and 99.9% 12C (isotopically enriched) synthetic diamonds, their behaviour was most like that of a type IIb diamond. Finally, by studying type la diamonds with a nitrogen concentration ranging from 14 - 750 ppm, evidence is obtained which supports the suggestion that this element reduces the intrinsic resistance to dislocation movement and encourages the initiation of cracks in the diamond structure.
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Tsakmaki, Anastasia. "Plasticity of the endoderm." Thesis, University of Bath, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.538557.
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Castell, Martin R. "Indentation plasticity in semiconductors." Thesis, University of Cambridge, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.363040.
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Kothari, Manish. "Rate independent crystal plasticity." Thesis, Massachusetts Institute of Technology, 1995. http://hdl.handle.net/1721.1/36611.
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Guinnee, Meghan A. "Plasticity in reproductive traits." Thesis, University of Edinburgh, 2005. http://hdl.handle.net/1842/16998.
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In this thesis, I explore how an individual’s environment, or the environment of its mother, affects its reproductive life-history characteristics (age at maturity, size at maturity, offspring size, offspring number). I attempt to explain observed responses using adaptive reasoning and/or mathematical modelling. I find that mean egg size decreases with increasing clutch size in Daphnia, and explore possible causes of this using a mathematical model. This pattern could be an adaptive response, if larger offspring have greater fitness advantages in food-limited environments. However, such a pattern can also result from a minimum viable egg size that is similar to the optimal egg size. I also empirically test the fitness effects of hatching from a small or large egg in Daphnia. I find that offspring from food-limited mothers are larger, but that they mature later, produce less offspring per clutch, do not produce larger offspring and produce fewer offspring per unit time. I find that the nematode parasites Strongyloides ratti and Nippostrongylus brasiliensis mature at different rates depending on the efficacy of the host immune response, but that differences are species-dependent. In addition, female N. brasiliensis suffer decreased fecundity at higher densities, but only in hosts with fully-functioning immune systems; in hosts with no thymus-based immune system, there is no density-dependent fecundity effect. This suggests that the density-dependent effects often observed in parasitic nematodes are mediated by the host immune system. This thesis reminds us that small differences in an individual’s surroundings, or even its mother’s surroundings, can profoundly affect when, how, and how successfully an animal reproduces. Often, these effects can be explained using adaptive reasoning, and/or mathematical modelling. When and how an animal reproduces is certain to have consequences for its fitness. Implications and future research directions are also discussed.
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Dekkers, Martijn. "Plasticity in Caenorhabditis elegans." [S.l.] : Rotterdam : [The Author] ; Erasmus University [Host], 2008. http://hdl.handle.net/1765/13961.
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Carney, Karen. "Caractérisation Protéomique Des Prolongements Astrocytaires au Cours de la Plasticité Synaptique." Thesis, Bordeaux, 2014. http://www.theses.fr/2014BORD0270/document.
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Les astrocytes sont les cellules les plus abondantes dans le cerveau où ils sontimpliquées dans une myriade de fonctions telles que la neurogénèse, l’homéostasieionique, le soutien métabolique, l’élimination des substances toxiques et dans laréponse aux lésions cérébrales. Des altérations fonctionnelles des astrocytes ont étéassociées avec des pathologies telles que l’épilepsie, la depression et laschizophrénie. A ce titre, l’étude de la contribution astrocytaire aux fonctionssynaptiques revêt un intérêt clinique et sociétal assez conséquent. Dans cette thèse,j’ai évalué le potentiel de plusieurs préparations permettant l’analyse des protéinesastrocytaires impliquées dans la plasticité synaptique et j’ai utilisé celle qui se prêtaitle mieux à la quantification des niveaux de protéines astrocytaires qui se trouventêtre régulées dans différent modèles de plasticité synaptique. J’ai caractériséplusieurs préparations qui peuvent être utilisées pour évaluer la contribution desastrocytes à la plasticité synaptique et j’ai identifié de nombreuses protéinesastrocytaires régulées par la plasticité synaptique et qui sont susceptibles d’êtreciblées lors de prochaines études destinées à identifier les mécanismes d’action desastrocytes dans un contexte physiologique et pathologiqueAstrocytes are the most abundant cell type in the brain and mediate a myriad offunctions, including neurogenesis, ion homeostasis, metabolic support, clearance oftoxic substances and responses to brain injuries. Alterations in astrocyte functionhave been linked with neurological disorders such as epilepsy, depression, dementiaand schizophrenia, and thus the continued study of astrocytic contributions tosynaptic function are of clinical and societal relevance. In this thesis I have evaluatedthe potential utility of several preparations for the assessment of astrocyte proteinsinvolved in the regulation of synaptic plasticity, and employed the most suitable ofthese preparations to measure regulation in astrocyte protein levels in models ofsynaptic plasticity. I have characterized several preparations that can be used toevaluate astrocyte contributions to synaptic plasticity and identified numerousastrocyte-enriched proteins regulated by synaptic plasticity that can be targeted infuture studies to elaborate upon the mechanisms of action of astrocytes in bothphysiological and pathological contexts
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Prokin, Ilia. "Synaptic plasticity emerging from chemical reactions : Modeling spike-timing dependent plasticity of basal ganglia neurons." Thesis, Lyon, 2016. http://www.theses.fr/2016LYSEI115/document.
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Notre cerveau prend en charge différentes formes d’apprentissage dans ses diverses parties. C’est par exemple le cas des ganglions de la base, un ensemble de noyaux sous-corticaux qui est impliqué dans la sélection de l’action et une forme spécifique de l’apprentissage / mémoire, la mémoire procédurale (mémoire des compétences ou d’expertise). A l’échelle du neurone unique, le support le plus plausible de l’apprentissage et de la mémoire est la plasticité synaptique, le processus par lequel l’efficacité de la communication entre deux neurones change en réponse à un pattern spécifique de conditions environnementales. Parmi les différentes formes de plasticité synaptique, la plasticité dépendante du timing des spikes (STDP) représente le fait que le poids synaptique (l’efficacité de la connexion) change en fonction du temps écoulé entre l’émission des deux potentiels d’action (spikes) présynaptiques et postsynaptiques consécutifs. Si la STDP est une forme de plasticité qui a récemment attiré beaucoup d’intérêt, on ne comprend pas encore comment elle émerge des voies de signalisation / biochimiques qui la sous-tendent. Pour répondre à cette question, nous combinons les approches expérimentales de nos collaborateurs (pharmacologie et électrophysiologie) avec la modélisation de la dynamique des réseaux de signalisation impliquées (décrite par des équations différentielles ordinaires). Après estimation des paramètres, le modèle reproduit la quasi-totalité des données expérimentales, y compris la dépendance de la STDP envers le nombre stimulations pré- et post-synaptiques appariées et son exploration pharmacologique intensive (perturbation des voies de signalisation par des produits chimiques). En outre, contrairement à ce qui était largement admis dans la communauté des neurosciences, notre modèle indique directement que le système endocannabinoïde contrôle les changements du poids synaptique de façon bi-directionnelle (augmentation et diminution). De plus, nous étudions comment une série de facteurs comme la recapture du glutamate régule la STDP. Notre modèle représente une première étape pour l’élucidation de la régulation de l’apprentissage et de la mémoire au niveau du neurone unique dans les ganglions de la baseOur brains support various forms of learning in their various subparts. This is for instance the case of the basal ganglia, a set of subcortical nuclei that is involved in action selection and a specific form of learning / memory, procedural memory (memory of skills or expertise). At the scale of single neurons, the most plausible support of learning and memory is synaptic plasticity, the process by which the efficiency of interneuronal communication changes in response to a pattern of environmental conditions. A recent focus of research is on spike-timing dependent plasticity (STDP), whereby the relative timing of activations (spikes) of connected pre- and postsynaptic neurons, determines the synaptic weight (the efficiency of synaptic connection). Notwithstanding, the dependence of STDP on underlying signaling pathways is not yet fully understood. To address this issue, we combine experimental approaches by our collaborators (pharmacology and electrophysiology) with modeling of the implicated signaling network (described by Ordinary-Differential Equations). After parameter estimation, the model reproduces much of experimental data, including the dependence of STDP on the number of paired stimuli of pre- and postsynaptic neurons and intensive pharmacological exploration (where signaling molecules are perturbed by chemicals). Furthermore, in opposition to what was widely believed in the neuroscience community, our model directly indicates that the endocannabinoid system supports bidirectional changes of the synaptic weight (increase and decrease). Moreover, we study how a range of factors including glutamate uptake regulates STDP. We expect our model to be a starting point to the elucidation of the regulation of learning and memory in the basal-ganglia at the single neuron level
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Adzima, Francis. "Modélisation et simulation de procédés de mise en forme de tôles métalliques ultrafines." Thesis, Paris, ENSAM, 2016. http://www.theses.fr/2016ENAM0066/document.
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La course à la miniaturisation entraine une forte hausse de la demande encomposants aux dimensions submillimétriques et donne un essor considérable aux procédés de micro-formage. Cependant le comportement mécanique des tôles ultrafines, employées dans ces procédés présente des singularités liées à la réduction du nombre de grains. Cette thèse a eu pour objet de mettre en place un outil d’aide à la prédiction du comportement mécanique des tôles ultrafines.Expérimentalement, le comportement de deux alliages de cuivre, le CuBe2 et le CuFe2P, a été caractérisé sous divers types de chargement. Diverses caractéristiques ont été mises en évidence, notamment l’anisotropie de la réponse mécanique, l’effet Bauschinger ou encore ladégradation du module de Young.Afin d’obtenir un cadre de modélisation apte à la description de tôles présentant un comportement plus ou moins homogène, deux approches ont été retenues. La première consiste en une modélisation phénoménologique inspirée des observations macroscopiques. La seconde est une description, en plasticité cristalline, à l’échelle du grain du comportement mécanique, basée sur les mécanismes physiques de déformation. Les modèles retenus ont été intégrés dansles logiciels ABAQUS et SiDoLo dans le formalisme des grandes transformations. Des stratégies d’identification paramétrique des différents modèles sont développées et une analyse comparative de l’impact de l’identification sur les prévisions des modèles est proposée.Enfin les approches développées sont mises en oeuvre sur des procédés industriels et des tests académiques. Une étude sur des facteurs influençant la prédiction du retour élastique estréalisée. Elle a montré qu’une attention particulière doit être portée à la modélisation de l’élasticitéThe on-going trend on device miniaturization has increased the demand forminiature parts and boosted micro forming processes. However, the mechanical behavior of ultra-thin sheet metals is subjected to certain peculiarities which are driven from the reduced number of grains in the sheets. The present work aimed to provide a numerical tool for the prediction of the mechanical behavior of ultra-thin sheet metals. The mechanical behavior of two copper alloys, CuBe2 and CuFe2P, was experimentally characterized through several strain paths. Various characteristics have been revealed, such as the anisotropic response, Bauschinger effect and the decrease of the Young modulus.In order to build a modeling frame capable of describing thin metal sheets which exhibit a highly heterogeneous behavior and those whose response is more homogeneous, two modeling approaches were considered. On one hand, a phenomenological model based on the experimental results is chosen. On the other hand, a crystal plasticity based model, which takes into account the physical deformation mechanisms, is adopted. Both models were implementedin ABAQUS and SiDoLo softwares, under the finite strain formalism. Parametric identification strategies are devised and the influence of calibration on models performance is assessed.Ultimately, the modeling approaches were applied to the simulation of industrial processes and academic tests. A numerical study on relevant parameters for the prediction of springback has been performed. The accurate modeling of elasticity proved highly influential
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Valtcheva, Silvana. "Conditions for the emergence of corticostriatal synaptic plasticity." Thesis, Paris 6, 2016. http://www.theses.fr/2016PA066627/document.
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D'après le postulat de Hebb, les réseaux neuronaux adaptent leur connectivité sous l'influence des activités pré- et post-synaptiques. La " spike-timing-dependent plasticity " (STDP) est une règle d'apprentissage synaptique de type Hebbien, qui repose sur la structure temporelle précise des patrons d'activités appariées de part et d'autre de la synapse. La plasticité cortico-striatale serait le substrat biologique de l'apprentissage procédural effectué par les ganglions de la base. Les neurones de sortie du striatum agissent comme des détecteurs de coïncidence des activités corticales et thalamiques. La STDP cortico-striatale pourrait donc jouer un rôle crucial dans les processus d'encodage de l'apprentissage et la mémoire procédurale. Nous avons exploré les conditions d'émergence et d'expression de la STDP cortico-striataleAccording to Hebbian theory, neural networks refine their connectivity by patterned firing of action potentials in pre- and postsynaptic neurons. Spike-timing-dependent plasticity (STDP) is a synaptic Hebbian learning rule relying on the precise order and the millisecond timing of the paired activities on either side of the synapse. Temporal coding via STDP may be essential for the role of the striatum in learning of motor sequences in which sensory and motor events are associated in a precise time sequence. Corticostriatal long-term plasticity provides a fundamental mechanism for the function of the basal ganglia in procedural learning. Striatal output neurons act as detectors of distributed patterns of cortical and thalamic activity. Thus, corticostriatal STDP should play a major role in information processing in the basal ganglia, which is based on a precise time-coding process. Here, we explored the conditions required for the emergence of corticostriatal STDP
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Ho, Shu Xian. "Silent synapses and postnatal development of the mouse cerebellar cortex." Thesis, Aix-Marseille, 2018. http://www.theses.fr/2018AIXM0604/document.
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Dans le cortex cérébelleux, au premier chef impliqué dans l’apprentissage moteur, chaque neurone de Purkinje reçoit des centaines de milliers d'entrées provenant de cellules granulaires. Etonnement, il a été suggéré qu'une grande majorité de ces connexions (synapses) sont silencieuses, c’est-à-dire qu’elles ne transmettent pas d’information détectable. Les propriétés et le rôle de ces synapses silencieuses restent mystérieux. Jouent-elles le rôle d’une réserve ou sont-elles le produit de l’apprentissage cérébelleux ? En combinant l’enregistrement électrique de la transmission synaptique et la cartographie des entrées synaptiques dans des tranches aigües de cervelet de souris, nous avons étudié l'évolution du pourcentage des synapses qui sont silencieuses entre deux âges : avant le sevrage et une fois que l’agilité d’adulte est acquise. Nous avons observé que le pourcentage de synapses qui sont silencieuses reste remarquablement stable malgré l’augmentation du nombre total de synapsesIn the cerebellar cortex, primarily involved in motor learning, any Purkinje neuron receives hundreds of thousands of inputs from granule cells. Disturbingly, it has been suggested that the vast majority of these connections (synapses) are silent, that is to say they do not transmit any detectable information. The properties and the role of these silent synapses remains mysterious. Do they serve as a reserve pool for additional information storage or are they a byproduct of cerebellar learning? Combining the electrical recording of synaptic transmission and the mapping of synaptic inputs in acute cerebellar slices from mice, we have studied how the percentage of synapses which are silent changes between two postnatal ages: before weaning and once adult agility is acquired. Our main finding is that the percentage of synapses which are silent remains remarkably stable despite the increase in the total number of synapses
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Zellner, Samantha R. "Charpy Impact Testing of Twinning Induced Plasticity and Transformation Induced Plasticity High Entropy Alloys." Thesis, University of North Texas, 2019. https://digital.library.unt.edu/ark:/67531/metadc1538702/.
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High entropy alloys (HEAs) are a new class of solid solution alloys that contain multiple principal elements and possess excellent mechanical properties, from corrosion resistance to fatigue and wear resistance. Even more recently, twinning induced plasticity (TWIP) and transformation induced plasticity (TRIP) non-equiatomic high entropy alloys have been engineered, promising increased strength and ductility as compared to their equiatomic counterparts. However, impact and fracture resistance of these HEAs has not been studied as much as their other mechanical properties. In this thesis, the hardness, tensile properties, and Charpy impact energy of Al0.3CoCrFeNi, a TWIP HEA, and 50Fe-30Mn-10Co-10Cr (at.%), a TRIP HEA, was explored. First, three processing conditions, (1) as-received, (2) recrystallized, and (3) peak hardness, were chosen for each alloy and verified with Vickers microhardness measurements. Next, the tensile properties of each alloy and condition were investigated. Charpy impact specimen size was then selected based on the final plate thickness, and the machined samples were tested. Plastic zone size and change in sample thickness in the deformed region of each condition after testing was measured. Post-impact test inspection of the samples in all conditions showed that the samples were in tension near the V-notch root and in compression at the impact surface. Plastic zone size is seen to change as a function of distance from the V-notch root moving towards the impact surface in conditions that exhibited higher ductility. Overall, the TWIP alloy displayed high fracture resistance, and further microstructural optimization will likely increase the fracture resistance of these alloys.
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Blaha, Jakub. "Výpočtová analýza zbytkových napětí u autofretovaných vysokotlakých zásobníků paliva." Master's thesis, Vysoké učení technické v Brně. Fakulta strojního inženýrství, 2015. http://www.nusl.cz/ntk/nusl-231712.
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The master‘s thesis is aimed on numerical simulation of autofrettage of high pressure fuel vessel – rail in Common Rail system. First there is described Chaboche model, which is later used for simulation of autofrettage. There are described different approaches which can be used to obtain sufficient material model. Then there is observed influence of these different approaches on stress state of rail within the process of autofrettage. Suitability of Chaboche model for autofrettage and re-autofrettage simulations is assessed by comparing with more complex Jiang model. In the end there is a study of influence of autofrettage pressure on different properties, especially on residual stresses.
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Nguyen, Tuan Hung. "Développement d’outils numériques pour la prise en compte du couplage hydrogène-plasticité dans un code éléments finis : application à l’essai de pliage en U." Thesis, Paris 13, 2014. http://www.theses.fr/2014PA132032/document.
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Dans le cadre de l’étude du couplage entre la plasticité et les interactions de l’hydrogène avec les matériaux métalliques, l’objectif de ce travail de thèse est l’implémentation dans le code de calcul par éléments finis Abaqus© de la loi de diffusion de l’hydrogène couplée aux champs mécaniques, tenant compte notamment du piégeage dû à la déformation plastique. La stratégie d’implémentation retenue permet de résoudre simultanément les problèmes de diffusion et de mécanique ; elle s’est appuyée sur les travaux de la littérature, et a nécessité le développement de procédures en fortran 77, et en particulier, de procédures utilisateur UMAT et UMATHT permettant de définir respectivement le comportement mécanique, et un flux de matière. Ces procédures ont été confrontées avec succès à plusieurs cas de la littérature. Les outils développés ont été appliqués à l’étude numérique d’un essai de pliage en U, utilisé pour la caractérisation de la rupture différée par fragilisation par l’hydrogène de tôles minces prédéformées plastiquement. Une étude paramétrique portant sur les conditions de l’essai, les conditions limites en hydrogène et la relation entre plasticité, hydrogène piégé et hydrogène diffusif a été menée. Enfin, une transposition à l’échelle du polycristal 3D a été effectuée, en utilisant une procédure UMAT de comportement polycristallin modifiée. Une étude sur les paramètres constitutifs d’un Volume Elémentaire Représentatif a été réalisée, puis, une étude de l’essai en U à l’échelle du polycristal effectuée grâce à un transfert de conditions limites entre un calcul global et le VER, afin de simuler l’effet de l’anisotropie cristalline sur les champs de concentration d’hydrogèneIn the framework of the coupling between plasticity and hydrogen interactions with the metallic material, the aim of this thesis is to implement in the finite element code Abaqus © the hydrogen diffusion law coupled with the mechanical fields, accounting particularly for the trapping caused by the plastic strain. The chosen implementation strategy allows to simultaneously solve the diffusion and mechanical problems. It is based on works from the literature and needs the development of procedures in fortran 77, in particular the user procedures UMAT and UMATHT allowing the definition of the mechanical behavior and the material flux respectively. These procedures were confronted with several cases in literature. The developed procedures were applied to the numerical study of the U-bend test, used for characterizing the delayed cracking caused by hydrogen embrittlement. A parametric study on test conditions, boundary conditions on hydrogen and relationship between plasticity, trapped hydrogen, diffusive hydrogen was carried out. Finally, a transposition to the scale of a 3D polycristal was performed using a modified UMAT procedure with crystalline elastoviscoplasticity. A numerical study on the relevant parameters for defining a Representative Volume Element was carried out. Then, the simulation of a virtual u-bend test at the polycristal scale was performed thanks to a boundary condition transfer between global calculation and the RVE, in order to simulate the effect of crystal anisotropy on hydrogen concentration field
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Londe, Sylvain. "Origines et potentiel évolutif des intercastes chez la fourmi Mystrium rogeri." Thesis, Paris 6, 2014. http://www.theses.fr/2014PA066320/document.
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Les colonies de fourmis produisent occasionnellement des individus intermédiaires entre les reines et les ouvrières (c.-À-D. intercastes). Les intercastes pourraient être impliquées dans l'évolution de nouvelles castes par un processus de réorganisation des phénotypes ancestraux. Afin d'évaluer cette hypothèse, nous avons étudié la validité de trois corollaires de ce modèle évolutif chez la fourmi Mystrium rogeri: (i) les intercastes résultent de la réorganisation de caractères de reines et d'ouvrières; (ii) les intercastes sont susceptibles d'être fonctionnelles parce qu'elles recombinent des comportements qui ont déjà été testé par la sélection chez les reines et les ouvrières; (iii) certains phénotypes intercastes ressemblent à ceux des nouvelles castes ayant évolué de cette façon.Les résultats suggèrent que les intercastes sont générées par des niveaux intermédiaires de facteurs environnementaux induisant des réponses différentielles entre les modules. Les intercastes effectuent les mêmes tâches que les reines et les ouvrières et elles ne sont pas associées à des comportements aberrants. Elles sont plus impliquées que les reines et les ouvrières dans les interactions agonistes et peuvent ainsi entraîner des coûts à l'échelle de la colonie. Les intercastes peuvent attirer les mâles, s'accoupler et pondre des ¿ufs, présentant ainsi un fort potentiel reproducteur. Des changements de pressions de sélection sur les stratégies de reproduction sont alors susceptibles d'entrainer la fixation d'un phénotype intercaste par accommodation génétique. Nos résultats soutiennent l'hypothèse selon laquelle les intercastes peuvent être à l'origine de l'évolution des nouvelles castesAnt colonies occasionally produce individuals called intercastes. These are morphologically highly variable, but always intermediate between queens and workers. Because of their rarity, intercastes have been little studied. However, they may be involved in the evolution of novel castes through the reorganization of ancestral phenotypes (i.e. developmental recombination). In order to evaluate this hypothesis, we investigated the validity of three corollaries of this evolutionary model in the ant Mystrium rogeri: (i) intercastes must be produce by the reorganization of queen and workers characters following new genetic or environmental input; (ii) they are likely to be functional because they recombine behaviors that have already been tested by selection in queens and workers, unlike a random mutational process that mainly produces deleterious variants; (iii) some intercaste phenotypes may resemble those of new castes suspected to have evolved by this way. In agreement with the phenotypic reorganization hypothesis, our morphometric analyses suggest that intercastes are generated by intermediate levels of environmental factors inducing differential responses among modules. Behavioral records showed that intercastes perform the same tasks than queens and workers and therefore they are not associated with aberrant and costly behaviors. Nevertheless, they are more involved in agonistic interactions than queens and workers and thus may cause significant costs at the colonial level. Behavioral tests showed that some intercastes may attract males, mate, and lay diploid eggs, thereby demonstrating their high reproductive potential. Consequently, new selective pressures on the reproductive strategy may result in the selection of these intercastes and then the fixation of a new canalized phenotype by genetic accommodation of change. This process may explain the multiple evolutions of new reproductive castes (e.g. ergatoid queens). Overall, results presented in this work support the hypothesis that intercastes may be at the origin of the evolution of novel castes by developmental recombination
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Benamar, Mehdi. "Modulation de la plasticité et des fonctions suppressives des lymphocytes T régulateurs par les molécules de signalisation Themis1 et Vav1." Thesis, Toulouse 3, 2018. http://www.theses.fr/2018TOU30249.
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Les lymphocytes T régulateurs Foxp3+ jouent un rôle crucial dans l'établissement de la tolérance au soi, le contrôle des réponses inflammatoires et le maintien de l'homéostasie du système immunitaire. La compréhension des mécanismes moléculaires impliqués dans la fonction de ces cellules représente un défi important. Chez le rat, la déficience en Themis1, une nouvelle molécule de la signalisation du TCR, associée à un locus de 117kb d'origine BN induit un défaut fonctionnel des Tregs et le développement spontané d'une maladie inflammatoire des intestins. Au sein de ce locus, le rat BN présente deux polymorphismes non-synonymes, un au niveau du gène C3 et un au niveau du gène Vav1 (R63W). Ce dernier est un candidat potentiel du fait du rôle joué par Vav1 dans l'activation des lymphocytes T et de sa régulation par Themis1. Dans ce travail de thèse, j'ai étudié l'effet de la déficience en Themis1 associé au polymorphisme R63W de Vav1 chez la souris de fond génétique C57BL/6 sur les fonctions des lymphocytes T régulateurs. J'ai montré que la déficience en Themis1 associé au polymorphisme R63W induit un défaut fonctionnel des Tregs in vitro et in vivo dans un modèle de colite. Ce défaut est associé à une production accrue de cytokines pro-inflammatoires par ces Tregs. J'ai également mis en évidence que l'association de ces deux mutations induit une sensibilité accrue à la colite induite par le DSS. Au niveau moléculaire, j'ai mis en evidence que ce défaut fonctionnel est associé à une réduction de la signalisation du TCR impliquant les vois Erk et NF-ĸB. De plus, j'ai montré que l'inhibition d'une phosphatase de la signalisation du TCR, SHP-1, permet de restaurer les fonctions suppressives des Tregs Vav1R63W-Themis1-/-. Cette étude souligne l'importance de l'intégrité du hub de la signalisation impliquant Vav1, Themis1 et SHP-1 dans la plasticité des lymphocytes T régulateurs et dans le maintien de leur fonction suppressive. Ainsi ce hub de signalisation représente une cible thérapeutique pour augmenter les fonctions des Tregs dans le cadre des maladies inflammatoires ou réduire leurs fonctions suppressives pour favoriser les réponses immunes anti-tumorales dans le cadre du cancerRegulatory T cells (Treg) are of paramount importance for restraining excessive immune responses and their manipulation holds enormous therapeutic potential. Our recent results using a congenic rat model suggested that the integrity of Vav1/Themis1 T-cell receptor signaling hub plays a crucial role in Treg suppressive function. Indeed, Themis1 deficiency in BN, but not in LEW rats, led to the development of inflammatory bowel disease (IBD), linked to a defect in Treg suppressive function. Genetic studies revealed that this phenotype depended on a 117 Kb genomic locus, containing the R63W polymorphism on Vav1 that impacted its expression and functions. To test the importance of the Vav1/Themis1 TCR signaling hub in Treg function, we generated Themis1-T-/- mice expressing conditionally Themis1 in thymocytes, but not in peripheral T cells. In contrast to regular germline Themis1 knockout mice, these mice were not lymphopenic and exhibited normal proportions of CD4+ T cells in the thymus and in peripheral lymphoid organs. Next, Themis1-T-/- mice were crossed with Vav1R63W mice to assess the impact of these combined mutations on Treg suppressive functions. Using in vitro approaches, together with in vivo analyses of IBD, we showed that suppressive activity of Treg was impaired in Themis1-deficient mice harboring the mutated Vav1; this defect is linked to higher production of IL-17 and IFNg. Functional studies showed that Themis1-deficient associated with the mutated Vav1 induced a defect in Erk and P65 phosphorylation after TCR engagement. Interestingly, the inhibition of the SHP-1 phosphatase restore the functional defect of Tregs. Together, these data showed that Themis1, Vav1 and SHP-1 cooperate in the signaling hub to regulate the suppressive function of regulatory T cells. Thus, this signaling hub represents a therapeutic target to enhance the suppressive functions of Tregs in the context of autoimmune and inflammatory diseases or to decrease their functions to favor anti-tumoral immune responses
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Avanzi, Ariel. "Biophysical model of synaptic plasticity." Bachelor's thesis, Alma Mater Studiorum - Università di Bologna, 2020. http://amslaurea.unibo.it/21967/.
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Nel 1982 Elie Bienestock, Leon Cooper e Paul Munro scrissero ”Theory for the development of neuron selectivity” proponendo uno schema di evoluzione sinaptica nel quale competono i modelli in arrivo piuttosto che la convergenza degli afferenti. Brevemente divenne nota come teoria BCM e fu il trampolino di lancio per ulteriori lavori sulla modificazione delle sinapsi corticali. Durante le ultime due decadi sono state fatte nuove formulazioni, come la IBCM di Nathan Intrator e Leon Cooper del 1992, e nuovi metodi sono stati introdotti permettendo la creazione di reti neurali più complicate ed efficienti. Lo studio di questi modelli evidenzia la capacità di adattamento a diverse situazioni in un modo semplice. Sono stati fatti studi allevando animali in un periodo critico per lo sviluppo sella selettività corticale e l’accordo tra i dati e la teoria è stato provato. Tutta la teoria, valida per i neuroni corticali, potrebbe essere migliorata con una maggiore capacità di calcolo che permetterebbe di sbarazzarsi di alcune approssimazioni.
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Rick, John Thomas. "Frequency, plasticity and information processing." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/NQ59069.pdf.
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Sayre, Eleanor C. "Plasticity: Resource Justification and Development." Fogler Library, University of Maine, 2007. http://www.library.umaine.edu/theses/pdf/SayreEC2007.pdf.
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Linnarsson, Sten. "Neurotrophic factors and neuronal plasticity /." Stockholm, 2001. http://diss.kib.ki.se/2001/91-628-4618-3/.
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Adkin, P. "Yield surfaces in cyclic plasticity." Thesis, Coventry University, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.374221.
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Samsel, Paulina Anna. "Retinal plasticity in experimental glaucoma." Thesis, Cardiff University, 2010. http://orca.cf.ac.uk/54163/.
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Our study confirmed the existence of a perineuronal net in the rat retina and indicated that molecular weight distribution and immunohistochemical tissue localisation of glycosaminoglycans varied in young, old and glaucomatous rat retinas.
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Billings, Guy. "Memory stability and synaptic plasticity." Thesis, University of Edinburgh, 2009. http://hdl.handle.net/1842/3853.
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Numerous experiments have demonstrated that the activity of neurons can alter the strength of excitatory synapses. This synaptic plasticity is bidirectional and synapses can be strengthened (potentiation) or weakened (depression). Synaptic plasticity offers a mechanism that links the ongoing activity of the brain with persistent physical changes to its structure. For this reason it is widely believed that synaptic plasticity mediates learning and memory. The hypothesis that synapses store memories by modifying their strengths raises an important issue. There should be a balance between the necessity that synapses change frequently, allowing new memories to be stored with high fidelity, and the necessity that synapses retain previously stored information. This is the plasticity stability dilemma. In this thesis the plasticity stability dilemma is studied in the context of the two dominant paradigms of activity dependent synaptic plasticity: Spike timing dependent plasticity (STDP) and long term potentiation and depression (LTP/D). Models of biological synapses are analysed and processes that might ameliorate the plasticity stability dilemma are identified. Two popular existing models of STDP are compared. Through this comparison it is demonstrated that the synaptic weight dynamics of STDP has a large impact upon the retention time of correlation between the weights of a single neuron and a memory. In networks it is shown that lateral inhibition stabilises the synaptic weights and receptive fields. To analyse LTP a novel model of LTP/D is proposed. The model centres on the distinction between early LTP/D, when synaptic modifications are persistent on a short timescale, and late LTP/D when synaptic modifications are persistent on a long timescale. In the context of the hippocampus it is proposed that early LTP/D allows the rapid and continuous storage of short lasting memory traces over a long lasting trace established with late LTP/D. It is shown that this might confer a longer memory retention time than in a system with only one phase of LTP/D. Experimental predictions about the dynamics of amnesia based upon this model are proposed. Synaptic tagging is a phenomenon whereby early LTP can be converted into late LTP, by subsequent induction of late LTP in a separate but nearby input. Synaptic tagging is incorporated into the LTP/D framework. Using this model it is demonstrated that synaptic tagging could lead to the conversion of a short lasting memory trace into a longer lasting trace. It is proposed that this allows the rescue of memory traces that were initially destined for complete decay. When combined with early and late LTP/D iii synaptic tagging might allow the management of hippocampal memory traces, such that not all memories must be stored on the longest, most stable late phase timescale. This lessens the plasticity stability dilemma in the hippocampus, where it has been hypothesised that memory traces must be frequently and vividly formed, but that not all traces demand eventual consolidation at the systems level.
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Nelson, Barry Declan. "Genetic factors affecting neural plasticity." Thesis, Queen's University Belfast, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.602694.
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Electrophysiological stimulation has been proffered as having the potential to improve rehabilitation in stroke survivors suffering residual motor deficits. Interindividual variation exists in the response to these interventions, undoubtedly mediated at least in part by genetic factors. The thesis identified 3 candidate genes in neural plasticity, and determined their impact on the efficacy of paired associative stimulation (PAS) and transcranial direct current stimulation tDeS in forearm muscles, which are often the target of rehabilitation therapies . Three candidate genes in neural plasticity were examined- BDNF, COMT and ApoE. Genotype-mediated baseline differences in cortical excitability were found. Females who were homozygous for the BDNF val allele had significantly larger VO curves than those who carried a met allele. COMT val homozygotes showed a trend towards smaller VO curve area at baseline, which approached significance (p=O.0504). Baseline I/O curve area was undifferentiated across ApoE genotype groups.
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Whitehouse, Mary Elizabeth Anora. "Behavioural plasticity in Argyrodes antipodiana." Thesis, University of Canterbury. Zoology, 1991. http://hdl.handle.net/10092/5858.
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In this thesis I look at the behavioural plasticity of A.antipodiana while foraging and interacting with conspecifics. The aim is to see how an animal, with apparently limited intelligence is able to deal with environmental variability. I conclude that A.antipodiana appears to have been able to overcome these limitations very effectively by using four methods, of which the first two effectively reduce the amount of learning necessary.
Firstly, A.antipodiana simplifies the situation as much as possible by ignoring some of the variability. For example, in social situations, A.antipodiana appears to recognize only a few categories of conspecifics, rather than recognize conspecifics as individuals. Consequently, the social groups of A.antipodiana are not characterized by complicating factors such as aggressive orders or dominance hierarchies.
Secondly, A.antipodiana largely ignores current situations and instead bases much of its behavioural decisions on its internal conditions. For example, in male-male conflicts, males respond to their opponents largely according to their own size, level of hunger, the number of contests in which they have participated, or their past experience of winning or losing; rather than to the characteristics of their opponents. Likewise in social interactions A.antipodiana is more inclined to be aggressive towards conspecifics if it itself is foraging, and less inclined if it is feeding with the host.
When the situation cannot be simplified, A.antipodiana adopts a third response which is to use the simplest method possible for adjusting its behaviour. For example, A.antipodiana's ability to develop
araneophagic skills appears to be governed by a critical period. Thus rather than developing araneophagic skills through trial and error with practise, the ability appears to be simply 'switched on' if required.
The fourth means by which A.antipodiana compensates for limited intelligence is to be very selective in the areas in which it does use learning. For example, A.antipodiana seems to use problem solving when foraging, but only when it is actually trying to reach the food bundle upon which the host is feeding. A.antipodiana also seems to learn to move more stealthfully on the host's web. There is even evidence that A.antipodiana may behave with intent when males are competing for opportunities to copulate.
Thus the intelligence of A.antipodiana appears to be severely limited. However, despite these limitations, by reducing the amount of learning necessary, and then channelling what learning it has to very restricted, but very poignant areas of its behaviour, A.antipodiana, is able to respond very effectively to its variable environment.
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Johnson, Richard James Ramsay. "Plasticity in adult automatic neurons." Thesis, University College London (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.299940.
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Hwang, Hongik. "Molecular mechanisms of synaptic plasticity." Thesis, Massachusetts Institute of Technology, 2016. http://hdl.handle.net/1721.1/105027.
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Thesis: Ph. D. in Biological Chemistry, Massachusetts Institute of Technology, Department of Chemistry, 2016.Cataloged from PDF version of thesis. Vita.
Includes bibliographical references.
Synaptic plasticity serves as a central molecular mechanism underlying learning and memory formation in the brain. An increase in intracellular calcium concentrations triggered by neuronal activity induces synaptic plasticity, and calmodulin is a key protein that detects the elevated calcium levels and propagates downstream signaling. Neurogranin is a neuron-specific protein that binds to calmodulin and regulates the availability of calmodulin in the postsynaptic compartments of excitatory neurons. Dysregulation of neurogranin has been reported to cause altered synaptic plasticity as well as impairment in hippocampus-dependent learning, and is also associated with the higher risk of developing neurodegenerative and psychiatric diseases. Therefore, it is critical to understand how neurogranin regulates the induction of synaptic plasticity in the brain at the molecular level. The focus of this thesis is to examine how the changes in neurogranin expression levels contribute to the induction of synaptic plasticity in the hippocampus with a spike-timing-dependent plasticity paradigm and to understand the underlying molecular mechanisms. Using lentivirus-mediated manipulations of neurogranin levels in hippocampal CAl neurons, we found that increasing neurogranin levels in CAI neurons prolongs the timing window for spike-timing-dependent long-term potentiation (LTP), whereas acute knockdown of neurogranin inhibits the expression of LTP via regulating PP2B activity. We have also found that neurogranin interferes with calcium-dependent inactivation of neuronal L-type calcium channels and allows a sustained influx of calcium during the membrane depolarization in hippocampal neurons. Our results indicate that dynamic changes in neurogranin levels play a crucial role in setting the threshold for inducing LTP in spike-timing-dependent plasticity in the hippocampus.
by Hongik Hwang.
Ph. D. in Biological Chemistry
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Howie, Philip Robert. "Measuring plasticity in brittle materials." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610682.
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Woollett, K. "Plasticity in the human hippocampus." Thesis, University College London (University of London), 2011. http://discovery.ucl.ac.uk/1310481/.
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If we are to approach rehabilitation of memory-impaired patients in a systematic and efficacious way, then it is vital to know if the human memory system has the propensity for plasticity in adulthood, the limiting factors on such plasticity, and the timescales of any plastic change. This thesis was motivated by an attempt to develop a body of knowledge in relation to these questions. There is wide agreement that the hippocampus plays a key role in navigation and memory across species. Evidence from animal studies suggests that spatial memoryrelated hippocampal volume changes and experience-related hippocampal neurogenesis takes place throughout the lifespan. Previous studies in humans indicated that expert navigators, licensed London taxi drivers, have different patterns of hippocampal grey matter volume relative to control participants. In addition, preliminary evidence also suggested there may be functional consequences associated with this grey matter pattern. Using licensed London taxi drivers as a model for learning and memory, the work undertaken centered on four key issues: (1) In a set of studies, I characterised the neuropsychological profile of licensed London taxi drivers in detail, which included devising a number of new table-top associational memory tests. This enabled me to assess the functional consequences of their expertise and hippocampal grey matter pattern in greater depth than previous studies. (2) In order to explore the effects of taxi drivers’ expertise in more naturalistic settings, I also examined how well they could learn the layout of an unfamiliar town compared with a group of non-taxi drivers, and how effectively taxi drivers could integrate a new district into their existing spatial representation of London. (3) I then conducted a study on experts whose knowledge was much less spatial than taxi drivers in order to examine if the effects on hippocampal grey matter and neuropsychology were general or whether they were specific to the spatial domain. (4) Given that previous taxi driver studies were cross-sectional, the question of whether the human hippocampus can exhibit spatial memory-related structural plasticity in adulthood was uncertain. I therefore conducted a longitudinal study which assessed participants both pre and post taxi driver training using structural MRI and neuropsychological measures. This enabled me to investigate, within subjects, whether hippocampal volume changes can be acquired in response to intense spatial stimulation. In addition, I explored whether ceasing to be a taxi driver (i.e. retiring after many years on the job) resulted in ‘reverse’ plasticity. I found evidence for hippocampal plasticity within individuals as a result of their intense acquisition of spatial knowledge over a number of years that was associated with qualifying to be a licensed London taxi driver, and preliminary evidence of reverse plasticity when taxi drivers retire. This suggests that hippocampal structure and memory ability can be modified in response to environmental factors and are not necessarily hard-wired. However, my results also provide some insights into the boundaries within which human memory operates, as I identified both positive and negative cognitive consequences of being an expert navigator, and also established that the MRI and neuropsychology effects of expertise on the hippocampus may be restricted to the spatial domain.
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Thomas, Adam G. "Brain plasticity and aerobic fitness." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:c941d5b2-4b37-420a-be3f-d71e753fc8d6.
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Regular aerobic exercise has a wide range of positive effects on health and cognition. Exercise has been demonstrated to provide a particularly powerful and replicable method of triggering a wide range of structural changes within both human and animal brains. However, the details and mechanisms of these changes remain poorly understood. This thesis undertakes a comprehensive examination of the relationship between brain plasticity and aerobic exercise. A large, longitudinal experiment was conducted in which healthy but sedentary participants were scanned before and after six-weeks of monitored aerobic exercise. Increases in the volume of the anterior hippocampus were observed, as previously reported in an older cohort after a longer exercise intervention. Multimodal imaging methods allowed an in-depth exploration of the mechanisms underlying this volume change, which proved to be dominated by white matter changes rather than the vascular changes that have been previously reported. A surprising global change in the balance of CSF, blood, and brain tissue within the cranial cavity was also observed. Cross-sectional differences in memory and brain structure associated with fitness were also observed. The volume of the anterior hippocampus was shown to correlate with a measure of working memory. Higher cerebral blood volume throughout the brain was found to correlate with greater fitness and better working memory. Focal associations between fitness and magnetic susceptibility, a measure of iron content, were also observed in the basal ganglia. These findings demonstrate that aerobic fitness is associated with improved cognition and brain structure throughout the lifespan rather than simply acting to mitigate age related brain atrophy or accelerate brain development. Finally, a new pipeline was developed for analysing hippocampal morphometry using high-resolution, 7 Tesla scans. Striking variability in the convolution of the hippocampal surface is reported. This technique shows promise for imaging the precise nature of the change in hippocampal volume associated with aerobic exercise. This thesis adds to the evidence that aerobic exercise is a potent catalyst for behavioural and brain plasticity while also demonstrating that the mechanisms for those plastic changes are likely different than previously supposed. Future work will refine these measurement techniques, perhaps to a point where brain changes can be monitored on a single subject level. This work will provide an important tool to understand how best to utilize aerobic exercise to facilitate adaptive behavioural changes, mitigate the negative effects of ageing and disease on the brain, and maximize the benefits of active lifestyles.
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Zahedi, S. Abolfazl. "Crystal-plasticity modelling of machining." Thesis, Loughborough University, 2014. https://dspace.lboro.ac.uk/2134/14588.
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A machining process is one of the most common techniques used to remove material in order to create a final product. Most studies on mechanisms of cutting are performed under the assumption that the studied material is isotropic, homogeneous and continuous. One important feature of material- its anisotropyis linked to its crystallographic nature, which is usually ignored in machining studies. A crystallographic orientation of a workpiece material exerts a great influence on the chip-formation mechanism. Thus, there is a need for developing fundamental understanding of material's behaviour and material removal processes. While the effect of crystallographic orientation on cutting-force variation is extensively reported in the literature, the development of the single crystal machining models is somewhat limited.
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Cheng, Yi Pik Helen. "Micromechanical investigation of soil plasticity." Thesis, University of Cambridge, 2004. https://www.repository.cam.ac.uk/handle/1810/272053.
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Walton, James C. "Photoperiod, Brain Plasticity, and Behavior." The Ohio State University, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=osu1364994837.
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Padrão, Ana Isabel Martins Novais. "Mitochondrial plasticity in pathophysiological conditions." Doctoral thesis, Universidade de Aveiro, 2013. http://hdl.handle.net/10773/12025.
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Doutoramento em BioquímicaBoth skeletal and cardiac muscles daily burn tremendous amounts of ATP to meet the energy requirements for contraction. So, it is not surprising that the maintenance of mitochondrial morphology, number, distribution and functionality in striated muscle are important for muscle homeostasis. In these tissues mitochondria present the added dimension of two populations, the intermyofibrillar (IMF) and the subsarcolemmal (SS) mitochondria, being IMF the most abundant one. In the present thesis, the molecular mechanisms harboured in mitochondria of striated muscles were studied using animal models, to better comprehend the role of mitochondrial plasticity in several pathophysiological conditions such as aging, diabetes mellitus and bladder cancer. The comparative analysis of IMF and SS populations isolated from heart evidenced a higher respiratory chain activity of mitochondria interspersed in the contractile apparatus. The higher susceptible of SS respiratory chain complexes subunits to carbonylation, but not to nitration, seems to justify the lower respiratory chain activity observed in this mitochondrial population. Our results showed that in heart from aged mice there is an accumulation of dysfunctional mitochondria. The age-related decrease of oxidative phosphorylation activity seems to be justified, at least partially, by the increased proneness of mitochondrial proteins as OXPHOS subunits and MnSOD to oxidative modifications. Moreover, a sedentary lifestyle seems to worsen the functional consequences of aging in heart by increasing mitochondrial proteins susceptibility to nitration. In skeletal muscle from rats with type 1 diabetes mellitus induced by streptozotocin administration, we verified the accumulation of dysfunctional mitochondria due, at least in part, to the impairment of PQC system. Indeed, the decreased activity of AAA proteases was accompanied by the accumulation of oxidatively modified mitochondrial proteins with impact in respiratory chain activity. The diminishing of mitochondria activity also underlies cancer-induced muscle wasting. Indeed, using a rat model of chemically induced urothelial carcinoma we verified that the loss of gastrocnemius mass was related to mitochondrial dysfunction due to, at least partially, the down-regulation of PQC system involving the mitochondrial proteases paraplegin and Lon. PQC impairment resulted in the accumulation of oxidatively modified mitochondrial proteins. In overall, regardless the pathophysiological stimuli that promote mitochondrial alterations, there are similarities in the pattern of disease-related mitochondrial plasticity. The diminished capacity for ATP production in striated muscle seems to be due to increased oxidative damage of mitochondrial proteins, namely subunits of respiratory chain complexes, metabolic proteins and MnSOD. Our data highlighted, for the first time, the impact of mitochondrial PQC system impairment in the accumulation of oxidized proteins, exacerbating the dysfunction of this organelle in striated muscle in several pathophysiological conditions.
O músculo-esquelético e o músculo cardíaco consomem diariamente grandes quantidades de ATP para a contração, pelo que não é de surpreender que a morfologia, a distribuição e a funcionalidade mitocondrial sejam importantes para a manutenção da sua homeostasia. Mais ainda, o músculo estriado apresenta duas populações de mitocôndrias, as intermiofibrilares (IMF), presentes em maior quantidade, e as subsarcolemais (SS). Na presente tese foram estudados, utilizando modelos animais, os mecanismos moleculares localizados na mitocôndria do músculo estriado para melhor compreender o papel da plasticidade mitocondrial em resposta a várias condições patofisiológicas nomeadamente o envelhecimento, a diabetes mellitus e o cancro. A análise bioquímica das populações de mitocôndrias isoladas do coração evidenciou uma maior atividade da cadeia respiratória nas mitocondriais IMF em comparação com as SS. A maior suscetibilidade das subunidades dos complexos da cadeia respiratória das mitocôndrias SS à carbonilação, mas não à nitração, parece justificar a menor atividade da cadeia respiratória observada nesta população de mitocôndrias. No estudo da adaptação mitocondrial ao envelhecimento verificou-se a acumulação de mitocôndrias disfuncionais no coração. A diminuição da atividade da cadeia respiratória parece ser justificada, pelo menos em parte, pelo aumento da suscetibilidade de proteínas mitocondriais a modificações oxidativas. Adicionalmente verificou-se que um estilo de vida sedentário tem um impacto negativo na funcionalidade mitocondrial do coração de animais idosos. No músculo-esquelético de animais com diabetes mellitus tipo 1 induzida pela administração de streptozotocina, verificou-se uma acumulação de mitocôndrias disfuncionais devido, pelo menos em parte, ao comprometimento do sistema de controlo de qualidade proteica mitocondrial. Efetivamente, a diminuição da atividade e da expressão de proteases AAA foi acompanhada pela acumulação de proteínas mitocondriais oxidadas. No músculo-esquelético de animais com caquexia associada ao carcinoma urotelial também se verificou a ocorrência de disfunção mitocondrial associada ao comprometimento do sistema de controlo de qualidade proteica, envolvendo as proteases mitocondriais paraplegina e Lon, com consequente acumulação de proteínas mitocondriais oxidadas. A disfunção mitocondrial observada no músculo gastrocnemius de animais com cancro ocorreu em paralelo com o aumento do catabolismo muscular e consequente perda de massa corporal. No global, os resultados sugerem que independentemente do estímulo patofisiológico que promove uma resposta adaptativa da mitocôndria no músculo estriado existem semelhanças no padrão de plasticidade mitocondrial. A redução da capacidade de produção de ATP parece ser devida ao aumento dos danos oxidativos das proteínas mitocondriais, nomeadamente das subunidades dos complexos da cadeia respiratória, de proteínas metabólicas e da MnSOD com consequente comprometimento das vias moleculares em que estão envolvidas. Os nossos resultados evidenciaram, pela primeira vez, a contribuição da disfunção do sistema de controlo de qualidade proteica mitocondrial para a acumulação de proteínas oxidadas e, consequentemente, para a disfunção mitocondrial.
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Focht, Eric M. "Transformation induced plasticity in ceramics." Thesis, This resource online, 1992. http://scholar.lib.vt.edu/theses/available/etd-12232009-020415/.
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Karakossian, Movses H. "Molecular substrates of cerebellar plasticity." Diss., Restricted to subscribing institutions, 2007. http://proquest.umi.com/pqdweb?did=1428839071&sid=1&Fmt=2&clientId=1564&RQT=309&VName=PQD.
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Mysore, Shreesh Pranesh Schuman Erin Margaret Quartz Steven. "Structural plasticity in neuronal networks /." Diss., Pasadena, Calif. : California Institute of Technology, 2007. http://resolver.caltech.edu/CaltechETD:etd-11102006-021149.
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Johnson, Hope Amy. "Plasticity of cortical network dynamics." Diss., Restricted to subscribing institutions, 2009. http://proquest.umi.com/pqdweb?did=1835448081&sid=7&Fmt=2&clientId=1564&RQT=309&VName=PQD.
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He, Kaiwen. "AMPA Receptor and synaptic plasticity." College Park, Md.: University of Maryland, 2009. http://hdl.handle.net/1903/9181.
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Thesis (Ph.D.) -- University of Maryland, College Park, 2009.Thesis research directed by: Dept. of Biology. Title from t.p. of PDF. Includes bibliographical references. Published by UMI Dissertation Services, Ann Arbor, Mich. Also available in paper.
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Kohengadol, Roni A. "Nonlinear solvers for plasticity problems." Link to electronic thesis, 2004. http://www.wpi.edu/Pubs/ETD/Available/etd-0408104-111231.
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Cziko, Anne-Marie. "Translational Control of Synaptic Plasticity." Diss., The University of Arizona, 2009. http://hdl.handle.net/10150/195589.
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Activity-dependent and synapse-specific translation of mRNAs is required for long-term changes in synaptic strength (or efficacy). However, many of the components mediating repression, transport and activation of mRNAs are unknown. Translational control in neurons is a highly conserved process and mediated by a ribonuclear particle (RNP). This study shows that RNPs in Drosophila neurons are similar not only to mammalian neuronal RNA granules but also to yeast P-bodies, cytoplasmic foci involved in translational repression and RNA decay. The evolutionarily conserved proteins Me31b and Trailer Hitch localize to RNA granules. Me31b and Trailer Hitch are required for normal dendritic growth. Mutations in Me31b and Trailer Hitch suppress phenotypes resulting from overexpression of Fragile X Mental Retardation protein, suggesting that both proteins may act as translational repressors. In addition, this study reports the identification of novel translational repressors in neurons. Using the overexpression phenotype of Fragile X Mental Retardation protein in a candidate-based genetic screen, I identified dominant suppressor mutations in five genes, including Doubletime/Discs Overgrown, Orb2/CPEB, PolyA Binding Protein, Rm62/Dmp68 and SmD3. Like Me31b and Trailer Hitch, all five proteins localize to neuronal RNPs. Overexpression of each proteins affects dendritic branching of sensory neurons in Drosophila. Identification and further characterization of these novel RNP granule components and dFMR1-interacting proteins may provide further insights into the mechanisms controlling translational in dendrites.
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Scholey, Andrew Belton. "Immunological investigations into synaptic plasticity." Thesis, Open University, 1991. http://oro.open.ac.uk/57339/.
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Antibody technology was applied to the study of synaptic plasticity resulting from passive avoidance training in the chick and long-term potentiation in the rat. These studies fell into three categories: 1) the disruption of memory for a one-trial passive avoidance task by intracranial injection of an anti-postsynaptic density antiserum 2) mapping time- and locus-specific changes in the chick brain using antisera to the cytoskeletal proteins (Xtubulin and microtubule-associated protein 2 following passive avoidance training and 3) using antibodies to synaptically-enriched antigens to map time- and locus-specific changes in hippocampal subfields following long-term potentiation in the rat. In the first series of experiments an antiserum (RI4) was raised against protein from chick forebrain postsynaptic densities (PSDs). The antiserum was characterised and was found to recognise six distinct antigens as determined by Western Blots. These antigens were found to have a primarily (but not exclusively) synaptic location. Intracranial injections of IgG isolated from R14 resulted in amnesia for a one-trial passive avoidance paradigm in the chick when administered 60min pre-training (but not 30min or 15min pre-training or 1000n post-training), in chicks tested 24hrs (but not Ihr or 3hrs) post-training. In the second set of experiments monoclonal antibodies were used to examine changes in levels of the cytoskeletal proteins a-tubulin and microtubule-associated protein 2 (MAP2) in specific forebrain loci following passive avoidance training in the chick. Of the regions examined, elevations in the titre of anti-a-tubulin were found in the left Intermediate Hyperstriatum Ventrale (IMHV) l hr, 6hrs and 24hrs following passive training, in the left Lobus Parolfactorius (LPO) 1hr following training and in the right LPO 6hrs and 24hrs following training. A hemispherically-asymmetrical change was found in the titre of anti-MAP2 which was interpreted as possibly reflecting a decrease in the amount of the antigen in the left IMHV 24hrs following training. No training-related changes were detected, using either antibody, in a third forebrain region, the Paleostriatum Augmentatum (PA). During the characterisation of antiserum R14 it was found that only one antigen (with an apparent molecular weight of 230kDa) is conserved between the chick and rat brain. The antigen is enriched in synaptic fractions isolated from the rat hippocampus and was used, as well as a PSD-specific monoclonal antibody, 411B, to examine possible changes in hippocampal subfields CAl, CA3 and the dentate area taken at several time-points following tetanisation of the right perforant path. 24hrs following tetanisation (but not at earlier time-points), the titre of R14 was elevated in the dentate area ipsilateral to tetanisation and in both the ipsi- and contralateral CAL The titre of 411B was increased specifically in the target, dentate area and only at 8hrs following tetanisation, an increase which was abolished in the presence of the protein synthesis inhibitor, anisomycin. These results are discussed in the context of current models of synaptic plasticity.
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Edwards, Thomas Edward James. "Plasticity of γ-TiAl alloys." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/275867.
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Gamma titanium aluminide alloys are emerging as a lightweight replacement to nickel superalloys, with current application in turbine stages of aero-engines, as well as in high performance automobiles and potentially the nuclear industry. The lack of toughness of its two constitutive intermetallic phases, γ-TiAl and α2-Ti3Al, prevents a conventional damage tolerant approach to fatigue lifing. To gain confidence in the use of γ-TiAl alloys and extend the temperature-stress envelope of applicability, the present work aims to achieve an understanding of the development of plasticity and flaw formation during cyclic loading. The general plasticity of a γ-TiAl alloy, Ti-45Al-2Nb-2Mn(at.%)-0.8vol.%TiB2, in compression was investigated by mapping the development of localised strain at the specimen surface. Methods were developed to produce speckle patterns for high resolution digital image correlation that were stable at test temperatures of 700 °C in air, in order to study the extent of plasticity generated by differing deformation mechanisms at application-relevant temperatures, with nano-scale resolution. At the colony scale (i.e. single stacks of co-planar α2-Ti3Al and γ-TiAl lamellae, where each stack is formed from a single high temperature disordered α-TiAl grain), macroscopic deformation bands were observed to develop at only a few percent strain. Within such bands, which propagated across many colonies of differing lamellar orientations, considerable lattice curvature and localised slip and twin operation occurred. This correlated with colony boundary failure in such bands. Twinning of the γ-TiAl phase parallel to the lamellar interfaces, longitudinal twinning, has rarely been studied, despite generalised twinning in equiaxed γ-TiAl grains being known to cause boundary decohesion. Here, the occurrence of longitudinal twinning in both microcompression and polycrystalline testpieces was investigated up to 700 °C by electron backscatter diffraction. The strength of constraint by surrounding lamellar domains was found to be the determining factor in the increased prominence of twinning at 700 °C, and hence determined whether twinning shear-induced flaws formed at colony boundaries. Using the high temperature digital image correlation strain mapping and electron backscatter diffraction techniques developed, along with transmission electron microscopy, the onset of plasticity at temperatures up to 700 °C was studied in both micro-scale and macro-scale test specimens for different lamellar thicknesses. Testpieces were loaded below the macroscopic yield stress in both monotonic and high cycle fatigue regimes, to 107 cycles, at a tensile stress ratio of R = 0.1. Longitudinal plasticity occurred in most colonies with soft mode lamellar orientations, and was located just 30 - 50 nm from lamellar interfaces. Lamellar refinement caused an increased number of slip bands to develop. In most cases, plastic strains decreased to zero by the colony boundary and strain transfer across such boundaries in high cycle fatigue was rare. At room temperature, the maximum applied stress was found to influence the number of slip bands more than the number of loading cycles.
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Fuhrmann, Delia Ute Dorothea. "Learning and plasticity in adolescence." Thesis, University College London (University of London), 2017. http://discovery.ucl.ac.uk/10040234/.
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Adolescence is the period of life between puberty and relative independence. It is a time during which the human brain undergoes protracted changes - particularly in the frontal, parietal and temporal cortices. These changes have been linked to improvements in cognitive performance; and are thought to render adolescence a period of relatively high levels of plasticity, during which the environment has a heightened impact on brain development and behaviour. This thesis investigates learning and plasticity in adolescence in four experimental studies. Study 1 examined age differences in face cognition, a key component of social cognition, by testing face perception and face memory performance in 661 participants aged 11 - 33. Study 2 tested whether the effects of social exclusion are age-dependent by measuring cognitive performance after social exclusion in 99 participants between ages 10 - 38. For Study 3, 663 participants aged 11 - 33 were asked to complete 20 days of cognitive training to probe whether the effects of cognitive training are also age-dependent. Study 4 investigated the neural correlates of academic diligence in 40 girls aged 14 - 15, using functional and structural neuroimaging. The research in this thesis demonstrates protracted development of cognitive functions in adolescence, consistent with previous studies. It highlights adolescence as a window of opportunity for learning but also as a vulnerable phase during which the brain is particularly susceptible to harmful effects of social exclusion. Finally, it highlights that individual variability in self-control and underlying frontal systems may be related to academic diligence, and thus educational outcomes.
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Sallagundala, Nagaraja. "Neuronal hypothalamic plasticity in chicken." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2007. http://dx.doi.org/10.18452/15600.
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Aufgabe der elektrophysiologischen Studie zur Charakterisierung der neuronalen hypothalamischen Plastizität beim Haushuhn war es, den Einfluss des Alters sowie GABAerger Substanzen auf die Feuerrate und die Temperatursensitivität (thermischer Koeffizient: TC) von Hypothalamusneuronen mittels extrazellulärer Ableitungen in Hirnschnitten zu untersuchen. Im Vergleich zu adulten Vögeln und Säugetieren wurde bei juvenilen Hühnern eine hohe neuronale Kältesensitivität nachgewiesen, die offensichtlich eine spezifische Eigenschaft juveniler Vögel ist. Die Ontogenese der neuronalen hypothalamischen Thermosensitivität ist deutlich artspezifisch. Einige Neurone wiesen eine inherente Kältesensitivität auf. Eine mögliche zentrale Rolle kältesensitiver Neurone im Rahmen der Thermoregulation juveniler Hühner wurde postuliert. Muscimol und Baclofen hemmen signifikant die Feuerrate der Hypothalamusneurone, unabhängig von der jeweiligen Thermosensitivität. Demgegenüber bewirken Bicucullin und CGP35348 einem Anstieg der Feuerrate. Nur bei kältesensitiven Neuronen wurde der TC signifikant durch GABAB-Rezeptor-Liganden verändert (signifikant erhöht durch Baclofen und durch CGP35348 gehemmt). Der Effekt von Muscimol und Baclofen auf Feuerrate und TC wurde durch Co-Perfusion mit einer 10-fach höheren Konzentration der entsprechenden Antagonisten Bicucullin und CGP35348 aufgehoben. Der wesentliche GABAerge Einfluss auf thermosensitive und –insensitive Hypothalamusneurone ist mit dem bei Säugetieren nachgewiesenen vergleichbar. Der einzige Unterschied betrifft die GABAB-Rezeptor vermittelte Änderung des TC. Beim Hühnerküken betraf dies die kältesensitiven und beim Säugetier die wärmesensitiven Neurone. Der grundlegende Mechanismus der GABAergen Beeinflussung thermosensitiver und –insensitiver Neurone scheint einen älteren evolutionären Ursprung zu haben. Eine funktionelle Rolle GABAerger Substanzen im Rahmen der zentralen Kontrolle der Körpertemperatur beim Vogel ist möglich.In the present electrophysiological studies, characterization of neuronal hypothalamic plasticity in the chicken aims to investigate the influence of age during development by extracellular recordings. High neuronal cold sensitivity has been found in juvenile chicken in contrast to adult mammals and birds. High hypothalamic cold sensitivity seems to be a specific characteristic feature in juvenile birds. Between species a species specificity of the early development of neuronal hypothalamic thermosensitivity could be clearly demonstrated. Existence of inherent nature to a certain degree suggests a possible thermoregulatory role of cold-sensitive neurons in chicken. The effects of the GABAergic substances on neuronal tonic activity (firing rate) and temperature sensitivity (temperature coefficient) in hypothalamic neurons have been examined. Muscimol and baclofen in equimolar concentrations significantly inhibited tonic activity, regardless of their type of thermosensitivity. In contrast bicuculline and CGP 35348 increased firing rate. Temperature coefficient was significantly changed by ligands of GABAB receptors, restricted to cold-sensitive neurons. The TC was significantly increased by baclofen and significantly decreased by CGP 35348. Effects of muscimol and baclofen on firing rate and TC were prevented by co-perfusion of appropriate antagonists bicuculline and CGP 35348, respectively in tenfold higher concentration. Thus the main effects of GABA in chicken are similar with that described in mammals. The only difference is in respect of the GABAB receptors mediated change restricted to cold-sensitive neurons in chicken but in mammals only seen in warm-sensitive neurons. However, the results indicate that the fundamental mechanism of GABAergic influence in chicken are conserved during evolution. The response of hypothalamic neurons to temperature changes suggest a possible functional role of GABAergic substances in the control of body temperature in birds.
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Forest, Jérémy. "Impact of adult neurogenesis versus preexisting neurons on olfactory perception in complex or changing olfactory environment." Thesis, Lyon, 2017. http://www.theses.fr/2017LYSE1326/document.
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L'olfaction est un sens clé dans l'adaptation du comportement. Pour permettre des actions appropriées le système olfactif doit effectuer des discriminations fines entre stimuli. Les performances de discrimination peuvent être améliorées via l'apprentissage perceptif et une structure cérébrale clé : le bulbe olfactif. Cette structure est cible d'une forme de plasticité particulière qui est la neurogenèse adulte. C'est là que des nouveaux neurones, majoritairement des cellules granulaires, régulent l'activité des cellules relais. Il a été montré que ces neurones sont requis pour un apprentissage perceptif.La question centrale de cette thèse est d'élucider le rôle et la spécificité des nouveaux neurones dans l'apprentissage olfactif complexe et changeant.Nous avons d'abord étudié l'effet d'un apprentissage perceptif complexe sur la neurogenèse adulte. Cette étude à démontré la nécessité et suffisance des nouveaux neurones dans l'apprentissage perceptif simple. Elle a aussi montré que lorsque l'apprentissage devient complexe, un réseau plus large est recruté, requérant les neurones préexistant.L'environnement olfactif est aussi changeant. Dans une seconde étude nous avons investigué comment la mémoire olfactive est altérée par nouvelle mémoire et le rôle de la neurogenèse adulte dans ce processus. Elle a montré le rôle des nouveaux neurones à sous tendre la mémoire olfactive et l'importance du délai entre apprentissages dans la stabilisation mnésique.Finalement, le recours aux neurosciences computationnelles a eu pour but de définir le rôle des nouveaux neurones granulaire au niveau du premier niveau de transformation de l'information et comment le raffinement des représentations sensorielles émerge par décorrelation.Pour conclure, la perception olfactive est changeante en fonction des modifications environnementales et cette plasticité est sous tendu par une plasticité du circuit du bulbe olfactif, due en grande partie à la neurogenèse adulteOlfaction is a key player in behavioral adaptation. To perform tasks accurately, the olfactory system has to perform fine discrimination between very close stimuli. The discrimination performances can be enhanced through perceptual learning and a key cerebral structure in this is the olfactory bulb. This structure is the target of a specific form of plasticity that is adult neurogenesis. In this structure, adult-born neurons differentiate mostly in granule cells that regulate the activity of the relay cells. It has previously been shown that these neurons are required to perform perceptual learning. The central question of this thesis work is to elucidate both the role and the specificity of adult born neurons during complex or changing olfactory learning.We first studied the effect of complex perceptual learning on adult neurogenesis. This study demonstrated the necessity and sufficiency of adult-born neurons for simple olfactory learning. It also showed that when learning becomes complex, a larger neural network is involved requiring preexisting neurons.The olfactory environment is also changing. In a second study we investigated how the memory of an olfactory information is altered by the acquisition of a new one and what is the role of adult neurogenesis in this process. This second study highlighted the role of adult-born neurons in underlying olfactory memory and the importance of delay between learning for memory stabilization.Lastly, an approach relying on computational neurosciences aimed at outlining a computational framework explaining the role of adult-born granule cells in early olfactory transformations and how sharpened sensory representations emerge from decorrelation.To conclude, olfactory perception is changing according to environmental modifications and this plasticity is underlain by an important plasticity of the olfactory bulb circuitry due in large part to adult neurogenesis