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1

Woodall, Lucy. "Population genetics and mating systems of European seahorses Hippocampus guttalatus and Hippocampus hippocampus." Thesis, Royal Holloway, University of London, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.538319.

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Molecular genetic studies of European seahorses revealed the presence of two native species (European long snouted seahorse Hippocampus guttulatus and European short snouted seahorse Hippocampus hippocampus) the primary focus of the present study. Ecological studies across the entire geographic range of the species confirmed low density and patchy population distribution. Habitat and holdfast preferences were different for the two seahorse species, with substantial variation between population locations. Morphological characteristics of the seahorses varied considerably across their range, but significant differences were observed within just one population of each species. No environmental parameters were consistent across all populations, and no specific indicators for seahorse presence were discovered. The tissue collection technique, fin clipping, was confirmed to not significantly affect seahorse mortality or growth; this technique was used for all tissue biopsies during this study. Genetic analysis using mitochondrial DNA sequences and data from five microsatellite markers revealed significant population structuring across both species' geographic range. Contemporary environmental factors for this structuring were both physical barriers to gene flow and geographic distance between populations. Most physical barriers identified have also affected other marine species; however a proposed barrier at Cape Finisterre, observed for both seahorse species, has previously only been documented in a few other species. Historic events appear to have influenced the contemporary structure of the two seahorse species differently, with H. hippocampus showing less population structuring. Population expansion and founder effects were seen in most geographic regions. Previously acknowledged refugia sites of the last glacial maximum were also seen in seahorses, but these were different in each species. Microsatellite markers revealed monogamy within broods and breeding cycles for the social polygamous H. guttulatus. Finally the findings of this study were used to suggest specific management and conservation practises for seahorse species across Europe.
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Darling, Ryan Daniel. "HIPPOCAMPAL THETA-TRIGGERED CONDITIONING: ENHANCED RESPONSES IN HIPPOCAMPUS AND PREFRONTAL CORTEX." Connect to this document online, 2005. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=miami1130446123.

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Thesis (M.A.)--Miami University, Dept. of Psychology, 2005.
Title from first page of PDF document. Document formatted into pages; contains [1], v, 48 p. : ill. Includes bibliographical references (p. 16-20).
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3

Cornish, S. "Hippocampal suspension grafts in the Kainic acid lesioned hippocampus of the rat." Thesis, University of Southampton, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.384375.

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4

Kremers, Wolfram. "Neuroprotektion durch Nikotin, Clenbuterol, Memantin und Prolin-reiches Peptid in einer Primärkultur von postnatalen Hippocampuszellen der Ratte." Aachen : Shaker, 2004. http://archiv.ub.uni-marburg.de/diss/z2004/0435/.

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5

Rooney, Alasdair Grant. "Matrix signalling and hippocampal neurogenesis." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/33168.

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The adult mammalian brain harbours at least two germinal - or neurogenic - niches in which new neurons are born throughout life. These neurogenic niches comprise the subependymal zone which lines the ventricular system, and the subgranular zone in the hippocampal dentate gyrus. Post-natal hippocampal neurogenesis was in fact first identified experimentally in the 1960s. However perhaps due partly to aforementioned institutionalised belief and partly to a lack of accessible experimental tools, the phenomenon of hippocampal neurogenesis was widely recognised by the scientific community only shortly before the millennium. Consequent study has established that adult hippocampal neurogenesis has been conserved through millions of years of evolution in nearly every mammalian species studied to date. Importantly, post-mortem studies and radioisotope carbon dating techniques suggest that it also occurs in humans. A great deal of this research has focused on understanding the inner workings of the cells that undergo the transformation to become new adult-born neurons. By contrast, relatively little is known about the potential regulatory role of the surrounding extracellular microenvironment. This might be useful to know in light of much evidence that the extracellular matrix is a key regulator of developmental neurogenesis. This thesis describes my study of whether extracellular matrix regulates hippocampal neurogenesis.
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Stening, Eva. "The Influence of APOE ε4 on the Hippocampus and Hippocampus-Dependent Memory." Doctoral thesis, Uppsala universitet, Institutionen för psykologi, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-302855.

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APOE ε4 is the major genetic risk factor for Alzheimer’s disease, a dementia characterized by memory impairment and hippocampal atrophy. While associated with episodic impairment and reduced hippocampal volume in healthy aging, APOE ε4 has been related to increased episodic memory performance in young adults. The effect of APOE ε4 on hippocampal volume in young age is uncertain, with studies showing comparable or smaller volumes in ε4 carriers. This thesis aims to further explore the effects of APOE ε4 on episodic memory and hippocampal volume in young adults. In addition to episodic memory, spatial memory will also be assessed, as both these memory types are hippocampus-dependent. Furthermore, potential modulating effects of sex are assessed, as sex differences has been found in relation to APOE-related pathology, episodic and spatial memory and hippocampal volume. Study I examined the effects of APOE ε4 on episodic and spatial memory and hippocampal volume in young adults. Hippocampal volume was assessed by manual tracing of the hippocampal head, body and tail. Study II considered whole-brain structural covariance patterns of the anterior and posterior hippocampus. Furthermore, the association between these patterns and episodic and spatial memory performance was assessed. Study III investigated the effects of APOE ε4 on episodic and spatial memory and hippocampal volume in three different age groups. This was done in order to further explore the different effects of APOE ε4 on cognition and hippocampal volume seen in young and older age. In summary, APOE ε4 was positively associated with spatial function and episodic memory in young adults. Although there were no effects of APOE ε4 on hippocampal volume, structural covariance patterns of the anterior and posterior hippocampus differed as a function of APOE ε4 and sex. Thus, structural covariance may provide an early measure of APOE ε4-related effects on brain structure. Moreover, sex was found to modulate the effects of APOE ε4 to the disadvantage of women. This was seen in both age-related hippocampal volume effects and in structural covariance patterns in young adults, as well as in spatial memory performance across age groups.
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7

Khanna, Sanjay. "The hippocampus in nociception." Thesis, University of British Columbia, 1990. http://hdl.handle.net/2429/30685.

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Limbic structures, including the hippocampus, are thought to be involved in pain though not much is known of their neuronal responses to noxious stimuli. Experiments were therefore performed in lightly anaesthetized rats to determine the effect of noxious heat stimuli on the excitability of dorsal hippocampal field CA1 pyramidal neurones. A prolonged and substantial depression of the CA1 population spike was produced by a brief but intense noxious stimulus applied to the tail. This depression was temperature-dependent and habituated to subsequent noxious stimuli applied more than 1 hr later. In other animals, a similar depression and habituation was also obtained with noxious heat stimuli applied to the left hind paw. However, following this habituation of the hind paw, a persistent depression of the CA1 population spike was seen if the tail was exposed to a noxious heat stimulus. The persistent depression was absent when noxious heat was applied in the presence of hippocampal theta rhythm. If, however, the hippocampal electroencephalographic ( EEG ) activity was in an irregular pattern at the time noxious heat was applied, a 4-6 Hz theta rhythm was produced along with the depression of the population spike. The latency and intensity of the reflex response was combined into a reflex-reaction score. There appeared to be a relationship between the reflex-reaction score and the duration of theta rhythm induced by different intensities of noxious heat stimuli but there was no habituation to these responses. The CA1 population spike evoked either by ipsilateral or contralateral CA3 stimulation was similarly depressed following a noxious stimulus. Concomitantly, the persistent depression and habituation of the commissural CA1 population spike was also accompanied by similar changes in the corresponding dendritic field excitatory postsynaptic potential ( EPSP ). However, the amplitude of the CA1 antidromic spike was increased in the majority of cases. These findings suggest that a presynaptically mediated decrease in synaptic transmission may account for the depression of the population spike and dendritic field EPSP. There is evidence to suggest that the noxious stimulus-induced persistent depression of CA1 pyramidal cell synaptic excitability is due to a cholinergic projection from the medial septal-vertical limb of the diagonal band of Broca complex ( MS-VLDBB ). Thus, atropine sulphate ( 40 mg/kg, i.p. ) prevented the persistent depression of the CA1 population spike to a noxious stimulus. It also antagonized the septal tetanus-evoked, cholinergic mediated facilitation of the CA1 commissural population spike but had no effect on the corresponding paired-pulse facilitation. Atropine, applied iontophoretically to the cell body region antagonized the iontophoretic acetylcholine-induced facilitation of the CA1 population spike but not its depression to a noxious stimulus. On the other hand, apical dendritic application of atropine antagonized iontophoretic acetylcholine and noxious stimulus-induced depression of the CA1 dendritic field EPSP. However, such iontophoretic application of atropine had no effect on dendritically applied gamma aminobutyric acid ( GABA )-induced depression of the CA1 dendritic field EPSP. These results support the notion that acetylcholine release in the dendritic region of CA1 neurones is involved in the depression of synaptic excitability of these neurones evoked by a noxious stimulus.
Pharmaceutical Sciences, Faculty of
Graduate
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8

Legrand, Marie. "Effets de l'uranium appauvri sur le processus de neurogenèse au cours du développement et à l'age adulte chez le rat." Thesis, Université Paris-Saclay (ComUE), 2016. http://www.theses.fr/2016SACLS054/document.

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Le projet de thèse s’inscrit dans la continuité de l’étude pilote développée dans le cadre du programme Doremi (Consortium européen de programmes de recherche portant sur les effets des faibles doses). En partant des résultats préliminaires déjà obtenus sur ce projet, l’objectif est d’approfondir les études sur les effets d’une contamination chronique à l’uranium via l’eau de boisson sur le processus de neurogénèse au cours du développement cérébral mais également au stade adulte. La première partie du projet de thèse consiste à comparer la prolifération, la survie et le potentiel de différentiation des cellules des zones neurogéniques (dans l’hippocampe principalement) à l’aide de marqueurs spécifiques de chaque stade de différentiation chez des rats contaminés ou non à l’uranium dès le stade in utero. Cette étude in vivo sera entreprise à différents stades : pendant le développement cérébral embryonnaire et post natal et à l’âge adulte. Cette première partie donnera des pistes pour étudier plus en détails les mécanismes d’action. La deuxième partie du projet de thèse vise donc à étudier comment l’uranium agit sur la neurogénèse à l’aide de modèles in vitro et ex vivo. Des cultures primaires de neurosphères seront utilisées afin d’étudier l’effet de l’uranium sur les capacités de multipotentialité des cellules souches neurales. En parallèle, un modèle de culture organotypique d’hippocampe sera développé. Ce modèle est particulièrement intéressant car il permet de réaliser des expositions aux radionucléides « à façon », d’en étudier les mécanismes d’action dans des aires cérébrales ayant une cytoarchitecture préservée et mettant en jeu différents types cellulaires, tout en combinant des méthodes d’analyse en histologie et en biologie moléculaire
The PhD project is a continuity of the Doremi program (European Consortium of research programs on low doses effects). The objective is to assess the effects a chronic uranium contamination via drinking water on neurogenesis during brain development and in adult rats. The first part of the project will evaluate proliferation, survival and cell differentiation in neurogenic zones (in particular in the hippocampus) using specific markers for each differentiation stage in control and contaminated rats from the in utero life. This in vivo study will be performed at different stages: during embryonic and postnatal brain development and at the adult age. This part of the project will provide some clues on the potential mechanisms of action that we aim to study more in details. For this purpose, the second part of the project will be performed on in vitro and ex vivo model. Neurosphere primary cultures will be performed to assess uranium effects on the multipotential properties of neural stem cells. We also plan to use a model of hippocampal organotypic culture which will allow the study of the mechanisms of action in a preserved ex vivo structure in terms of cytoarchitecture, cell interactions, and being able to test different uranium concentrations and combine multiple analyses methods (histology, molecular biology…)
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9

Mercer, Audrey. "Hippocampal circuitry and characterisation of interneurones in the CA2 subfield of the rat hippocampus." Thesis, University College London (University of London), 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.420370.

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10

Rennó, Costa César. "The Hippocampus code : a computational study of the structure and function of the hippocampus." Doctoral thesis, Universitat Pompeu Fabra, 2012. http://hdl.handle.net/10803/94196.

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Actualment, no hi ha consens científic respecte a la informació representada en la activitat de les célules del hipocamp. D'una banda, experiments amb humans sostenen una visión de la funció de l'hipocamp com a un sistema per l'emmagatzematge de memóries episódiques, mentre que la recerca amb rodents enfatitza una visió com a sistema cognitiu espacial. Tot i que existeix abundant evidència experimental que indica una possible sobreposició d'ambdues teories, aquesta dissociació també es manté en part en base a dades fisiològiques aparentment incompatibles. Aquesta tèsi poposa que l'hippocamp té un rol funcional que s'hauría d'analitzar en termes de la seva estructura i funció, enlloc de mitjança estudis correlació entre activitat neuronal i comportament. La identificació d'un codi a l'hipocamp, es a dir, el conjunt de principis computacionals que conformen les transformacions d'entrada i sortida de l'activitat neuronal, hauría de proporcionar un explicació unificada de la seva funció. En aquesta tèsi presentem un model teòric que descriu quantitativament i que interpreta la selectivitat de certes regions de l'hipocamp en funció de variables espaials i no-espaials, tal i com observada en experiments amb rates. Aquest resultat suggereix que multiples aspectes de la memòria expressada en humans i rodents deriven d'uns mateixos principis. Per aquest motius, proposem nous principis per la memòria, l'auto-completat de patrons i plasticitat. A més, mitjançant aplicacions robòtiques, creem d'un nexe causal entre el circuit neural i el comportament amb el que demostrem la naturalesa conjuntiva de la selectivitat neuronal observada en el hipocamp es necessària per la solució de problemes pràctics comuns, com per example la cerca d'aliments. Tot plegat, aquests resultats avancen en l'idea general de que el codi de l'hipocamp es genèric i aplicable als diversos tipus de memòries estudiades en la literatura.
There is no consensual understanding on what the activity of the hippocampus neurons represents. While experiments with humans foster a dominant view of an episodic memory system, experiments with rodents promote its role as a spatial cognitive system. Although there is abundant evidence pointing to an overlap between these two theories, the dissociation is sustained by conflicting physiological data. This thesis proposes that the functional role of the hippocampus should be analyzed in terms of its structure and function rather than by the correlation of neuronal activity and behavioral performance. The identification of the hippocampus code, i.e. the set of computational principles underlying the input-output transformations of neural activity, might ultimately provide a unifying understanding of its role. In this thesis we present a theoretical model that quantitatively describes and interprets the selectivity of regions of the hippocampus to spatial and non-spatial variables observed in experiments with rats. The results suggest that the multiple aspects of memory expressed in human and rodent data are derived form similar principles. This approach suggests new principles for memory, pattern completion and plasticity. In addition, by creating a causal tie between the neural circuitry and behavior through a robotic control framework we show that the conjunctive nature of neural selectivity observed in the hippocampus is needed for effective problem solving in real-world tasks such as foraging. Altogether, these results advance the concept that the hippocampal code is generic to the different aspects of memory highlighted in the literature.
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11

Sanderson, David John. "The hippocampus and structural learning." Thesis, Cardiff University, 2005. http://orca.cf.ac.uk/55382/.

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The hippocampus has been implicated in the learning and memory of arrays of spatial cues. Certain theories of the function of the hippocampus have stressed the importance of the hippocampus in learning about configurations of stimuli that have non-linear associations. Recent evince has suggested that the hippocampus may not be responsible for learning about unique configurations but rather the unique spatial relationships formed by a configuration of visual cues. This thesis examines the effects of hippocampal lesions on visual configural discriminations, in which the solution relies on learning the features that are necessary for configural learning, and also discriminations in which the solution of the task relies on learning the spatial structure of the features that form the configurations. It was found that hippocampal lesions made after acquisition impaired performance of a structural discrimination. Hippocampal lesions did not impair performance of previously acquired configural discriminations. A probe test revealed that although hippocampal lesioned and control rats do not differ on performance of a configural discrimination that does not require learning structural information, control rats learn the structural features of the configurations to a greater extent than hippocampal lesioned rats. Hippocampal lesioned rats were impaired at learning structural information when a task explicitly demanded, and when the structural features were incidental to the requirements of a task. The results are discussed with regards to a configural account of hippocampal dependent allocentric spatial learning, and also theories of hippocampal dependent stimulus representation
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12

Kammerer, Axel. "Memory capacity in the hippocampus." Diss., Ludwig-Maximilians-Universität München, 2015. http://nbn-resolving.de/urn:nbn:de:bvb:19-184549.

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Neural assemblies in hippocampus encode positions. During rest, the hippocam- pus replays sequences of neural activity seen during awake behavior. This replay is linked to memory consolidation and mental exploration of the environment. Re- current networks can be used to model the replay of sequential activity. Multiple sequences can be stored in the synaptic connections. To achieve a high mem- ory capacity, recurrent networks require a pattern separation mechanism. Such a mechanism is global remapping, observed in place cell populations. A place cell fires at a particular position of an environment and is silent elsewhere. Multiple place cells usually cover an environment with their firing fields. Small changes in the environment or context of a behavioral task can cause global remapping, i.e. profound changes in place cell firing fields. Global remapping causes some cells to cease firing, other silent cells to gain a place field, and other place cells to move their firing field and change their peak firing rate. The effect is strong enough to make global remapping a viable pattern separation mechanism. We model two mechanisms that improve the memory capacity of recurrent net- works. The effect of inhibition on replay in a recurrent network is modeled using binary neurons and binary synapses. A mean field approximation is used to de- termine the optimal parameters for the inhibitory neuron population. Numerical simulations of the full model were carried out to verify the predictions of the mean field model. A second model analyzes a hypothesized global remapping mecha- nism, in which grid cell firing is used as feed forward input to place cells. Grid cells have multiple firing fields in the same environment, arranged in a hexagonal grid. Grid cells can be used in a model as feed forward inputs to place cells to produce place fields. In these grid-to-place cell models, shifts in the grid cell firing patterns cause remapping in the place cell population. We analyze the capacity of such a system to create sets of separated patterns, i.e. how many different spatial codes can be generated. The limiting factor are the synapses connecting grid cells to place cells. To assess their capacity, we produce different place codes in place and grid cell populations, by shuffling place field positions and shifting grid fields of grid cells. Then we use Hebbian learning to increase the synaptic weights be- tween grid and place cells for each set of grid and place code. The capacity limit is reached when synaptic interference makes it impossible to produce a place code with sufficient spatial acuity from grid cell firing. Additionally, it is desired to also maintain the place fields compact, or sparse if seen from a coding standpoint. Of course, as more environments are stored, the sparseness is lost. Interestingly, place cells lose the sparseness of their firing fields much earlier than their spatial acuity. For the sequence replay model we are able to increase capacity in a simulated recurrent network by including an inhibitory population. We show that even in this more complicated case, capacity is improved. We observe oscillations in the average activity of both excitatory and inhibitory neuron populations. The oscillations get stronger at the capacity limit. In addition, at the capacity limit, rather than observing a sudden failure of replay, we find sequences are replayed transiently for a couple of time steps before failing. Analyzing the remapping model, we find that, as we store more spatial codes in the synapses, first the sparseness of place fields is lost. Only later do we observe a decay in spatial acuity of the code. We found two ways to maintain sparse place fields while achieving a high capacity: inhibition between place cells, and partitioning the place cell population so that learning affects only a small fraction of them in each environment. We present scaling predictions that suggest that hundreds of thousands of spatial codes can be produced by this pattern separation mechanism. The effect inhibition has on the replay model is two-fold. Capacity is increased, and the graceful transition from full replay to failure allows for higher capacities when using short sequences. Additional mechanisms not explored in this model could be at work to concatenate these short sequences, or could perform more complex operations on them. The interplay of excitatory and inhibitory populations gives rise to oscillations, which are strongest at the capacity limit. The oscillation draws a picture of how a memory mechanism can cause hippocampal oscillations as observed in experiments. In the remapping model we showed that sparseness of place cell firing is constraining the capacity of this pattern separation mechanism. Grid codes outperform place codes regarding spatial acuity, as shown in Mathis et al. (2012). Our model shows that the grid-to-place transformation is not harnessing the full spatial information from the grid code in order to maintain sparse place fields. This suggests that the two codes are independent, and communication between the areas might be mostly for synchronization. High spatial acuity seems to be a specialization of the grid code, while the place code is more suitable for memory tasks. In a detailed model of hippocampal replay we show that feedback inhibition can increase the number of sequences that can be replayed. The effect of inhibition on capacity is determined using a meanfield model, and the results are verified with numerical simulations of the full network. Transient replay is found at the capacity limit, accompanied by oscillations that resemble sharp wave ripples in hippocampus. In a second model Hippocampal replay of neuronal activity is linked to memory consolidation and mental exploration. Furthermore, replay is a potential neural correlate of episodic memory. To model hippocampal sequence replay, recurrent neural networks are used. Memory capacity of such networks is of great interest to determine their biological feasibility. And additionally, any mechanism that improves capacity has explanatory power. We investigate two such mechanisms. The first mechanism to improve capacity is global, unspecific feedback inhibition for the recurrent network. In a simplified meanfield model we show that capacity is indeed improved. The second mechanism that increases memory capacity is pattern separation. In the spatial context of hippocampal place cell firing, global remapping is one way to achieve pattern separation. Changes in the environment or context of a task cause global remapping. During global remapping, place cell firing changes in unpredictable ways: cells shift their place fields, or fully cease firing, and formerly silent cells acquire place fields. Global remapping can be triggered by subtle changes in grid cells that give feed-forward inputs to hippocampal place cells. We investigate the capacity of the underlying synaptic connections, defined as the number of different environments that can be represented at a given spatial acuity. We find two essential conditions to achieve a high capacity and sparse place fields: inhibition between place cells, and partitioning the place cell population so that learning affects only a small fraction of them in each environments. We also find that sparsity of place fields is the constraining factor of the model rather than spatial acuity. Since the hippocampal place code is sparse, we conclude that the hippocampus does not fully harness the spatial information available in the grid code. The two codes of space might thus serve different purposes.
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13

Farrow, Tom F. D. "Hippocampus, cognitive function and epilepsy." Thesis, University of Sheffield, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.322874.

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14

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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Retailleau, Aude. "Activités normales et pathologiques du réseau hippocampique chez le rat : implication des systèmes monoaminergiques." Thesis, Bordeaux 1, 2011. http://www.theses.fr/2011BOR14405/document.

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Les représentations mentales, en particulier les représentations spatiales, sont étroitement associées à l'activation coordonnée de groupes de cellules dans l'hippocampe. Nous avons entrepris l'étude des propriétés et activités spontanées du réseau hippocampique (et plus particulièrement de la région CA3) afin de mieux en comprendre le fonctionnement, dans les situations normales et pathologiques. En effet, certaines pathologies neurodégénératives telle que la maladie de Parkinson serait potentiellement associées à des troubles cognitifs hippocampo-dépendants. Ainsi dans la première partie de ma thèse, nous avons caractérisé la dynamique temporelle des signaux excitateurs et inhibiteurs spontanés de l'hippocampe par une approche électrophysiologique in vitro sur tranches d'hippocampe mais aussi chez l'animal anesthésié grâce des enregistrements multi-unitaires multi-sites. Ces travaux nous a permis de mettre en évidence que les caractéristiques de la dynamique du réseau CA3 remplissent quelques critères essentiels au concept d'assemblées cellulaires. De plus, cette étude a mis en évidence les caractéristiques fonctionnelles de l'hippocampe chez l'animal normal. Ces résultats peuvent donc être utiles pour de futures études sur les pathologies hippocampo-dépendantes touchant le codage ou la mémoire spatiale telle que la maladie de Parkinson. Ainsi, dans la deuxième partie de ma thèse, nous avons étudié les altérations fonctionnelles du circuit hippocampique chez un modèle rat de la maladie de Parkinson. La maladie de Parkinson est une maladie neurologique qui affecte le système nerveux central et entraine des symptômes essentiellement moteurs. La cause est une dégénérescence des neurones dopaminergiques mais aussi noradrénergiques et sérotoninergiques. Cependant, en dehors des troubles moteurs, cette pathologie est aussi caractérisée par des troubles cognitifs notamment des déficits spatiaux. Notre projet a donc consisté à analyser les mécanismes par lesquels les déplétions monoaminergiques entraîneraient des troubles de l'apprentissage spatial. Ce travail a été réalisé chez le rongeur à l'aide d'une étude associant une approche comportementale et des enregistrements électrophysiologiques chez l'animal anesthésié mais aussi chez l'animal éveillé en comportement. Nous avons ainsi pu mettre en évidence des dysfonctionnements hippocampiques causés par des lésions contrôlées des différents systèmes mono-aminergiques (plus particulièrement dopaminergique et noradrenergique) impliqués dans la maladie de Parkinson
Mental representations, especially spatial ones are closely related to correlated activity in cellular assembly in the hippocampus. In this work, we analyzed the properties and the spontaneous activity of the hippocampal network in order to unravel its functioning in normal and pathological conditions. Several neurodegenerative disorders such as Parkinson's disease seems to be also associated to cognitive disorder related to hippocampus dysfunction. We first characterized the temporal dynamic properties of spontaneous excitatory and inhibitory signal. We then studied the functional alteration of the hippocampal network in a rat model of Parkinson's disease using behavioral and electrophysiological investigations. Our work showed that controlled lesion of the various monoaminergic systems induced hippocampus dysfunction related to spatial disorientation.In the first part of my thesis, we characterized the temporal dynamic of excitatory and inhibitory signals with electrophysiological recordings in vivo on hippocampal slices but also in anesthetized animals with multi-units multi-sites recordings. These studies allowed us to highlight that dynamic of CA3 network meets the criteria of cells assembly concept. Moreover, we characterize the functional properties of hippocampus in physiological conditions. These results could be useful for further studies on hippocampo-dependant pathologies in the context of spatial coding and memory.Thus, in the second part of my work, we studied the functional alterations of hippocampal network in the context of Parkinson disease. This pathology is a neurodegenerative disease which affects the central nervous system and leads essentially to motor symptoms. The cause is the degeneration of dopamine neurons but also of noradrenalin and serotonin neurons. Nevertheless, this pathology is also associated to cognitive disorders notably a form of spatial disorientation. Our project consisted to analyze the mechanisms by which monoamines depletions led to spatial learning impairments. This work was realized on rats with a study combinating behavioral approach with electrophysiological recordings in anesthetized animals but also in awake animals. We showed that some monoamines depletions (and notably dopamine and noradrenalin depletions) led to spatial impairments in behavioral tasks correlated to a change in firing and coding of neurons of hippocampus
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16

Langlois, Anaïs. "Rôle du BDNF dans le développement des synapses GABAergiques de l'hippocampe de rat." Thesis, Aix-Marseille, 2012. http://www.theses.fr/2012AIXM4089/document.

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Le cerveau immature est le siège de processus développementaux qui permettent de passer d'une structure primitive à un réseau mature et fonctionnel. L'activité synaptique spontanée générée dans le système nerveux en développement joue un rôle fondamental dans ces processus. Un des principaux moyens par lesquels cette activité peut être traduite en changement phénotypique au niveau neuronal est la sécrétion de neurotrophines. Les neurotrophines sont sécrétées par les neurones et contrôlent toutes les étapes du développement neuronal. Dans l'hippocampe en développement, la neurotrophine principale est le BDNF (brain derived neurotrophic factor). Cette protéine est synthétisée sous forme immature, le proBDNF, dont le rôle est encore méconnu. Durant ma thèse, j'ai montré que le BDNF exerce un contrôle bidirectionnel sur l'efficacité des synapses GABAergiques en développement. La polarité de la plasticité est déterminée par le type d'activité endurée par les neurones et la forme sous laquelle le BDNF est présenté à ces derniers. J'ai ainsi décrit une séquence développementale qui pourrait s'inscrire dans les processus développementaux permettant la maturation du réseau GABAergique dans l'hippocampe de rat
The immature brain is the place of developmental processes that allow the switch from a primitive structure to a mature and functional network. Spontaneous synaptic activity generated in the developing nervous system plays a fundamental role in these processes. One of the principal ways this activity is translated into phenotypical changes at the neuronal level is the secretion of neurotrophins. Neurotrophins are secreted by neurons and control each step of neuronal development. In the developing hippocampus, the major neurotrophin is BDNF (brain derived neurotrophic factor). This protein is synthetized under an immature form, proBDNF, which role is still poorly known. During my thesis, I showed that BDNF exerts a bidirectional control on the efficacy of developing GABAergic synapses, which polarity is set by the type of activity endured by neurons and the form of BDNF that is presented to them. I described a developmental sequence which could be a part of the developmental processes allowing the maturation of the GABAergic network in the developing rat hippocampus
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17

Yotter, Rachel A. "A network model of the hippocampus /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/5887.

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18

Yim, Tonia Tan-Ling, and University of Lethbridge Faculty of Arts and Science. "Multiple-object memory requires the hippocampus." Thesis, Lethbridge, Alta. : University of Lethbridge, Faculty of Arts and Science, 2007, 2007. http://hdl.handle.net/10133/678.

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This thesis investigates the role of the hippocampus in object memory. Currently, the role of the hippocampus in object recognition is unclear, with some studies demonstrating a delay-dependent impairment after hippocampal damage, others showing no impairment. The present thesis used the novel object recognition task and its variants to investigate various types of object memory in hippocampal lesion rats. In the first study, impairments were observed in discriminating object order and associating objects with contexts, while no impairment was observed in novel object recognition. In the second study, it was found that encountering another object shortly prior to or after encountering a target object impairs the recognition of the target object. In a control procedure, encountering a novel context either shortly before or after encountering the target object did not impair object recognition. In sum, in the absence of the hippocampus, object memory becomes vulnerable to interference, rendering rats unable to discern memories of multiple objects. The present thesis concludes that the hippocampus discriminates multiple objects via pattern separation. A stimulus-response model relating the role of the hippocampus to object memory is proposed.
vii, 150 leaves : ill. ; 29 cm. --
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19

Casey, Stephen Patrick. "Conservation genetics of seahorses (Hippocampus species)." Thesis, Queen Mary, University of London, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.311943.

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20

Strange, Bryan Andrew. "Imaging the functions of human hippocampus." Thesis, University College London (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.406949.

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21

Mutalik, Prabhanjan. "Hippocampus as an Echo State Network." Thesis, KTH, Skolan för elektroteknik och datavetenskap (EECS), 2018. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-241368.

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The Hippocampus is a brain region responsible for learning, memoryand spatial navigation. In that, the interactions between the CA3 andCA1 subregions have been the most studied due to the interesting dynamicsbetween the two regions. The excitatory auto-associative connectionsin the CA3 and the lack thereof in CA1 can be modelled asan Echo State Network (ESN) with the reservoir and readout approximatingCA3 and CA1 respectively. However, CA1 possesses somedegree of recurrent connections between the excitatory and the inhibitoryneurons, thereby posing an important problem from the computationaland Machine Learning perspective. The aim of this thesisis to introduce the recurrent connections in the readout and exploringits implications. By doing so, we observed that the recurrent connectionsperform a dynamic mapping of the readout output that makesthe system susceptible to noise, thereby affecting the performance.However, we also observed that by controlling certain parameters, themodel with the recurrent readout connections could perform comparablywith the basic ESN.
Hippocampus är en hjärnregion som är involverad i inlärning, minne och navigering. För att öka vår kunskap om detta har interaktionerna mellan delregionerna CA3 och CA1 varit de mest studerade, detta på grund av den intressanta dynamik som uppstår mellan de två regionerna. De excitatoriska auto-associativa kopplingarna i CA3 samt avsaknaden av sådana i CA1 kan modelleras som ett Echo State Network (ESN) där reservoaren och readout kan mappas på CA3 respektive CA1. CA1 har emellertid en viss grad av rekurrenta kopplingar mellan de excitatoriska och de hämmande neuronerna, vilket kan ses som en utmaning att förstå utifrån ett maskinlärningsperspektiv. Syftet med detta projekt är att introducera de rekurrenta kopplingarna i readoutmodulen och utforska konsekvenserna. Vi observerade att de rekurrenta kopplingarna utför en dynamisk mappning av readout vilket gör systemet känsligt för brus och därigenom påverkar prestandan. Vi observerade emellertid också att genom att anpassa vissa parametrar kunde modellen med de rekurrenta readout-kopplingarna prestera jämförbart med ett standard-ESN.
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22

Zeidman, P. S. "Scene processing and the human hippocampus." Thesis, University College London (University of London), 2014. http://discovery.ucl.ac.uk/1426971/.

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The hippocampus is one of the most extensively studied structures of the brain, and yet its diverse set of cognitive functions is still being identified. It is particularly associated with episodic memory in humans and spatial processing in animals, but more recently it has also been implicated in processes beyond memory, including imagination of fictitious and future experiences and even visual perception. The relationship between these cognitive functions, and the underlying involvement of the hippocampus, is not well understood. In this dissertation, I draw upon and extend the hypothesis that the feature common to episodic memory, imagination and visual perception, which necessitates them all to engage the hippocampus, is scene construction – the creation of internal representations of spatially coherent scenes. In a series of experiments, I improved our understanding of scene construction by directly comparing the imagination of scenes (the hippocampus being driven endogenously) against scene perception (being driven by visual stimuli), and further by comparing imagination against memory recall, using functional Magnetic Resonance Imaging (fMRI). Two experiments had the added advantage of using high-resolution structural MRI (0.5mm3) and fMRI (1.5mm3), for the first time making inferences about scene processing at the level of the sub-units of the hippocampus, termed the hippocampal subfields. Furthermore, by capitalising on recent developments in connectivity analysis (Generalized Psychophysiological Interactions and Stochastic Dynamic Causal Modelling), I examined the interactions of the hippocampus with other brain regions, and inferred the flow of information between the hippocampal subfields using fMRI. Together, my findings provide new insights into the relationship between scene perception, imagination and memory, and develop our understanding of the heterogeneous functional anatomy of the hippocampus. This has important implications for understanding why patients with hippocampal lesions may lose their ability to construct scenes in their imagination and recall episodes from their past.
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23

May, Patrick B. Y. "Studies on the induction of short- and long-term synaptic potentiation in the hippocampus." Thesis, University of British Columbia, 1987. http://hdl.handle.net/2429/26497.

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High frequency repetitive stimulation of an excitatory input in the hippocampus results in a post-tetanic potentiation (PTP) of short duration (about 3 min) that can be followed by a long-term synaptic potentiation (LTP) of the same excitatory input (Schwartzkroin and Wester, 1975; Andersen et al., 1977). It has been reported that this tetanus-induced LTP cannot be elicited in a Ca²⁺-free medium and is therefore a Ca²⁺-dependent process (Dunwiddie et al., 1978; Dunwiddie and Lynch, 1979; Wigstrӧm et al., 1979). Whether the induction of LTP is directly dependent upon Ca²⁺, or whether, Ca²⁺ is required because synaptic transmission is needed to initiate certain postsynaptic process(es) (a postsynaptic depolarization, for instance) leading to LTP, is unknown. Recent studies from this laboratory showed that both short-term potentiation (STP; with a duration resembling PTP) and LTP can be associatively induced if activation of a test input co-occured with either a tetanic stimulation of separate excitatory inputs or a sufficient depolarization of the postsynaptic neurone (Sastry et al., 1985). In this study, experiments were performed to investigate (1) whether associative STP could be induced when activation of the test input preceded or followed the onset of the conditioning train and (2) whether LTP could be induced in the absence of Ca²⁺ in the extracellular medium if sufficient depolarizations of the presynaptic terminals and postsynaptic neurones were provided. All experiments were performed using the transversely sectioned hippocampal slice preparation. Test stimuli were delivered via an electrode located in the stratum radiatum while the conditioning tetani (100 Hz, 10 pulses per train) were delivered via another electrode located in the recorded from the apical dendritic area of CA₁ neurones. After the initial control stimulation period, 5 conditioning tetani were given at a frequency of 0.2 Hz. The test stimuli either preceded (-) or followed ( + ) the onset of each conditioning train by 0 to 100 ms. When the test stimulus followed the onset of each conditioning train, there was significant STP of the test EPSP up to a conditioning-test interval of +80 ms. When the test stimulus preceded the onset of each conditioning train, there was significant STP of the test EPSP up to a conditioning-test interval of -50 ms. Conditioning tetani that were given without co-activation of the test input resulted in a subsequent depression of the test EPSP. It is suggested that either the test or the conditioning input can initiate some postsynaptic process(es) which can in turn affect the activated presynaptic terminals to increase transmitter release or alter the subsynaptic dendritic properties. For studying the possibility of the induction of LTP in the absence of Ca²⁺ in the extracellular medium, population EPSPs were recorded from apical dendritic area of CA₁ neurones in response to stratum radiatum stimulation. After the control stimulation period, slices were exposed either to Ca²⁺-containing or Ca²⁺-free (with Mn²⁺ and Mg²⁺ replacing Ca²⁺) medium, with the concentration of KC1 at 10 to 80 mM. Long-term potentiation of the population EPSPs was observed following the exposure to high K⁺ in Ca²⁺-free media. Following a brief period of potentiation initially, population EPSPs often exhibited a tendency toward depression after exposure to high K⁺ in Ca²⁺-containing media. LTP induced by high K⁺ in Ca²⁺-free medium could also be observed when a fixed number of axons were being activated, indicating that a recruitment of presynaptic fibres cannot entirely account for the potentiation. LTP of the depolarizing commands were paired with activation of the stratum radiatum while the slices were exposed to Ca²⁺ -free medium (normal concentration of KC1). These results suggest that extracellular Ca²⁺, synaptic transmission and thus subsynaptic receptor activation are not necessary for the induction of LTP as long as sufficient depolarizations of the presynaptic terminals and postsynaptic neurones are provided.
Medicine, Faculty of
Anesthesiology, Pharmacology and Therapeutics, Department of
Graduate
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24

Gulbrandsen-MacDonald, Tine L., and University of Lethbridge Faculty of Arts and Science. "The role of the hippocampus and post-learning hippocampal activity in long-term consolidation of context memory." Thesis, Lethbridge, Alta. : University of Lethbridge, Dept. of Neuroscience, c2011, 2011. http://hdl.handle.net/10133/2635.

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Sutherland, Sparks and Lehmann (2010) proposed a new theory of memory consolidation, termed Distributed Reinstatement Theory (DRT), where the hippocampus (HPC) is needed for initial encoding but some types of memories are established in non-HPC systems through post-learning HPC activity. An evaluation of the current methodology of temporary inactivation was conducted experimentally. By permanently implanting two bilateral guide cannulae in the HPC and infusing ropivacaine cellular activity could be reduced by 97%. Rats were trained in a context-fear paradigm. Six learning episodes distributed across three days made the memory resistant to HPC inactivation while three episodes did not. Blocking post-learning HPC activity following three of six training sessions failed to reduce the rat’s memory of the fearful context. These results fail to support DRT and indicate that one or more memory systems outside the HPC can acquire context memory without HPC post-event activity.
x, 85 leaves : ill. ; 29 cm
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25

Sparks, Fraser T. "Interactions of the hippocampus and non-hippocampal long-term memory systems during learning, remembering, and over time." Thesis, Lethbridge, Alta. : University of Lethbridge, Dept. of Neuroscience, c2012, 2012. http://hdl.handle.net/10133/3116.

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The hippocampus and non-hippocampal long-term memory systems each have the capacity to learn and express contextual fear memory. How these systems interact during learning and remembering revolves around hippocampal mediated interference, where the hippocampus dominates for both the acquisition and expression of long-term memory. Hippocampal interference during learning can be overcome by modifying learning parameters such that learning is distributed across multiple independent sessions. The standard view of the role of the hippocampus in long-term memory retrieval is that it is temporally limited, where recently acquired memory is dependent on hippocampal function though as a memory ages, dependency is transferred to other memory systems by a process called systems consolidation. Distributed training demonstrates that learning parameters create a memory that is resistant to hippocampal damage. We find little evidence to support temporally based systems consolidation, and present data that supports the view that if the hippocampus is initially involved in learning a memory, it will always be necessary for accurate retrieval of that memory. A critical assessment of the rat literature revealed that initial memory strength, and/or lesion techniques might be responsible for the few studies that report temporally graded retrograde amnesia using contextual fear conditioning. Our experiments designed to directly test these possibilities resulted in flat gradients, providing further evidence that the hippocampus plays a permanent role in long-term memory retrieval. We propose and assess alternatives to the standard model and conclude that a dual store model is most parsimonious within the presented experiments and related literature. Interactions of the hippocampus and non-hippocampal systems take place at the time of learning and remembering, and are persistent over time.
xvi, 161 leaves : ill. (some col.) ; 29 cm
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26

Dannenberg, Holger [Verfasser]. "Direct and indirect cholinergic septo-hippocampal pathways cooperate to structure spiking activity in the hippocampus / Holger Dannenberg." Bonn : Universitäts- und Landesbibliothek Bonn, 2015. http://d-nb.info/1079273441/34.

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27

Bellace, Matthew John Williams J. Michael. "Activation of the hippocampus during emotional learning /." Philadelphia, Pa. : Drexel University, 2005. http://dspace.library.drexel.edu/handle/1860/480.

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28

Lafenêtre, Pauline. "Regulation der Proliferation im Hippocampus adulter Mäuse." [S.l.] : [s.n.], 2005. http://deposit.ddb.de/cgi-bin/dokserv?idn=979107407.

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29

Kempermann, Gerd. "Aktivitätsabhängige Regulation von Neurogenese im erwachsenen Hippocampus." [S.l.] : [s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=964507862.

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30

Elliott, Audrea Elizabeth. "Emotional modulation of hippocampus-dependent spatial learning." Texas A&M University, 2005. http://hdl.handle.net/1969.1/4302.

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Previous research has indicated that the amygdala exerts a modulatory influence on multiple memory systems. Evidence also indicates that emotional state can influence the use of multiple memory systems and that this effect is mediated by the amygdala. Anxiogenic drugs administered during acquisition in a task that can be acquired either through hippocampus-dependent “place” learning or caudate dependent “response” learning, resulted in the predominant use of response learning. It is not known whether inducing anxiety at other behavioral time points will also influence the relative use of multiple memory systems. In experiment 1, male Long-Evans rats were trained to swim from the same start point to an escape platform constantly located in a goal arm. Prior to memory retrieval rats were administered either alpha- two adrenoceptor antagonist RS 79948-197, peripherally (0.03, 0.01, 0.3 mg/kg) or into the basolateral amygdala (0.1 µg), or saline vehicle. Rats treated with RS 79948-197 prior to memory retrieval exhibited caudate-dependent response learning. Previous studies examining the effects of RS 77948-197 on memory were conducted with rats trained in an anxiogenic state and subsequently probed in a drug free state. Experiment 2 examined whether state dependency may account for those results. Animals received peripheral (0.1 mg/kg) or intra-amygdala (0.1 µg) administration of RS 79948-197, prior to both acquisition and memory retrieval. Rats treated with RS 79948- 197 predominantly exhibited response learning. Finally, experiments 3 and 4 examined whether the use of response learning produced by RS79948-197 was due to the impairing effect on hippocampus-dependent memory. Rats that were administered peripheral (0.03 mg/kg) or intra-amygdala (0.1 µg) injections of RS 79948-197 displayed impaired acquisition of the single solution place task relative to control animals. This indicates that place learning was impaired. Over, all the present findings indicate 1) peripheral and intra-amygdala anxiogenic drug administration results in the use of habit memory at both acquisition and retrieval, 2) state dependency does not play a role in the influence of RS 799948-197 on memory system use, 3) the use of response learning produced by peripheral and intra-amygdala injections of RS 79948-197 may result from an impairing effect of hippocampusdependent memory.
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31

MacPherson, Cameron Ross. "Transcriptional Regulatory Networks in the Mouse Hippocampus." Thesis, University of the Western Cape, 2007. http://etd.uwc.ac.za/index.php?module=etd&action=viewtitle&id=gen8Srv25Nme4_1683_1259931126.

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This study utilized large-scale gene expression data to define the regulatory networks of genes expressing in the hippocampus to which multiple disease pathologies may be associated. Specific aims were: ident i fy key regulatory transcription factors (TFs) responsible for observed gene expression patterns, reconstruct transcription regulatory networks, and prioritize likely TFs responsible for anatomically restricted gene expression. Most of the analysis was restricted to the CA3 sub-region of Ammon&rsquo
s horn within the hippocampus. We identified 155 core genes expressing throughout the CA3 sub-region and predicted corresponding TF binding site (TFBS) distributions. Our analysis shows plausible transcription regulatory networks for twelve clusters of co-expressed genes. We demonstrate the validity of the predictions by re-clustering genes based on TFBS distributions and found that genes tend to be correctly assigned to groups of previously identified co-expressing genes with sensitivity of 67.74% and positive predictive value of 100%. Taken together, this study represents one of the first to merge anatomical architecture, expression profiles and transcription regulatory potential on such a large scale in hippocampal sub-anatomy.

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32

Goh, Joanne Wan Yoong. "Studies on synaptic potentiation in the hippocampus." Thesis, University of British Columbia, 1986. http://hdl.handle.net/2429/27080.

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The present investigation was conducted on transversely sectioned rat hippocampal slices to examine the mechanisms involved in synaptic potentiation. Results indicate that long-term potentiation (LTP) induced by input tetanization requires extracellular Ca⁺⁺, because during the induction of LTP postsynaptic depolarization must accompany presynaptic activity (LTP could be induced by raised K⁺ [10 to 80 mM] in Ca⁺⁺-free medium). Since LTP (induced by raised K⁺) occurs in the absence of Ca⁺⁺ and, therefore, presumably in the near absence of transmitter release, N-methyl-D-aspartate (NMDA) receptor activation is not obligatory. Moreover, NMDA receptors appear not to be involved in the CA₃ area. A necessity for both pre- and postsynaptic depolarization also accounts for the need for co-stimulation of afferents for LTP induction. Associative potentiation was found not to require tetanic stimulation of the test input; single pulse activation of the test input (at 0.2 Hz) paired with tetanic trains to a conditioning input (presumably to the same postsynaptic neurones) could produce LTP. A short-term potentiation (STP), which resembled post-tetanic potentiation (PTP) in time course, could be induced in an associative fashion by conditioning tetanic trains (paired with single test stimuli), that were insufficient to produce LTP. In the absence of conditioning stimuli, interruption of a regular 0.2 Hz test input stimulation for 10 minutes disclosed a subsequent potentiation. This potentiation could be distinguished from associative potentiation in that it was not associated with a decrease in presynaptic terminal excitability. A decrease in presynaptic terminal excitability was characteristic of associative STP and LTP, and followed similar time courses. Since raised K⁺ reversed rather than accentuated the decreased excitability, it was concluded that it is not due to Na⁺ -inactivation and may be caused by a hyperpolarization which might also lead to an increase in evoked transmitter release. The hypothesis of Baudry and Lynch (1980a) that LTP is due to an increase in glutamate receptors seems unlikely; there was no increase in Na-independent glutamate binding sites (determined by the same method as used by Lynch et- al: [1982]) in association with LTP induced by a single brief 400 Hz (200 pulses) input tetanus. A decrease in the uptake of glutamate occurs with tetanic stimulation under conditions where there is no LTP (absence of Ca⁺⁺ and raised Mg⁺⁺ and Mn⁺⁺) and, therefore, does not appear to be a mechanism producing LTP.
Medicine, Faculty of
Anesthesiology, Pharmacology and Therapeutics, Department of
Graduate
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33

Robillard, Julie. "Modulators of synaptic plasticity in the hippocampus." Thesis, University of British Columbia, 2010. http://hdl.handle.net/2429/29653.

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The two main forms of hippocampal synaptic plasticity, long-term potentiation (LTP) and long-term depression (LTD) represent a cellular model for learning and memory. While synaptic plasticity has been studied extensively, questions still remain on how exogenous and endogenous modulators can impact hippocampal LTP and LTD. Here, we use electrophysiology and imaging to investigate the effects of two types of modulators on synaptic plasticity. First, we look at the effects of an antagonist of the 5-HT6 re ceptor on LTP and LTD in two regions of the hippocampus, the CAl and the dentate gyrus (DG). We find that our 5-HT6 antagonist differentially affects LTP in each region and blocks hippocampal LTD. These findings are the first report of an involvement of the 5-HT6 receptor in synaptic plasticity and are particularly relevant in light of evidence showing a key role of the 5-HT6 receptor in cognition and memory. Second, we look at the effects of glutathione (GSH) supplementation on LTP in aged animals. We show that supplementing aged mice with a precursor for GSH formation reverses the mechanisms underlying hippocampal LTP from L-type calcium channel dependence back to NMDA receptor-dependence. These results suggest an important role for GSH as a modulator of synaptic plasticity in aging.
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34

Epp, Jonathon, and University of Lethbridge Faculty of Arts and Science. "The hippocampus, retrograde amnesia, and memory deconsolidation." Thesis, Lethbridge, Alta. : University of Lethbridge, Faculty of Arts and Science, 2005, 2005. http://hdl.handle.net/10133/219.

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There are numerous clinical and experimental accounts of retrograde and anterograde amnesia resulting from damage to the hippocampus (HPC). Several theories on the HPC hold that only certain types of recent memories should be affected by HPC damage. These theories do not accurately predict the circumstances within which memories are vulnerable to HPC damage. Here I show the HPC plays a role in the formation and storage of a wider range of memories than is posited in contemporary theories. I will demonstrate that an important factor in elciting retrograde amnesia is the number of similar learning episodes. Exposure to multiple problems in the same task context leads to retorgrade amnesia that is not observed when only one problem is learned under otherwise identical parameters. When multiple discriminations are learned, the output of the HPC blocks recall from and future use of the extra-HPC memory system.
x, 78 leaves : ill. ; 29 cm.
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35

Haber, Michael. "Investigating glial dynamics in the developing hippocampus." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=115681.

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Glial cells represent the most abundant cell population in the central nervous system (CNS), and yet, have historically been thought of as merely support cells for neurons. Over the past few decades, however, the number of identified roles that glial cells play in the CNS has expanded at an exponential rate, revealing new and exciting functions in neuron-glial communication. At synapses, astrocytes are now recognized as part of a "tripartite" complex with pre- and postsynaptic structures and can modulate synaptic transmission and plasticity. Accumulating evidence has also revealed new roles for oligodendrocytes in regulating axon diameter and integrity, and ion channel clustering. Despite our knowledge of the physiological connections between neurons and glia, relatively little is known about the morphological interplay of these cells during development and in the mature brain. The results presented in this thesis reveal the extent and time-course of rapid remodelling of astrocytes and oligodendrocytes in close proximity to dendritic spines and axons respectively. These findings provide further evidence that glia play an important role in regulating the structural plasticity of the brain. The methodology developed also provides a powerful system for the study of neuron-glial structural dynamics and may contribute to the development of novel therapeutic strategies for diseases affecting the central nervous system.
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36

Burnett, Dean. "Role of the hippocampus in configural learning." Thesis, Cardiff University, 2010. http://orca.cf.ac.uk/54380/.

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Contemporary theories of animal learning propose that memory for a specific event can be based upon either an elemental network of associations, a configural associative network or a hybrid of these possibilities. The two aims of this thesis were (1) to assess whether rats form configural representations of the spatiotemporal features of specific cues, and (2) to test the hypothesis that the hippocampus plays a critical role in configural representations that encode the spatiotemporal properties of an event, more commonly known as episodic memory. Chapter 2 investigated rats' ability to represent the spatiotemporal context in which objects were presented. These experiments failed to find robust evidence for such an ability. Chapter 3 discusses the development of a novel task, based on a sensory preconditioning procedure, that demonstrated configural memory for the spatiotemporal features of auditory cues in normal rats. In addition, it was shown that excitotoxic lesions of the hippocampus disrupted such configural memories. The experiments reported in Chapter 4 used the procedure developed in Chapter 3 to show that temporary inactivation of the hippocampus during memory retrieval disrupted configural, but not elemental memory retrieval. The results presented in this thesis support the hypothesis that normal rats are able to form elemental and configural representations involving the spatiotemporal properties of cues, and that the hippocampus has a role in configural but not elemental associative memory.
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37

Roberts, Lindsay A. "Plasticity related gene expression in the hippocampus." Thesis, University of Glasgow, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.360278.

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38

Kay, Kenneth. "Novel patterns of activity in the hippocampus." Thesis, University of California, San Francisco, 2016. http://pqdtopen.proquest.com/#viewpdf?dispub=10133436.

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The observation that the hippocampus is required for memory and spatial navigation has led to extensive study of the hippocampal neural circuit. Past research has focused on established patterns of hippocampal neural activity, such as the classic place cell code and the theta network pattern. However, we still have only a preliminary understanding of how the hippocampus performs cognitive functions. This may be the case because there still remain unknown yet fundamental patterns of hippocampal neural activity.

To investigate this possibility, we recorded neural activity in the hippocampus of rats engaged in a spatial memory task. In this thesis I describe four previously unidentified patterns of hippocampal neural activity: (1) spatially specific neural firing that is more active when animals are at rest, (2) a ∼200 ms network pattern that is associated with spatial firing at rest, (3) spatially specific, transient neural firing at the time of behavioral transitions between movement and rest, and (4) a high frequency (65-140 Hz) network pattern that entrains neural firing throughout the hippocampus. I postulate that these patterns of activity have essential roles in complex hippocampal functions.

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Armstrong, Beth Diane. "Hippocampus: seahorse; brain-structure; spatial map; concept." Thesis, Rhodes University, 2010. http://hdl.handle.net/10962/d1002224.

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Through an exploration of both sculptural and thought processes undertaken in making my Masters exhibition, ‘Hippocampus’, I unpack some possibilities, instabilities, and limitations inherent in representation and visual perception. This thesis explores the Hippocampus as image (seahorse) and concept (brain-structure involved in cognitive mapping of space). Looking at Gilles Deleuze’s writings on representation, I will expand on the notion of the map as being that which does not define and fix a structure or meaning, but rather is open, extendable and experimental. I explore the becoming, rather than the being, of image and concept. The emphasis here is on process, non-representation, and fluidity of meaning. This is supportive of my personal affirmation of the practice and process of art-making as research. I will refer to the graphic prints of Maurits Cornelis Escher as a means to elucidate a visual contextualization of my practical work, particularly with regard to the play with two- and three-dimensional space perception. Through precisely calculated ‘experiments’ that show up the partiality of our visual perception of space, Escher alludes to things that either cannot actually exist as spatial objects or do exist, but resist representation. Similarly I will explore how my own sculptures, although existing in space resist a fixed representation and suggest ideas of other spaces, non-spaces; an in-between space that does not pin itself down and become fixed to any particular image, idea, objector representation.
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Durán, Ernesto [Verfasser]. "Hippocampus-cortex communication during sleep / Ernesto Durán." Tübingen : Universitätsbibliothek Tübingen, 2020. http://d-nb.info/1214640141/34.

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41

Kempermann, Gerd. "Aktivitätsabhängige Regulation von Neurogenese im erwachsenen Hippocampus." Doctoral thesis, Humboldt-Universität zu Berlin, Medizinische Fakultät - Universitätsklinikum Charité, 2002. http://dx.doi.org/10.18452/13790.

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Das erwachsene Gehirn enthält neuronale, multipotente Stammzellen, aus denen in den beiden bekannten neurogenen Regionen des Gehirn, im Hippocampus und im olfaktorischen System, neue Nervenzellen hervorgehen. Aus Transplantationsstudien und anderen Untersuchungen weiß man, daß es die zelluläre Umgebung ist, die die neurogene Permissivität und damit die Entwicklung einer reifen neuen Nervenzelle aus einer Stamm- oder Vorläuferzelle, bestimmt. Die Schlüsselfrage lautet daher: Was macht eine neurogene Region neurogen? Neurogenität ist mehr als die Präsenz von neuralen Stammzellen. Die aktivitätsabhängige Regulation adulter hippocampaler Neurogenese stellt eine physiologische, positive Modulation von Neurogenität im erwachsenen Gehirn dar. Aktivitätsabhängige Regulation adulter hippocampaler Neurogenese ist vielstufig und kein An/Aus-Phänomen. Die unterschiedlichen Stufen der Regulation unterliegen unterschiedlicher genetischer Determination und unterschiedlicher Empfindlichkeit auf aktivitätsabhängige Stimuli. Die Steuerung des Überlebens neugeborener Zellen stellt möglicherweise den entscheidenden Schritt auf dem Weg zu einem neuen Neuron dar. Die aktivitätsabhängige Selektion durch eine überlebensfördernde Wirkung rekrutiert jedoch aus einem Pool proliferierender Vorläuferzellen, die das neurogene Potential darstellen. Die subtile Regulation adulter hippocampaler Neurogenese durch funktionsabhängige Stimuli legt eine Relevanz für hippocampale Funktion, insbesondere Lern- und Gedächtnisvorgänge nahe. Entsprechend muß aber auch eine Bedeutung für hippocampale Pathologie diskutiert werden. Das Verständnis darüber, wie Neurogenität funktions- und aktivitätsabhängig modulierbar ist, ist von größter Relevanz für die Frage, ob und wie sich Neurogenese aus ruhenden neuronalen Stamm- und Vorläuferzellen auch außerhalb neurogener Regionen induzieren und in therapeutischer Absicht nutzen läßt.
The adult brain contains neuronal, multipotent stem cells. In two neurogenic regions of the adult brain, hippocampus and olfactory system, new neurons are generated from these stem cells. From transplantation studies and other investigations it is known that the cellular microenvironment provides the neurogenic permissiveness and determines the development of a mature new neuron from a stem or progenitor cell. Thus, the key question is, what defines a neurogenic region as neurogenic, if it is not the presence of neural stem cells alone. The activity-dependent regulation of adult hippocampal neurogenesis represents a physiologic and positive modulation of neurogenic permissiveness in the adult brain. Activity-dependent regulation of adult hippocampal neurogenesis occurs on multiple steps and is not an on/off phenomenon. The different levels of regulation are differentially influenced by genetic determination and different susceptibility to activity-dependent stimuli. The regulation of the survival of a newly generated cells might be the key step in the development of a new neuron. The activity-dependent recruitment of new neurons by means of a survival-promoting effect acts upon a pool of proliferating progenitor cells, which represent the neurogenic potential. The subtle regulation of adult neurogenesis by functional stimuli suggests a relevance of adult hippocampal neurogenesis for hippocampal function, in particular learning and memory. Accordingly, a potential relevance for hippocampal pathology has to be considered. Insights on how neurogenic permissiveness can be modulated in response to functional stimuli has important implications for the question, if and how neurogenesis from quiescent neuronal stem or progenitor cells can be induced inside and outside of neurogenic regions of the adult brain and can be used for therapeutic purposes.
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42

Janác̆ková, Son̆a. "Functional maturation of postnatal hippocampus in rodents : electrophysiological approach." Thesis, Paris 5, 2013. http://www.theses.fr/2013PA05T050.

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Les réseaux neuronaux, pendant leur période de développement, génèrent des patrons d’activité immatures qui sont supposés participer à la formation des circuits neuronaux. Ces activités synchronisées créent des conditions favorables pour la plasticité hebbienne qui soutient la formation des circuits locaux. Les travaux menés notamment sur les systèmes sensoriels ont montré que les circuits pauci-neuronaux locaux sont capables de présenter une activité synchrone tout en étant isolés du reste des structures cérébrales. La moelle épinière isolée produit des bursts qui sont à l’origine des secousses musculaires, la rétine insensible à la lumière génère des ondes d’activité, d’autres régions cérébrales génèrent des activités synchrones avant de remplir la fonction à laquelle ils sont destinés. De manière similaire, l’hippocampe du rat nouveau-né ou primate prématuré in vitro, ainsi que les néocortex immature in vitro, génèrent une activité neuronale synchronisée, appelée giant depolarising potentials (GDPs). En se basant uniquement sur ces études et en prenant en compte la maturation tardive de certaines projections neuronales à distance, il serait tentant de conclure que le cerveau immature fonctionne comme un ensemble de petits modules fonctionnels qui auto-entretiennent leur activité intrinsèque avant de se connecter entre eux pour créer un cerveau fonctionnel adulte. Cependant, certaines connexions à longue distance sont formées très tôt pendant le développement et permettent la propagation des oscillations immatures entre les structures connectées. En effet, les ondes rétinales se propagent au noyau géniculé latéral et ensuite jusqu’au cortex visuel ; les GDPs hippocampiques se propagent à l’hippocampe controlatéral, septum et cortex entorhinal et finalement, les secousses musculaires, en créant un feed-back sensoriel, déclenchent des oscillations gamma immatures ainsi que les spindle bursts dans le réseau thalamo-cortical. Un fonctionnement similaire est décrit chez le nouveau-né prématuré. Il paraît donc plus probable, que le cerveau soit, dès les stades précoces du développement, organisé en sous-systèmes fonctionnels reliés entre eux anatomiquement et fonctionnellement. Au sein des unités fonctionnelles sont générés des patrons d’activité immatures synchrones afin de créer des connexions organisées topographiquement qui serviront de base anatomique de la fonction finale. Si ces étapes développementales sont perturbées pendant les périodes critiques, le système ne pourra pas assurer sa fonction de manière adéquate au stade mature. L’hippocampe mature, ou plus exactement les circuits cortico-hippocampiques, jouant un rôle primordial dans la mémoire déclarative, l’orientation spatiale et l’inhibition du comportement. L’établissement de ces fonctions est progressif au cours du développement. Par exemple les adultes humains n’ont que rarement des souvenirs personnels datant avant l’âge de trois ans. Or, nous savons aujourd'hui que le bébé humain est capable de garder des souvenirs dans la mémoire déclarative (dépendante de l’hippocampe) au cours de la première année de vie avec une efficacité croissante, mais il ne se rappellera pas ces souvenirs à l’âge adulte (Bauer, 2006). Nous ne savons pas s’il s’agit d’un encodage différent d’emblée ou d’un processus secondaire supprimant l’accès à ces souvenirs précoces. Nous pouvons présumer qu’il existe des modifications des activités électrophysiologiques pendant le développement qui soutiennent la modification de ces fonctions. Au cours de ce travail de thèse, nous voulions savoir comment et à partir de quand l’hippocampe, qui reçoit des informations convergentes de nombreuses régions néocorticales, acquiert son mode de fonctionnement adulte. Afin de répondre à cette question nous avons étudié le système cortex entorhinal – hippocampe, le cortex entorhinal étant la principale entrée excitatrice de l’hippocampe et recevant des afférences de nombreuses régions du néocortex. (...)
Neuronal networks spontaneously generate “immature” patterns of activity during development, which are thought to participate on the formation of neural circuits. Local neocortical as well as hippocampal circuits generate synchronised neuronal discharges providing support for Hebbian plasticity. Studies of sensory systems showed that local pauci-neuronal circuits were able to generate synchronous activity while isolated from other brain structures. Isolated spinal cord produces bursts evoking muscle twitching, light insensitive retina generates waves of activity, as well as other brain regions generate synchronous activities before fulfilling the function for which they are intended. Similarly, the hippocampus of newborn rat or premature primate in vitro, as well as immature neocortex in vitro, generates synchronised neuronal activity called giant depolarising potentials (GDPs). Based solely on these studies and taking into account the delayed maturation of certain long-distance neuronal projections, it would be tempting to conclude that the immature brain functions as a set of small functional modules that self-maintain their intrinsic activity before connecting together to create a functional adult brain. However, some long-distance connections are formed very early during development and allow the propagation of oscillations between immature connected structures. Indeed, retinal waves propagate to the lateral geniculate nucleus and then to the visual cortex, hippocampal GDPs propagate to the contralateral hippocampus, septum and entorhinal cortex, and finally, twitching, creating a sensory feedback, triggers immature gamma oscillations and spindle bursts in the thalamo-cortical network. A similar functioning is described in the premature newborn. It therefore seems more likely that the brain is, during the early stages of development, organised into functional subsystems interconnected anatomically and functionally. Within functional units are generated immature patterns of synchronous activity to create topographically organised connections that serve as anatomical basis of the final function. If these developmental stages are disturbed during critical periods, the system cannot perform its function adequately in mature stage. The mature hippocampus, or more precisely the cortico-hippocampal circuits, plays a key role in declarative memory, spatial organisation and behavioural inhibition. The establishment of these functions is progressive during development. For example, human adults rarely have personal memories dating before the age of three years. However, we now know that the human baby is able to keep memories in declarative memory (hippocampus-dependent) during the first year of life with increasing efficiency, but will not remember them in the adulthood. We do not know if the encoding of the memories is different or a secondary process inhibits the access to the early memories. We can assume that changes in electrophysiological activity during development support modification of these functions. In this thesis, we wanted to know how and from when the hippocampus, which receives convergent information from many cortical areas, acquires his adult mode of functioning. To answer this question we studied the entorhinal cortex-hippocampus system, entorhinal cortex being the main excitatory input to the hippocampus and receiving afferents from many parts of the neocortex. We were able to distinguish several periods in the development of the immature hippocampus: Period from P1 till P12 characterised by the sole presence of immature sharp waves triggered by the entorhinal cortex. Period from P13, when two types of sharp waves coexisted: the immature sharp waves and sharp waves as described in the adult animals newly emerged. The mature sharp waves, unlike the immature, can be accompanied by ripples. (...)
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43

Cornejo, Brandon John. "A single early life seizure permanently alters working memory, hippocampal plasticity and glutamate receptor localization /." Connect to full text via ProQuest. IP filtered, 2006.

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Thesis (Ph.D. in Pharmacology) -- University of Colorado, 2006.
Typescript. Includes bibliographical references (leaves 125-149). Free to UCDHSC affiliates. Online version available via ProQuest Digital Dissertations;
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44

Maingret, Nicolas. "A causal role for the hippocampo-cortical dialogue in memory consolidation : temporal coupling of rhythmic patterns and cortical network reorganization during sleep in rats." Thesis, Paris 6, 2016. http://www.theses.fr/2016PA066620.

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La théorie de la formation de la mémoire "en deux étapes" postule que la consolidation mnésique repose sur un dialogue pendant le sommeil entre l'hippocampe, où les traces mnésiques sont initialement formées, et le néocortex (notamment le cortex préfrontal médian, CPm), où elles seraient stockées à long terme. En particulier, la coordination entre oscillations au sein du réseau hippocampo-cortical pendant le sommeil apparaît comme un mécanisme plausible pour la consolidation. Nous avons augmenté la coordination temporelle entre ces deux structures pendant le sommeil suivant un apprentissage d'une tâche de mémoire spatiale limité en temps n'induisant pas de consolidation. Les rats ayant suivi le protocole permettant l'augmentation des intéractions entre ondulations hippocampiques, ondes delta corticales et fuseaux thalamo-corticaux par le biais d'impulsions électriques intra-corticales ont fait preuve d'un haut niveau de performance de rappel 24 h plus tard, contrairement à des rats de contrôle qui ne faisaient pas mieux que le hasard. Ainsi, cette augmentation des intéractions hippocampo-corticales pendant le sommeil a-t-elle stabilisé des traces mnésiques qui autrement n'auraient pas subsisté entre l'entraînement et le test. De plus, nous avons observé une réorganisation des réseaux neuronaux du CPm pendant le sommeil, ainsi qu'une réponse accrue du CPm à la tâche le lendemain. Ces travaux constituent une mise en évidence directe du rôle causal du dialogue hippocampo-cortical pendant le sommeil dans la consolidation mnésique, dont les mécanismes sous-jacents impliquent une coordination temporelle précise entre ondulations, ondes delta et fuseaux (Maingret et al., 2016)
The `two-stage' theory of memory posits that memory consolidation involves a dialogue during sleep between the hippocampus, where traces are initially formed, and the neocortex (notably the prefrontal cortex), where they are stored for long-term retention. Temporally coordinated oscillations in the hippocampo-cortical network could be a key mechanism for sleep-dependent memory consolidation. We dynamically manipulated the temporal coordination between the two structures during sleep following training on a spatial memory task specifically designed to trigger encoding, but not memory consolidation. Reinforcing the endogenous coordination between hippocampal sharp wave-ripples, cortical delta waves and spindles by timed electrical stimulation resulted in a high recall performance on the next day, contrary to control rats which performed at chance levels. Thus, this enhancement of hippocampo-cortical interactions during sleep stabilized memory traces that would have otherwise vanished between training and test. In addition, we observed a reorganization of prefrontal cortical networks during sleep, along with subsequent increased prefrontal responsivity to the task on the next day. These results provide direct evidence for a causal role of a hippocampo-cortical dialogue during sleep in memory consolidation, and indicate that the underlying mechanism involves a fine-tuned coordination between sharp wave-ripples, delta waves and spindles (Maingret et al., 2016)
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45

Brackmann, Marian. "Beteiligung des Calciumsensors VILIP-1 (Visinin-like-Protein-1) an synaptischer Plastizität Regulation der Expression in Modellen der hippokampalen Plastizität und Einfluss auf Signaltransduktionsmechanismen /." [S.l. : s.n.], 2004. http://www.diss.fu-berlin.de/2004/232/index.html.

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46

Doğancı, Beril. "The generation and characterisation of mice with conditional knock-out of the NMDA receptor subunit NR2B." [S.l. : s.n.], 2007. http://nbn-resolving.de/urn:nbn:de:bsz:16-opus-73853.

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47

Canepari, Marco. "Intrinsic variability and short-term changes in synaptic transmission in the rat hippocampal CA3 region." Doctoral thesis, SISSA, 1999. http://hdl.handle.net/20.500.11767/4432.

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48

Olson, Emelie. "Effects on the Hippocampal Volume and Function : Stress and Depression Versus Physical Exercise." Thesis, Högskolan i Skövde, Institutionen för biovetenskap, 2018. http://urn.kb.se/resolve?urn=urn:nbn:se:his:diva-15525.

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In this essay, changes in the human hippocampal volume and function induced by stress, depression and physical exercise are examined. Hippocampus is crucially involved in the acquisition and retrieval of episodic and spatial memory, and hippocampal volume correlates with episodic and spatial memory performance. Hippocampus has substantial plasticity and changes with age, but also in response to experiential factors across life. Stress and, under at least some circumstances, also depression have negative effects on hippocampal volume and memory function. The negative effects are believed to accelerate age-related decline in volume and function, mediated by exaggerated cortisol levels and dysfunction in the HPA-axis. Physical exercise is examined from two perspectives; aerobic and strength exercise. Aerobic exercise increases hippocampal volume across various ages and decelerates age-related hippocampal degeneration, whereas support for strength exercise-induced effects are mixed and need to be studied further. The positive effects are believed to be mediated by increased BDNF levels and regional cerebral blood volume. Although hippocampal volume normally correlates with hippocampus-dependent memory, studies on exercise-induced changes in human hippocampus-dependent memory have reported inconsistent results. Animal studies have observed both the negative and positive effects on hippocampal volume to relate to changes in neurogenesis, cell proliferation, and dendritic complexity. The negative and positive effects on hippocampal volume have been observed to be non-permanent, suggesting that physical exercise may prevent, attenuate and possibly reverse hippocampal degeneration induced by stress and depression. Further, more studies on sex and age differences, exercise intervention designs and functional values of physical exercise would be of value.
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49

Todorova, Ralitsa. "Profils d'activité neurale lors d'événements oscillatoires soutendant la consolidation des souvenirs dépendant de l'hippocampe." Thesis, Paris Sciences et Lettres (ComUE), 2018. https://tel.archives-ouvertes.fr/tel-03091987.

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Le stockage à long terme des souvenirs épisodiques requiert la formation de la mémoire pendant l'expérience d'éveil ainsi que la consolidation de la mémoire, un processus de renforcement de la mémoire qui a lieu pendant le sommeil. L'encodage rapide des traces mnésiques a lieu dans l'hippocampe pendant l'éveil. Pendant le sommeil, les traces mnésiques de l'hippocampe sont « rejouées » pendant les ondulations -- de brefs motifs oscillatoires hippocampiques (50-150 ms) à haute fréquence associés à une activité synchrone élevée. Les bouffées d'activité synchrone des neurones de l'hippocampe pendant les ondulations font d'eux des acteurs clés dans la consolidation de la mémoire des systèmes -- le processus de communication des mémoires vers le néocortex pour un stockage à long terme.L'activité corticale dans le sommeil est dominée par l'oscillation lente -- l'alternance synchrone des neurones corticaux entre un état dépolarisé (état HAUT) associé à des niveaux élevés d'activité endogène, et un état bref (~200ms) hyperpolarisé (état BAS) lorsque les neurones restent silencieux. Les états BAS sont accompagnés de grandes déviations du potentiel de champ local -- ondes delta, tandis que les états HAUTS sont associés à une activité élevée et des fuseaux thalamocorticaux, deux processus pouvant entraîner une plasticité synaptique. On pense que la consolidation de la mémoire des systèmes implique une coordination entre les rythmes hippocampiques et corticaux -- notamment, les ondulations hippocampiques précèdent (~130ms) les ondes delta corticales, qui sont ensuite suivies par des fuseaux thalamocorticaux.Pour vérifier si ce couplage temporel entraîne une consolidation de la mémoire, nous avons déclenché des ondes delta corticales suite à des ondulations hippocampiques afin d'améliorer la cooccurrence d'événements ondulation-delta couplés. Cela a augmenté la consolidation de la mémoire et la performance du rat sur une tâche de mémoire spatiale, et a entraîné une réorganisation des réseaux corticaux préfrontaux suite à des ondes delta induites ainsi qu'une réponse accrue du cortex préfrontal à la tâche le lendemain. De manière cruciale, ces améliorations n'ont pas été observées lorsqu'un retard (160-240 ms) a été introduit en plus du couplage endogène, indiquant que la stabilisation des traces mnésiques nécessite une interaction très fine entre les ondulations et les ondes delta.Comment l'interruption de l'activité corticale par des périodes de silence généralisées pendant les ondes delta peut-elle sous-tendre la consolidation de la mémoire lorsqu'elle se produit précisément entre le transfert d'informations (réactivation hippocampique) et la plasticité du réseau (état HAUT) ? Contrairement à un principe généralement accepté, nous avons constaté que les ondes delta ne sont pas des périodes de silence complet, et que l'activité résiduelle n'est pas un simple bruit neuronal. Au lieu de cela, nous avons montré que les cellules corticales émettent des « delta spikes » pendant les ondes delta en réponse à la réactivation transitoire d'ensembles hippocampiques pendant les ondulations, et que cela se produit sélectivement pendant la consolidation endogène ou induite de la mémoire. Ces résultats suggèrent un nouveau rôle pour les ondes delta, à savoir que le silence synchronisé de la grande majorité des cellules isole le réseau des entrées concurrentes, tandis qu'une sous-population sélectionnée de neurones reste active en réponse aux réactivations de l'hippocampe, faisant le pont entre les états HAUTs et coordonnant la consolidation de la mémoire
Long term storage of episodic memories requires memory formation during awake experience as well as memory consolidation, a process strengthening the memory taking place during sleep. The rapid encoding of memory traces takes place in the hippocampus during awake behaviour. In sleep, hippocampal memory traces are `replayed' during sharp wave-ripples -- brief (50-150 ms) high-frequency oscillatory patterns of high synchronous activity. The synchronous bursting of hippocampal neurons during ripples makes them a key player in systems memory consolidation -- the process of communicating memories to the neocortex for long-term storage.Cortical activity in sleep is dominated by the slow oscillation -- the synchronous alternation of cortical neurons between a depolarised (UP) state associated with high levels of endogenous activity, and a brief (~200 ms) hyperpolarized (DOWN) state when neurons remain silent. DOWN states are accompanied by large deflections of the local field potential -- delta waves, while UP states bring elevated activity and thalamocortical spindles, both of which can drive synaptic plasticity. Systems memory consolidation is thought to involve the coordination between hippocampal and cortical rhythms -- notably, hippocampal ripples precede (~130 ms) cortical delta waves, which are then followed by thalamocortical spindles.To test if this temporal coupling drives memory consolidation, we triggered cortical delta waves following ripples to enhance the co-occurrence of coupled ripple-delta events. This boosted memory consolidation and rat performance on a spatial memory task, and resulted in a reorganisation of prefrontal cortical networks following induced delta waves as well as increased prefrontal responsivity to the task on the next day. Crucially, these enhancements were not observed when a small delay (160-240 ms) was introduced in addition to the endogenous coupling, indicating the stabilization of memory traces requires a very fine-tuned interaction between ripples and delta waves.How can the 'interruption' of cortical activity by generalised periods of silence during delta waves underlie memory consolidation when it occurs precisely between information transfer (hippocampal replay) and network plasticity (UP state)? Contrary to a generally accepted tenet, we found that delta waves are not periods of complete silence, and that the residual activity is not mere neuronal noise. Instead, cortical cells fired `delta spikes' during delta waves in response to transient reactivation of hippocampal ensembles during ripples, and this occurred selectively during endogenous or induced memory consolidation. This suggests a new role for delta waves -- namely, that the synchronised silence of the large majority of cells isolates the network from competing inputs, while a select subpopulation of neurons remain active in response to hippocampal replay, bridging information between UP states and coordinating memory consolidation
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50

Rosay, Sophie. "A statistical mechanics approach to the modelling and analysis of place-cell activity." Thesis, Paris, Ecole normale supérieure, 2014. http://www.theses.fr/2014ENSU0010/document.

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Les cellules de lieu de l’hippocampe sont des neurones aux propriétés intrigantes, commele fait que leur activité soit corrélée à la position spatiale de l’animal. Il est généralementconsidéré que ces propriétés peuvent être expliquées en grande partie par les comporte-ments collectifs de modèles schématiques de neurones en interaction. La physique statis-tique fournit des outils permettant l’étude analytique et numérique de ces comportementscollectifs.Nous abordons ici le problème de l’utilisation de ces outils dans le cadre du paradigmedu “réseau attracteur”, une hypothèse théorique sur la nature de la mémoire. La questionest de savoir comment ces méthodes et ce cadre théorique peuvent aider à comprendrel’activité des cellules de lieu. Dans un premier temps, nous proposons un modèle de cellulesde lieu dans lequel la localisation spatiale de l’activité neuronale est le résultat d’unedynamique d’attracteur. Plusieurs aspects des propriétés collectives de ce modèle sontétudiés. La simplicité du modèle permet de les comprendre en profondeur. Le diagrammede phase du modèle est calculé et discuté en comparaison avec des travaux précedents.Du point de vue dynamique, l’évolution du système présente des motifs particulièrementriches. La seconde partie de cette thèse est à propos du décodage de l’activité des cellulesde lieu. Nous nous demandons quelle est l’implication de l’hypothèse des attracteurs surce problème. Nous comparons plusieurs méthodes de décodage et leurs résultats sur letraitement de données expérimentales
Place cells in the hippocampus are neurons with interesting properties such as the corre-lation between their activity and the animal’s position in space. It is believed that theseproperties can be for the most part understood by collective behaviours of models of inter-acting simplified neurons. Statistical mechanics provides tools permitting to study thesecollective behaviours, both analytically and numerically.Here, we address how these tools can be used to understand place-cell activity withinthe attractor neural network paradigm, a theory for memory. We first propose a modelfor place cells in which the formation of a localized bump of activity is accounted for byattractor dynamics. Several aspects of the collective properties of this model are studied.Thanks to the simplicity of the model, they can be understood in great detail. The phasediagram of the model is computed and discussed in relation with previous works on at-tractor neural networks. The dynamical evolution of the system displays particularly richpatterns. The second part of this thesis deals with decoding place-cell activity, and theimplications of the attractor hypothesis on this problem. We compare several decodingmethods and their results on the processing of experimental recordings of place cells in afreely behaving rat
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