In discussions of heterogeneous catalysis and other surface-related phenomena, the dynamical properties of the catalytic material are often neglected, even at elevated temperatures. An example is the three-way catalyst (TWC), used for treatment of exhaust gases from combustion engines operating at several hundred degrees Celsius. In the TWC, reduced ceria (CeO2-x) is one of the key components, where it functions as an oxygen buffer, storing and releasing oxygen to provide optimal conditions for the catalytic conversion of the pollutants. In this process it is evident that dynamics plays a crucial role, not only ionic vibrations, but also oxygen diffusion. In this thesis, the structure and dynamics of several ionic crystalline compounds and their surfaces have been studied by means of Molecular dynamics (MD) simulations and Lattice dynamics (LD) calculations. The main focus lies on CeO2-x, but also CeO2, MgO and CaF2 have been investigated. The presence of oxygen vacancies in ceria is found to lead to significant distortions of the oxygen framework around the defect (but not of the cerium framework). As a consequence, a new O-O distance emerges, as well as a significantly broadened Ce-O distance distribution. The presence of oxygen vacancies in ceria also leads to increased dynamics. The oxygen self-diffusion in reduced ceria was calculated from MD simulations in the temperature range 800-2000 K, and was found to follow an Arrhenius behaviour with a vacancy mechanism along the crystallographic <100> directions only. The cation and anion vibrational surface dynamics were investigated for MgO (001) using DFT-LD and for CaF2 (111) in a combined LEED and MD study. Specific surface modes were found for MgO and increased surface dynamics was found both experimentally and theoretically for CaF2, which is isostructural with CeO2. Many methodological aspects of modeling dynamics in ionic solids are also covered in this thesis. In many cases, the representation of the model system (slab thickness, simulation box-size and the choice of ensemble) was found to have a significant influence on the results.

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Les canaux ioniques sont des déterminants majeurs de la forme et de la durée du potentiel d'action (PA) cardiaque. Leur expression fonctionnelle à la membrane plasmique résulte d'une balance entre les voies antérograde et rétrograde du trafic intracellulaire, ainsi que de leur prise en charge par des compartiments endosomaux afin d'être recyclés ou dégradés. Le canal KV1.5 porte le courant principal de repolarisation atriale chez l'homme, IKur, et est impliqué dans la physiopathologie de la fibrillation atriale (FA). La FA est caractérisée par un raccourcissement de la durée du PA lié à un courant IKur augmenté et un courant ICaL diminué et est favorisée par l'augmentation des contraintes mécaniques. Ainsi, le canal KV1.5 constitue une cible majeure pour le développement d'anti-arythmiques spécifiques de l'oreillette. Ce projet avait pour but de mieux comprendre comment est régulée l'expression fonctionnelle des canaux KV1.5 dans les myocytes atriaux. Dans un premier temps, nous avons montré que le shear stress entraîne une augmentation du courant IKur impliquant la voie de mécanotransduction intégrine?1/FAK et l'endosome de recyclage lent. Dans les cellules hypertrophiées, cette voie de mécanotransduction est hyperactivée et le courant IKur est ainsi augmenté. Dans un second temps, nous avons montré que la voie d'endocytose des canaux KV1.5 est dépendante de la clathrine et que les microtubules sont principalement impliqués dans l'internalisation et la dynamique du canal à la surface des cellules. Ainsi, ce travail a permis de mieux caractériser les acteurs du trafic impliqués dans la régulation de l'expression fonctionnelle du canal KV1.5 dans les cardiomyocytes atriaux. / Ion channels are major determinants of shape and duration of the cardiac action potential (AP). Their functional expression at the sarcolemma is a dynamic process resulting from a balance between anterograde (exocytosis) and retrograde (endocytosis) pathways, and the involvement of the endosomal compartments which direct ion channels towards recycling or degradation. KV1.5 channel carries IKur current which constitutes the main atrial repolarizing current in human and which is involved in atrial fibrillation (AF). Mechanical forces and shortening of the AP duration are linked to an increased in IKur current and decreased ICaL current. Therefore, KV1.5 channel constitutes a major target for the development of atria-selective antiarrhythmic drugs. The aim on this project was to better understand how functional expression of KV1.5 channels in atrial myocytes is regulated. Firstly, we showed that shear stress triggers an increase in IKur current implying the integrinβ1/FAK mecanotransduction pathway. This process requires an intact microtubule network and involves the Rab11-associated recycling endosome. In hypertrophied cells, the mecanotransduction pathway is overactivated. Consequently, IKur is increased. Secondly, we demonstrated that KV1.5 channel endocytosis is mediated by the clathrin pathway. We showed that microtubules are involved in the internalization and dynamics of KV1.5 channel in the membrane. Therefore, this work provides a better understanding of the different players involved in the trafficking of KV1.5 channel and shed new lights on the functional regulation of this atria-specific channel.

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Initialement encodés dans l’hippocampe, les nouveaux souvenirs déclaratifs deviennent progressivement dépendants d’un réseau distribué de neurones corticaux au cours de leur maturation dans le temps. Cependant, les mécanismes cellulaires et moléculaires sous-­‐tendant la consolidation et le stockage à long terme de ces nouveaux souvenirs au sein des réseaux corticaux restent à élucider. Les récepteurs N-­‐méthyl-­‐D-­‐aspartate (RNMDA) jouent un rôle essentiel dans l’induction et la régulation des changements synaptiques sous-­‐tendant les processus mnésiques de type associatifs. Sur la base de leurs propriétés biophysiques respectives, nous avons formulé l’hypothèse que la redistribution synaptique des deux formes principales de sous-­‐unités GluN2 exprimées dans le néocortex adulte (GluN2A and GluN2B), pourrait constituer un mécanisme de régulation de la plasticité synaptique supportant l’intégration et la stabilisation progressive des souvenirs au niveau cortical au cours du processus de consolidation mnésique. En combinant, chez le rat adulte, une approche comportementale, biochimique, pharmacologique et des stratégies innovantes consistant à manipuler le trafic de sous-­‐unités des RNMDA à la surface synaptique, nos résultats mettent en évidence un changement cortical dans la composition synaptique en sous unités GluN2, lequel régule la stabilisation progressive de la mémoire à long terme au sein des réseaux corticaux. Nous avons d'abord établi que les RNMDA contenant la sous-­‐unité GluN2B, via leur interaction spécifique avec une protéine clé de la signalisation synaptique, la CaMKII, sont préférentiellement recrutés lors de la phase d’encodage pour permettre l’allocation des nouveaux souvenirs olfactifs associatifs dans un réseau de neurones corticaux spécifique. Au cours du processus de consolidation, nous avons révélé que la redistribution des RNMDA corticaux contenant les sous-­‐unités GluN2B vers l’extérieur ou l’intérieur de l’espace synaptique suite à l’apprentissage, contrôle respectivement la stabilisation de la mémoire à long terme et son oubli au cours du temps. Enfin, renforcer l’acquisition initiale conduit à une augmentation plus rapide du ratio post-­‐synaptique GluN2A/GluN2B et accélère la cinétique du dialogue hippocampo-­‐cortical, ce qui se traduit par une stabilisation accélérée des souvenirs au sein des réseaux corticaux. Pris dans leur ensemble, nos travaux montrent que le trafic des GluN2B-­‐RNMDA corticaux représente un mécanisme cellulaire majeur conditionnant le devenir des traces mnésiques (i.e. stabilisation versus oubli) et apporte un éclairage nouveau sur la façon dont le cerveau organise les souvenirs récents et anciens. / Initially encoded in the hippocampus, new declarative memories are thought to become progressively dependent on a broadly distributed cortical network as they mature and consolidate over time. Although we have a good understanding of the mechanisms underlying the formation of new memories in the hippocampus, little is known about the cellular and molecular mechanisms by which recently acquired information is transformed into remote memories at the cortical level. The N-­‐methyl-­‐D-­‐aspartate receptor (NMDAR) is widely known to be a key player in many aspects of long-­‐term experience-­‐dependent synaptic changes underlying associative memory processes. Based on their distinct biophysical properties, we postulated that the activity-­‐dependent surface dynamics of the two predominant GluN2 subunits (GluN2A and GluN2B) of NMDARs present in the adult neocortex could provide a metaplastic control of synaptic plasticity supporting the progressive embedding and stabilization of long-­‐lasting associative memories within cortical networks during memory consolidation. By combining, in adult rats, behavioral, biochemical, pharmacological and innovative strategies consisting in manipulating trafficking of NMDAR subunits at the cell membrane, our results identify a cortical switch in the synaptic GluN2-­‐containing NMDAR composition which drives the progressive embedding and stabilization of long-­‐lasting memories within cortical networks. We first established that cortical GluN2B-­‐containing NMDARs and their specific interactions with the synaptic signaling CaMKII protein are preferentially recruited upon encoding of associative olfactory memories to enable neuronal allocation, the process via which a new memory trace is thought to be allocated to a given neuronal network. As these memories are progressively processed and embedded into cortical networks, we observed a learning-­‐induced surface redistribution of cortical GluN2B-­‐containing NMDARs outwards or inwards synapses which respectively drives the progressive stabilization and subsequent forgetting of remote memories over time. Finally, increasing the strength, upon encoding, of the initial memory leads to a faster increase of the cortical GluN2A/GluN2B synaptic ratio and accelerates the kinetics of hippocampal-­‐cortical interactions, which translated into a faster stabilization of memories within cortical networks. Taken together, our results provide evidence that GluN2B-­‐NMDAR surface trafficking controls the fate of remote memories (i.e. stabilization versus forgetting), shedding light on a novel mechanism used by the brain to organize recent and remote memories.