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1
Li, Daqing. "Entorhino-hippocampal projections in organotypic cultures". Thesis, University College London (University of London), 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.315340.
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Sandin, Johan. "The hippocampal opioid system : role in spatial learning /". Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4332-x/.
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Overington, D. W. "Resolution of spatial ambiguity by the hippocampal place system". Thesis, University College London (University of London), 2017. http://discovery.ucl.ac.uk/1557213/.
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External space is coded in the brain by a network of spatially modulated neurons (including place, grid, border and head direction cells), known as the ‘cognitive map’.This internal map allows flexible and efficient navigation through the external world. These neurons use both self-motion and visual landmark information to update their spatial activity and form an accurate representation of space. Sometimes, the spatial meaning of a landmark can be ambiguous, e.g. when it can be approached from different directions (for example, a tree on the border between two fields). In such cases context information, such as odour, colour or texture, can provide clues to separate one environment from another. Recent work has shown that head direction (HD) cells in the retrosplenial cortex can use these non-metric cues to resolve visually symmetrical spaces with directional landmark ambiguity. In this study, we asked whether animals can also use these nonmetric cues to guide their behaviour, in this case in order to solve spatial tasks across multi-compartment space. Here we show that, behaviourally, rodents can correctly encode relative object positions in visually ambiguous space, and can resolve the directional ambiguity of two visually symmetrical spaces based only on odour information. Electrophysiological recordings of hippocampal place and anterior thalamus HD cells confirmed that both cell types can use odour-context information to discriminate these spaces; therefore, we tested potential involvement of the HD system by temporarily inactivating the anterior thalamus with an awake muscimol infusion. In the behavioural task, HD-disrupted animals show impairment in task performance compared to sham but retain response to novelty. Overall, these results indicate that rodents can use odour-context information to resolve directional ambiguity in otherwise identical multi-compartment environments, and suggest an involvement of the HD system in this process.
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Krebs, Desiree L. "Glucose modulation of the septo-hippocampal system implications for memory /". unrestricted, 2006. http://etd.gsu.edu/theses/available/etd-09272006-142645/.
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Thesis (Ph. D.)--Georgia State University, 2006.Marise B. Parent, committee chair; Timothy J. Bartness, Kim L. Huhman, Kyle J. Frantz, committee members. Electronic text (352 p. : ill.)) : digital, PDF file. Description based on contents viewed July 12, 2007. Includes bibliographical references (p. 307-352).
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Krebs-Kraft, Desiree Lynne. "Glucose Modulation of the Septo-Hippocampal System: Implications for Memory". Digital Archive @ GSU, 2006. http://digitalarchive.gsu.edu/psych_diss/22.
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Extensive evidence suggests that glucose has both positive and negative effects on memory and these effects likely involve an influence on the brain. For instance, direct infusions of glucose into the septum (MS) or hippocampus can enhance or impair memory. The present set of experiments attempted to determine the different conditions that dissociate the memory-enhancing and -impairing effects of glucose in rats. Specifically, these experiments examined the effects of glucose in spontaneous alternation, a measure of spatial working memory and shock avoidance, an index of emontional long-term memory. The results showed that the memory-impairing effects of MS infusions of glucose are not concentration-dependent. These data also indicated that the memory-impairing effects of MS glucose elevations are specific to gamma-aminobutyric acid GABA receptor activation but do not depend on increases in MS GABA synthesis or release. Importantly, we showed that the memory-impairing interaction between MS glucose and GABA agonists does not generalize to the hippocampus, suggesting the memory-modulating effects of glucose are brain region-dependent. We showed further that these brain region-dependent effects of glucose are not due to difference in basal extracellular glucose levels. Moreover, these findings showed that the memory-enhancing effects of hippocampus glucose override the memory-impairing interaction between MS glucose and GABA. These findings are important because they are the first to show that the memory-modulating effects of glucose are both neurotransmitter- and brain region-dependent. Furthermore, these findings provide preliminary evidence suggesting that the memory-impairing effects of MS glucose may involve compromised hippocampal function. These data also suggest the memory-impairing effects of MS co-infusions of glucose with GABA agonists likely involve an influence on the GABAergic SH projection. Finally, these findings demonstrate the mnemonic and neurochemical consequences of glucose in the MS and hippocampus, two brain regions affected by normal aging, Alzheimer’s disease, and diabetes.
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Christiansen, Kathleen Yolande. "An integrated analysis of the extended hippocampal system across species". Thesis, Cardiff University, 2017. http://orca.cf.ac.uk/100977/.
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The objective of this thesis was to investigate functional differences within the extended hippocampal system by 1. analysing its connectional topography and 2. looking at evidence for differential functions within its component structures. The main areas under examination were A. the subiculum and B. its diencephalic targets, along with C. the fornix, the principle white matter tract connecting these structures. Retrograde tracer experiments in rodents and primates revealed consistent topographies in the subiculum projections to these diencephalic target sites, with distinctions occurring primarily along the proximal-distal and laminar subicular axes in rodents and primarily along the anterior-posterior and laminar subicular axes in primates. Based on different input patterns to the proximal subiculum (principally from sites processing object information) and distal subiculum (principally from sites processing spatial/context information) it was predicted that this proximal-distal axis would show functional activation differences in rodents for matched object:spatial tasks. Immediate early gene imaging (using zif268 expression) did not, however, reveal clear-cut gradient differences, although there were indications of the expected bias to object memory in the proximal subiculum. Diffusion MRI was used to study the fornix by separating its precommissural and postcommissural connections in a healthy older and cognitively impaired human population. Reliable topographic differences were found for the precommissural and postcommissural fornix in each group but cognitive function proved difficult to differentiate between the tracts for the tasks used. Lastly, fornix reconstructions were also found to be separable according to their links with either the anterior or posterior hippocampus in a healthy population. These distinctions provide another way of studying the fornix in terms of relating different functional properties with different sets of hippocampal connections. It is assumed that different populations of fornical fibres should underlie different aspects of memory/cognitive tasks involving the fornix, making their segregation informative in future studies researching this tract. Detailing the nature of the connections within the extended hippocampal system, this thesis lays the groundwork for future studies investigating the relative roles of its component structures in cognitive function.
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Crawford, Freya. "Ultrastructure-function properties of recycling synaptic vesicles in acute hippocampal slices". Thesis, University of Sussex, 2015. http://sro.sussex.ac.uk/id/eprint/57953/.
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Synaptic vesicles are the substrate of neurotransmission in most nerve terminals in the central nervous system. These small membrane spheres fuse with the synaptic membrane in an activity-dependent manner and release neurotransmitter into the synaptic cleft. Subsequently, vesicles are reclaimed through endocytosis prior to reuse. This recycling process is key to supporting ongoing signalling in the brain. While substantial effort has gone into defining basic characteristics of vesicle recycling, for example elucidating the timing of vesicle turnover, key questions remain unanswered. An important area with significant knowledge deficits relates to the relationship between vesicle function and ultrastructural organisation in the terminal. The aim of this thesis is to address this issue, exploiting new methodologies which provide novel insights into function-structure relationships of vesicle populations in acute brain slices. Specifically, this study considers organisational principles of three defined vesicle pools as well as examining the impact of an established plasticity protocol on pool properties. The first results chapter, Chapter 3, outlines and validates the novel protocol used for fluorescently labelling functional recycling vesicle populations in acute rat brain slices using the vesicle-labelling dye FM1-43 and new antibody based probes (syt1-Oyster, CypHer5E). Reporter-labelling and release properties are compared to similar approaches using cultured neurons. We conclude that this approach provides a more physiologically relevant method to study the functional properties of cells than used previously in cultured neurons. Chapter 4 outlines experiments utilising the capability of FM 1-43 to be photoconverted to an electron-dense form to allow a defined vesicle population, the readily releasable pool (RRP), to be characterised ultrastructurally. The RRP is arguably the most significant pool class, released first in response to an activity train. Functional assays and time-stamped electron microscopy are used to define basic properties of this pool, including its size, functional release kinetics, and temporal organisation. Specifically, the results demonstrate that retrieved vesicles are close to the active zone after stimulation, but mixed randomly in the terminal volume over 20 min. These findings address fundamental questions about vesicle reuse, the composition of future vesicle pools, and thus the mechanism of ongoing signalling in the brain. The same approach was used in Chapter 5 to examine the influence of Long Term Depression (LTD) on pool function and ultrastructure. LTD was induced in presynaptic terminals in CA1 via Schaffer collateral activation, and the following effects were observed: 1) a change in release kinetics; 2) a reduction in the total recycling pool size; and 3) no change in the composition of the docked pool. These findings demonstrate that there is a presynaptic component to LTD and that vesicle recruitment into the recycling pool appears to be an important possible substrate. However, the results suggest that such changes appear to be selective for specific pool subsets. Overall, work in this chapter offers new insights into fundamental principles supporting synaptic plasticity. Chapter 6 expands on previous studies which have demonstrated that recycling vesicles are constitutively shared between neighbours. This sharing of a ‘superpool' of vesicles has implications for the ability of synapses to adapt to changes in input weighting. In this chapter, the methods outlined above, as well as a new 3D EM technology, are used to define the size, positional organisation, and clustering properties of this pool in native hippocampal slice system. The findings in this chapter reveal that extrasynaptic vesicles appear to show a greater degree of motility than vesicles which remain in the intrasynaptic cluster, perhaps implying differential interactions with structural proteins in the synapse. Characterising the superpool is increasingly relevant, as it is now implicated in models of plasticity and disease. Taken together, these results show that the ultrastructural arrangement of recycling vesicles is highly activity-dependent, and that the cytoarchitecture plays a large role in determining the functionality of individual vesicles and synapses.
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Devan, Bryan David. "Functional organization of the dorsal striatum : comparison to the hippocampal system". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ44408.pdf.
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Káli, Szabolcs 1972. "From space to episodes : modeling memory formation in the hippocampal-neocortical system". Thesis, Massachusetts Institute of Technology, 2001. http://hdl.handle.net/1721.1/8186.
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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Brain and Cognitive Sciences, 2001.Includes bibliographical references (p. 171-196).
This thesis describes the use of mathematical, statistical, and computational methods to analyze, in two paradigmatic areas, what the hippocampus and associated structures do, and how they do it. The first model explores the formation of place fields in the hippocampus. This model is constrained by hippocampal anatomy and physiology and data on the effects of environmental manipulations on the place cell representation. It is based on an attractor network model of area CA3 in which recurrent interactions create place cell representations from location- and direction-specific activity in the entorhinal cortex, all under neuromodulatory influence. In unfamiliar environments, mossy fiber inputs impose activity patterns on CA3, and recurrent collaterals and perforant path inputs are subject to graded Hebbian plasticity. Attractors are thus sculpted in CA3, and are associated with entorhinal activity patterns. In familiar environments, place fields are controlled by the way that perforant path inputs select amongst the attractors. Depending on training experience, the model generates place fields that are either directional or non-directional, and whose changes when the environment undergoes simple geometric transformations are in accordance with experimental data. Representations of multiple environments can be stored and recalled with little interference, and have the appropriate degrees of similarity in visually similar environments.
(cont.) The second model provides a serious test of the consolidation theory of hippocampal-cortical interactions. The neocortical component of the model is a hierarchical network structure, whose primary goal is to extract statistical structure from its set of inputs through unsupervised learning. This interacts with a hippocampal component, which is capable of fast learning, cue-based recall, and off-line replay of stored patterns. The model demonstrates the feasibility of hippocampally-dependent memory consolidation in a more general and realistic setting than earlier models. It reproduces basic characteristics of retrograde amnesia, together with some related phenomena such as repetition priming. The model clarifies the relationship between memory for general (semantic) and specific (episodic) information, suggesting that part of their underlying substrate may be shared. The model highlights some problematic aspects of consolidation theory, which need to be addressed by further experimental and theoretical studies.
by Szabolcs Káli.
Ph.D.
10
Patel, Kaushal S. "Post-TBI Hippocampal Neurogenesis in Different TBI Models". VCU Scholars Compass, 2016. http://scholarscompass.vcu.edu/etd/4134.
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Traumatic brain injury (TBI) leads to short-term and long-term consequences that can cause many different life-long disorders. Studies of TBI have generally focused on the acute stage; however, it is now becoming important to investigate chronic responses following TBI as clinical reports of dementia and cognitive impairments have been linked to a history of TBI. Recent data have established that cognitive function is associated with hippocampal neurogenesis. Chronic injury induced changes in the brain may affect this endogenous process. Chronic responses following TBI include cell death pathways and inflammatory responses that are persistent in the brain for months to years after injury. In this study we investigate the chronic consequences of TBI on adult neurogenesis and the possible involvement of chronic-inflammation in regulating adult neurogenesis. We used two popular TBI animal models, Control Cortical Impact (CCI) and Lateral Fluid Percussion Injury (LFPI) models, to examine focal and diffuse injury responses respectively. Adult rats received CCI, LFPI, or sham injury and were sacrificed at either 15 days or 3 months after injury to examine either subacute or chronic TBI-induced responses respectively. We found no change in levels of proliferation activity at both time points in both TBI models compared to sham animals. Using Doublecortin immunolabeling we found an enhanced generation of new neurons at 15 days after injury and by 3 months this activity was significantly reduced in both TBI models compared to sham animals. We also found persistent inflammation in the injured brains at both time points. Morphological assessment showed that LFPI model of TBI causes shrinkage of the ipsilateral hippocampus. Our results show that moderate TBI induced hippocampal neurogenesis in both models at the early time post-injury. However, at chronic stage, reduced hippocampal neurogenesis is observed in both models and this is accompanied by chronic inflammation. These results suggest that persistent inflammatory responses maybe detrimental to normal neurogenic activity, leading to cognitive impairment and neurodegeneration in long-term TBI survivors.
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Louie, LeeAnn N. "Inhibition of the Ubiquitin Proteasome System Enhances Long-Term Depression in Rat Hippocampal Slices". Scholarship @ Claremont, 2013. http://scholarship.claremont.edu/scripps_theses/274.
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The ubiquitin proteasome system (UPS) depends on three enzymes called E1, E2, and E3 to ubiquitinate proteins and several isopeptidases to de-ubiquitinate them. Ubiquitination serves as a post-translational modification that either tags proteins for degradation by the proteasome or serves to modulate their function. This dynamic system plays a role in synaptic plasticity and dysfunction of the UPS is associated a variety of neurodegenerative diseases. In this study, three inhibitors the UPS, ziram, clasto-lactacystin β-lactone (lactacystin) and G5 were employed to illuminate involvement of the UPS in long-term and short term plasticity in area CA1 of rat hippocampal slices. Ziram, lactacystin and G5 inhibits the E1 ubiquitin-activating enzyme, the proteasome and isopeptidases, respectively. It was found that UPS inhibition enhanced long-term plasticity, by specifically increasing the magnitude of long-term depression (LTD) and altered short term plasticity, measured with paired pulse facilitation (PPF), to varying degrees. These findings establish that the UPS may play a regulatory role in LTD and PPF, and the changes in PPF further indicate that the UPS may be acting presynaptically. Overall, the results suggest ubiquitination and proteasome-mediated proteolysis are important in both long-term and short-term plasticity.
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Harp, Phillip Allan. "System to compress while electrically stimulating hippocampal brain slices (SCWESH) : design, development, and electromechanical validation". Thesis, Georgia Institute of Technology, 1999. http://hdl.handle.net/1853/16828.
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Simpson, E. L. "Scene memory in rats : the hippocampal system and the encoding of two-dimension visual scenes". Thesis, University of Reading, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.297624.
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McNamara, Colin. "Relating the midbrain dopaminergic system to hippocampal cell assembly dynamics associated with spatial memory function". Thesis, University of Oxford, 2015. https://ora.ox.ac.uk/objects/uuid:5c116cc9-0d9a-4dd8-a343-abd233c68511.
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Central to the understanding of memory is a detailed understanding of the processes contributing to how some information is retained as memories, yet other information is not. Relevant to this is the question, does value and saliency information coded by dopaminergic neurons of the ventral tegmental area (VTA) affect hippocampal memory function and how might this arise? In order to address this question, I performed large scale extracellular recordings combined with optogenetic activation of dopaminergic neurons in mice. Tetrodes were located in the VTA and pyramidal cell layer of the CA1 subfield of the dorsal hippocampus. Midbrain dopaminergic neurons were made to express a chimeric protein formed of the light activated ion channel channelrhodopsin-2 and enhanced yellow florescent protein (ChR2-eYFP) through injection of a Cre activated viral construct in the VTA of DAT-IRES-Cre+/- mice. Mice explored familiar and novel open fields in the presence or absence of photostimulation. Periods of sleep and rest were recorded before and after each exploration in order to calculate the reactivation strength of hippocampal waking firing activity during subsequent sleep; a process thought to aid the stabilisation of representations enhancing their retention as memories. ChR2-eYFP expressing axons were present in the dorsal hippocampus demonstrating a direct dopaminergic projection from the midbrain to the hippocampus. Units isolated from midbrain tetrodes showed a sustained increase in mean firing rate during exploration of a novel over a familiar environment, indicating they have the potential to drive sustained dopamine release in target structures in response to such a sustained novelty cue. Hippocampal reactivation strength after exploration of a novel environment was higher than that seen after exploration of a familiar environment and this was further enhanced by burst mode photoactivation of dopaminergic neurons at their cell bodies in the VTA or at the afferent dopaminergic fibres in the dorsal CA1. A second group of mice performed a spatial learning task on a maze dubbed the 'crossword maze'. Photostimulation during learning trials did not increase the rate of learning but it did increase performance in a probe test held one hour after the end of the learning trials. Additionally, there was enhanced reinstatement of the hippocampal spatial representation during the probe test and it was preceded by enhanced reactivation of the newly formed representation in the intervening rest period. These findings reveal that midbrain dopaminergic neurons, encoding salient information about an environment, promote hippocampal network dynamics associated with memory persistence, thus modulating hippocampal memory function according to the value of the information to be remembered.
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Song, Jun. "Neuronal Adaptations in Rat Hippocampal CA1 Neurons during Withdrawal from Prolonged Flurazepam Exposure: Glutamatergic System Remodeling". Connect to Online Resource-OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=mco1177519349.
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Thesis (Ph.D.)--University of Toledo, 2007."In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Biomedical Sciences." Major advisor: Elizabeth Tietz. Includes abstract. Title from title page of PDF document. Bibliography: pages 88-94, 130-136, 178-189, 218-266.
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Gruber, David [Verfasser]. "The Role of the Hippocampal GABAergic System in the Development of Posttraumatic Stress Disorder / David Gruber". Berlin : Freie Universität Berlin, 2015. http://d-nb.info/1073868974/34.
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Döhring, Juliane [Verfasser]. "Structure function relationship of the hippocampal memory system in patients with an amnestic syndrome / Juliane Döhring". Kiel : Universitätsbibliothek Kiel, 2015. http://d-nb.info/1072410230/34.
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Littlejohn, Erica Latrice. "INSULIN-LIKE GROWTH FACTOR-1 OVEREXPRESSION MEDIATES HIPPOCAMPAL REMODELING AND PLASTICITY FOLLOWING TBI". UKnowledge, 2018. https://uknowledge.uky.edu/physiology_etds/39.
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Every year over 2.5 million traumatic brain injuries (TBI) occur and are the leading cause of death and disability among adolescents. There are no approved treatments for TBI. Survivors suffer from persistent cognitive impairment due to posttraumatic tissue damage and disruption of neural networks which significantly detract from their quality of life. Posttraumatic cognitive impairment depends in part on the brain's limited ability to repair or replace damaged cells. Immature neurons in the hippocampus dentate gyrus, a brain region required for learning and memory, are particularly vulnerable to TBI. Insulin-like growth factor-1 (IGF1) is a potential therapeutic for TBI because it is a potent neurotrophic factor capable of mediating neuroprotection, neuro-repair, and neurogenesis. We hypothesized that conditional IGF1 overexpression in the mouse hippocampus following experimental controlled cortical impact injury (CCI) would enhance posttraumatic neurogenesis chronically. To this end, conditional astrocyte-specific IGF1 overexpressing mice (IGFtg) and wild-type (WT) mice received CCI or sham injury. The proliferation marker BrdU was used to label neurons born the first week after injury. Six weeks after injury, when surviving posttrauma-born neurons would be fully developed, we counted proliferated cells (BrdU+) and the subset expressing a mature neuronal marker (NeuN+/BrdU+) in the hippocampus. We also assessed cognitive performance during radial arm water-maze reversal (RAWM-R) testing, a neurogenesis-sensitive assay. IGF1 promoted end-stage maturity and decreased mis-migration of neurons born after trauma. These effects coincide with IGF1 induced improvements in performance on neurogenesis sensitive cognition following TBI.
Mammalian target of rapamycin (mTOR), an early signaling molecule downstream of IGF1, has been identified as a potential target for TBI interventions because of its regulatory role in neuronal plasticity and neurogenesis. However, recent studies have also reported maladaptive plasticity and recovery associated with posttraumatic mTOR activation. It is imperative to elucidate the mechanism of action of IGF1 during pre-clinical evaluations. We hypothesized that IGF1 mediates posttraumatic neurogenic effects through IGF1 induction of mTOR activation. We injured cohorts of IGFtg and WT mice and harvested their brains for immunohistochemistry to assess IGF1 overexpression effects on posttraumatic mTOR activation at 1, 3, and 10 days post-injury (dpi). We found that IGF1 upregulated mTOR activation following TBI in a region-specific manner at 1 and 3dpi. To determine if IGF1 regulated differentiation and arborization through the mTOR pathway, injured WT and IGFtg mice received daily i.p. injections of rapamycin (10mg/kg), the inhibitor of mTOR, or its vehicle for 7 days. Vehicle and rapamycin administration began 3dpi, after the cells dividing at the peak of posttraumatic proliferation were labeled with BrdU. IGF1 enhancement of posttraumatic neurogenesis was not dependent on mTOR activation.
In summary, IGF1 directs newborn neuron localization, promotes end-stage maturation, and chronically improves cognition. IGF1 can stimulate posttraumatic neurogenesis and plasticity independent of mTOR activation. These data suggest that IGF1 can stimulate neuron replacement following trauma-induced hippocampal neuron loss and cognitive improvement. Further studies should investigate IGF1 and mTOR inhibition as a combination therapy for neurorehabilitation.
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Morris, Renée. "The association fiber system linking the mid-dorsolateral frontal cortex with the retrosplenial cortex and the posterior hippocampal region in the rhesus monkey". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0007/NQ30342.pdf.
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Morris, Renée. "The association fiber system linking the mid-dorsolateral frontal cortex with the retrosplenial cortex and the posterior hippocampal region in the rhesus monkey /". Thesis, McGill University, 1996. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=42100.
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The study of patients has shown that certain higher cognitive processes, such as those involved in the monitoring and the manipulation of information within working memory, depend on the integrity of both the dorsolateral frontal cortex and the medial temporal lobe memory system, as well as on their functional interaction (Petrides, 1994). Small surgical removal of the anterior temporal region, including the entorhinal cortex, is not sufficient to interrupt that fronto-hippocampal relationship. More extensive removals, however, that include a sizeable portion of the hippocampus and the surrounding parahippocampal cortex do disrupt such a fronto-hippocampal functional interaction (Petrides and Milner, 1982). Based on these data, it was postulated that the fronto-hippocampal functional interaction is not entirely dependent upon the integrity of the entorhinal cortex. To test this hypothesis, injections of tritiated amino acids were placed within individual cytoarchitectonic units of the frontal cortex, and the resulting labeling in the hippocampal region was analyzed. It was shown that the mid-dorsolateral frontal cortex, together with its medial cortical extension, is the only frontal region that sends efferent fibers, running caudally as part of the cingulum bundle, to the presubiculum, the posterior parahippocampal gyrus, as well as to the retrosplenial cortex. A light contingent of these fibers, congregating in the outermost layer of both the retrosplenium and the presubiculum, course into the molecular layer of the hippocampus proper. In complete agreement with the work with patients, these findings have confirmed the hypothesis that the mid-dorsolateral frontal cortex is closely affiliated with the hippocampal system, and demonstrated that this hodological relationship bypasses the entorhinal cortex.Another major contribution of the present work has been to provide the first architectonic analysis of a gross morphological region, referred to as the caudomedial lobule, which receives inputs from the mid-dorsolateral frontal cortex and its medial extension. This architectonic analysis has revealed that the caudomedial lobule is nothing but the postero-ventral extension, below the splenium of the corpus callosum, of areas 29 and 30, which together form the retrosplenial cortex, and of area 23, which partly forms the posterior cingulate cortex. Among the cortical fields that comprise the postero-ventral part of the retrosplenial cortex, area 30 is the major recipient of the mid-dorsolateral frontal inputs.
By virtue of the close anatomical relation of area 30 with the mid-dorsolateral frontal cortex and its medial extension, it is suggested that this part of the retrosplenial cortex may be a critical relay-station along the dorsomedially directed fronto-hippocampal pathway. In order to validate this hypothesis, the connections of area 30 were investigated by placing injections of anterograde and retrograde tracers within the limits of this retrosplenial area. This study has demonstrated that area 30 is bi-directionally connected with and only with that part of the lateral frontal cortex that lies above the sulcus principalis, namely the mid-dorsolateral frontal cortex, along with all the structures of the posterior hippocampal region that are the recipients of the inputs from the mid-dorsolateral frontal cortex. Since the fronto-hippocampal association fiber system described in the present thesis is most probably subserving certain aspects of working memory, area 30, by virtue of its bi-directional connections with both the mid-dorsolateral frontal cortex and the posterior parahippocampal cortex, is in a privileged position to exert a major influence in working memory processing.
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Silva, Daniel Giura da. "Extrapolação a partir de padrões seriais de estímulos é prejudicada por danos no tálamo anteroventral, em ratos". Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/41/41135/tde-17082017-092655/.
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De acordo com Gray (1982) o sistema nervoso monitora o ambiente e o comportamento continuamente, sendo capaz de inibir o comportamento em curso quando se depara com novidades ou com discrepâncias entre expectativas geradas com base em memórias de regularidades passadas e a informação sensorial presente, de modo a explorar a fonte de novidade ou discrepância e, assim, obter informações que possibilitem gerar previsões melhores no futuro. O sistema septo-hipocampal compararia estímulos presentes com informações antecipadas (ou previstas). Tal sistema envolve um comparador, o subículo, que receberia informações do presente através de aferências neocorticais, via córtex entorrinal, e informações \"previstas\" geradas em um \"circuito gerador de previsões\". Gray (1982) propôs que esse circuito gerador de previsões inclui o subículo, os corpos mamilares, o tálamo anteroventral, o córtex cingulado e, novamente, o subículo. Destas estruturas, o tálamo anteroventral encontra-se em posição privilegiada, do ponto de vista hodológico e experimental, para investigar este postulado circuito gerador de previsões. O objetivo do presente trabalho foi investigar o efeito da lesão seletiva no tálamo anteroventral, pela aplicação tópica de ácido N-metil-D-aspártico (NMDA), sobre a habilidade de ratos extrapolarem a partir de padrões seriais de estímulos. Tampão fosfato foi aplicado em sujeitos controle. Ratos da linhagem Wistar, machos, foram treinados a correr em uma pista reta para receberem reforço ao seu final. Em cada sessão (uma sessão por dia), os animais correram 4 tentativas sucessivas, recebendo quantidades diferentes de sementes de girassol em cada tentativa. No padrão monotônico decrescente os sujeitos receberam 14, 7, 3 e 1 sementes de girassol, enquanto os sujeitos expostos ao padrão não-monotônico receberam 14, 3, 7 e 1 sementes de girassol. Os animais foram treinados ao longo de 31 sessões. No 32° dia do experimento, uma quinta tentativa, nunca antes experienciada pelos animais, foi adicionada à sessão. Como esperado, os tempos de corrida na quinta tentativa dos animais controle expostos ao padrão monotônico decrescente foram substancialmente maiores se comparados aos animais controle expostos ao padrão não-monotônico, indicando a ocorrência de extrapolação. Em contraste, os sujeitos lesados expostos ao padrão monotônico não exibiram esse aumento de latência na quinta corrida, indicando que esses animais não extrapolaram. Em conclusão, os resultados indicam que extrapolação a partir de padrões seriais de estímulos é prejudicada pela lesão seletiva do tálamo anteroventralAccording to Gray (1982) the brain continuously monitors environment and behavior, being capable of inhibiting ongoing behaviors when facing novelty or detecting discrepancies involving predictions generated from memories of past regularities and the actual sensorial information, in order to explore the source of novelty and/or discrepancy, and thus to gather information for generating better predictions in the future. The septo-hippocampal system compares anticipated and present information. The comparator would be the subiculum. This brain structure would receive present information from neocortical afferents, via the entorhinal cortex, and expected information from a \"generator of predictions system\" including the subiculum, mammillary bodies, anteroventral thalamus, cingulate cortex and, again, the subiculum. The anteroventral thalamus is in a privileged position, both hodologically and experimentally, to allow investigation of this postulated generator of predictions system. This study investigated the effect of selective damage to the anteroventral thalamus, by topical application of N-Methyl-D-Aspartic acid (NMDA), on the ability of rats to extrapolate relying on serial stimulus patterns. Control subjects were injected with phosphate buffer. Male Wistar rats were trained to run through a straight alleyway to get rewarded. In each session (one session per day) the animal run four successive trials, one immediately after the other, receiving different amounts of sunflower seeds in each trial. While subjects exposed to the monotonic decremental schedule received 14, 7, 3, 1 sunflower seeds along trials, subjects exposed to the non-monotonic schedule received 14, 3, 7, 1 sunflower seeds. Subjects were trained along 31 sessions. Then, on the 32nd testing session, a fifth trial never experienced before by all subjects was included immediately after the fourth trial. As expected, running times on the fifth trial for Control subjects exposed to the monotonic schedule were significantly longer as compared to the corresponding scores of Control subjects exposed to the non-monotonic schedule, thus indicating the occurrence of extrapolation. In contrast, lesioned subjects exposed to the monotonic schedule did not exhibit this increase in running times on the fifth trial thus indicating that these subjects did not extrapolate. In conclusion, results indicate that extrapolation relying on serial stimulus patterns is disrupted following selective damage to the anteroventral thalamus
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Harland, Bruce. "Recovery of function after lesions of the anterior thalamic nuclei: CA1 neuromorphology". Thesis, University of Canterbury. Psychology, 2013. http://hdl.handle.net/10092/7644.
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The anterior thalamic nuclei (ATN) are a critical part of an extended hippocampal system that supports key elements of episodic memory. Damage or disconnection of the ATN is a component of clinical conditions associated with severe anterograde amnesisa such as the Korsakoff’s syndrome, thalamic stroke, and neurodegenerative disorders. Previous studies have demonstrated that the ATN and hippocampus are often interdependent, and that ATN damage can result in ‘covert pathology’ in ostensibly healthy distal regions of the extended hippocampal system. Adult male rats with neurotoxic bilateral ATN lesions or sham surgery were post-operatively housed in an enriched environment or standard housing after a lesion-induced spatial working memory deficit had been established. These rats were retested on cross-maze and then trained in radial-arm maze spatial memory tasks. Other enriched rats received pseudo-training only after the enrichment period. The detailed neuromorphology of neurons was subsequently examined in the hippocampal CA1. Soma characteristics were also examined in the retrosplenial granular b cortex and the prelimbic cortex. In Experiment 1, ATN lesions produced clear deficits in both the cross-maze and radial-arm maze tasks and reduced hippocampal CA1 dendritic complexity, length, and spine density, while increasing the average diameter of the dendrites. Post-operative enrichment reversed the ATN lesion-induced deficits in the cross-maze and radial-arm maze, and returned CA1 basal and apical spine density to a level comparable to that of sham standard housed trained rats. The sham enriched rats exhibited improved radial-arm maze performance and increased CA1 branching complexity and spine density in both basal and apical arbors compared to sham standard housed rats. The neuromorphological changes observed in the enriched ATN and sham rats may be in part responsible for the spatial working memory improvements observed. Experiment 2 provided support for this contention by demonstrating that the CA1 spine changes were explicitly relevant to spatial learning and memory, because trained enriched sham and ATN rats had increased spines, particularly in the basal tree when compared to closely comparable pseudo-trained enriched rats. Interestingly, spatial memory training increased the numbers of both thin and mushroom spines, whereas enrichment was only associated with an increase in thin spines. In Experiment 3, ATN lesions increased cell body size in layer II of the retrosplenial granular b cortex, whereas enrichment decreased cell body size in layer V of this region. Neither ATN lesions nor enrichment had any effect on cell body morphology in the prelimbic cortex. The current research provides some of the strongest evidence to date of ATN and hippocampal interdependence within the extended hippocampal system, and provides the first evidence of neuromorphological correlates of recovery after ATN lesions.
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Đorđević, Miloš [Verfasser], Stefanie [Gutachter] Schreiber i Michael [Gutachter] Falkenstein. "Hippocampal and cortical neuroplasticity and functional changes induced by vestibular system stimulation through various methods of balance training / Miloš Đorđević ; Gutachter: Stefanie Schreiber, Michael Falkenstein". Magdeburg : Universitätsbibliothek Otto-von-Guericke-Universität, 2019. http://d-nb.info/1220036293/34.
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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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Hu, Wen [Verfasser], Gabriele [Akademischer Betreuer] Flügge, Ralf [Akademischer Betreuer] Heinrich, Hubertus [Akademischer Betreuer] Jarry i Swen [Akademischer Betreuer] Hülsmann. "Effects of stress on the GABAergic system in the hippocampal formation and medial prefrontal cortex of the adult male rat / Wen Hu. Gutachter: Ralf Heinrich ; Hubertus Jarry ; Swen Hülsmann. Betreuer: Gabriele Flügge". Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2011. http://d-nb.info/1043030069/34.
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Santiago, Adriana Celestino. "Conexões aferentes da área de transição amígdalo-piriforme (APir) no rato". Universidade de São Paulo, 1999. http://www.teses.usp.br/teses/disponiveis/42/42137/tde-27032001-133255/.
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A área de transição amígdalo-piriforme (APir) está situada na confluência dos córtices piriforme, periamigdalóide e entorrinal lateral (ENTl). Com técnicas de rastreamento retrógrado foi observado que as principais aferências da APir se originam do bulbo olfativo, dos córtices piriforme, insular disgranular e agranular posterior, perirrinal, da formação hipocampal e da amígdala. Outras estruturas como o núcleo da banda diagonal de Broca, o pálido ventral, a substância inominada sublenticular, o tálamo da linha média, o núcleo dorsal da rafe, o locus coeruleus e a área parabraquial são fontes de aferências mais modestas a esta área de transição. A APir e o ENTl diferem no que diz respeito à origem de suas aferências mesocorticais, amigdalianas e talâmicas. Assim, a APir está em condições de integrar informações olfativas, gustativas, interoceptivas gerais e polissensoriais complexas e, através de suas projeções para a amígdala expandida, striatum ventral e formação hipocampal, influenciar a expressão de comportamentos motivados.The amygdalo-piriform transition area (APir) lies at the junction of the piriform, periamygdaloid and entorhinal cortices. The afferent connections of this olfactory district were studied with retrograde tracing methods using the cholera toxin B subunit and Fluoro-Gold as tracers. Our retrograde experiments showed that the main input sources to APir derive from the olfactory bulb, mesocortical and allocortical areas including the dysgranular insular, posterior part of the agranular insular, piriform, lateral entorhinal and perirhinal cortices, temporal field CA1 of Ammon horn, ventral subiculum, as well as the endopiriform nucleus and the amygdaloid complex (anterior basomedial, posterior basolateral and anterior, posterolateral, posteromedial cortical nuclei). Several other structures among which the diagonal band, ventral pallidum, sublenticular substantia inominatta, midline thalamic nuclei, dorsal raphe nucleus, locus coeruleus and parabrachial area provide more modest inputs to APir. Our results suggest in addition that projections from mesocortical areas, hippocampal formation and the posterior basolateral amygdaloid nucleus to APir are topographically organized. Fluoro-Gold injections in the ventrolateral entorhinal cortex indicate that the afferent connections of this district differ in many regards from the afferent connections of APir. Cortical and amygdaloid inputs suggest tha APir is chiefly involved in the processing of olfactory, gustatory, visceral and somesthesic information, whereas the ventrolateral entorhinal cortex seems to be more crucially related with visual and auditory processes. APir is also less densely projected upon by midline thalamic nuclei than the lateral entorhinal cortex. Taken as a whole our results suggest that APir is in position to relay highly integrated olfactory, gustatory, interoceptive and somesthesic information to the extended amygdala, ventral striatum and ventral subiculum, and as such modulate the expression of motivated and emotional behavior.
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Langlais, Valentin. "Contrôle de l'activité des récepteurs NMDA par la D-sérine : rôle des récepteurs astrocytaires EphB3 et CB1". Thesis, Bordeaux, 2016. http://www.theses.fr/2016BORD0211/document.
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Les astrocytes sont des partenaires clés des neurones. Dans l’hippocampe, et tout particulièrement au niveau des synapses CA3-CA1, en libérant la D-sérine, ces cellules gliales régulent l’activité des récepteurs glutamatergiques de type N-methyl-D-aspartate (NMDA) et de ce fait la mémoire synaptique, aussi connue sous le nom de plasticité synaptique à long terme. Cependant, le signal synaptique à l’origine de la libération de la D-sérine par les astrocytes reste à ce jour méconnu. De par des données rapportées dans la littérature nous nous sommes tout particulièrement intéressés aux récepteurs astrocytaires aux ephrins de type B3 (EphB3) et aux endocannabinoïdes de type 1 (CB1). Pour ce faire nous avons principalement utilisé une approche électrophysiologique sur des tranches aiguës d’hippocampe de souris adulte. Dans une première étude, nos données indiquent que l’activation des récepteurs EphB3 augmente la présence de D-sérine synaptique et en conséquence l’activité des récepteurs NMDA synaptiques. A l’inverse, leur inhibition diminue à la fois l’activité des récepteurs NMDA synaptiques et la potentialisation à long-terme qui en dépend (LTP ; une forme de plasticité synaptique à long terme). L’interaction EphB3-ephrinB3 contrôle donc la LTP en contrôlant la disponibilité en D-sérine synaptique. Dans une seconde étude, nous avons utilisé un modèle transgénique permettant d’inhiber l’expression des récepteurs CB1 astrocytaires (souris GFAP-CB1-KO). Nous avons découvert que la suppression de ces récepteurs diminue la disponibilité en D-sérine synaptique. De plus, nos travaux montrent que les récepteurs CB1 astrocytaires sont nécessaires à l’induction de la LTP via la D-serine. En conclusion, ces travaux de Thèse révèlent que les récepteurs astrocytaires EphB3 et CB1 régulent les fonctions dépendantes des récepteurs NMDA via le contrôle qu’ils exercent sur la disponibilité en D-sérineAstrocytes are key partners of neurons. In the hippocampus, and more particularly at CA3-CA1 synapses, by releasing D-serine, these glial cells regulate the activity of synaptic Nmethyl-D-aspartate (NMDA) receptors and thus synaptic memory, also known as long-term synaptic plasticity. Yet, the synaptic signal inducing D-serine release by astrocytes is still unknown. Based on interesting data from the literature we have investigated the role of the astrocytic receptors for ephrinB3 (EphB3) and endocannabinoids (CB1). To this end we used electrophysiological approaches on acute hippocampal slices of adult mice. In a first study, our data indicate on one hand that the activation of EphB3 receptors increases synaptic D-serine availability and in consequences the activity of synaptic NMDA receptor activity. On the other hand, inhibition of EphB3 receptors induces a decrease of synaptic NMDA receptor activity as well as the induction of the long-term potentiation (LTP; a form of long-term plasticity). Thus, EphB3-ephrinB3 interaction controls LTP induction through the availability of synaptic D-serine. In a second study, we used a transgenic model allowing the inhibition of CB1 receptors expression in astrocytes (GFAP-CB1-KO mice). We discovered that their deletion reduced synaptic D-serine availability. Our work shows that astrocytic CB1 receptors are necessary for LTP induction via this D-serine. All together, this PhD work reveals that astrocytic EphB3 and CB1 receptors regulate synaptic NMDA receptor functions through the control of D-serine availability
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Pins, Benoit de. "Pathophysiological role of Pyk2 in the nervous system Pyk2 in the amygdala modulates chronic stress sequelae via PSD-95-related microstructural changes Pyk2 modulates hippocampal excitatory synapses and contributes to cognitive deficits in a Huntington’s disease model". Thesis, Sorbonne université, 2019. http://www.theses.fr/2019SORUS073.
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Proline-rich tyrosine kinase 2 (Pyk2) est une tyrosine kinase dépendante du calcium de la famille de focal adhésion kinase (FAK). Cette thèse rapporte l’étude Pyk2 dans des conditions neuropathologiques in vivo, en utilisant des délétions conditionnelles ou totales de Pyk2 chez la souris. La délétion de Pyk2 dans l’hippocampe provoque des altérations synaptiques associées à des défauts de LTP et d’apprentissage lié à l’hippocampe confirmant l’importance de Pyk2 dans l’expression de la plasticité synaptique. Les maladies de Huntington et d’Alzheimer sont associées à un déficit du niveau total ou activé de Pyk2 dans l’hippocampe. Une surexpression de Pyk2 en utilisant un virus adéno-associé restaure les propriétés synaptiques ainsi que la mémoire. En parallèle, nous avons montré le bénéfice de la production de BDNF (un activateur connu de Pyk2) dans un modèle murin de la maladie d’Alzheimer. Dans l’amygdale en revanche, la délétion de Pyk2 empêche l’altération des épines et le développement de symptômes dépressifs induits par un stress chronique. Enfin, dans le striatum, le déficit de Pyk2 n’est pas associé aux mêmes altérations synaptiques observées ailleurs. Cependant, il s’accompagne d’une réponse altérée à une injection aiguë de cocaïne sans affectation de la sensibilisation locomotrice ou de la préférence de place conditionnée. Ce phénotype est récapitulé par la délétion de Pyk2 dans le noyau accumbens ou dans les neurones exprimant le récepteur D1, suggérant un rôle spécifique de Pyk2 dans ces neurones. Ce travail démontre un rôle important de Pyk2 dans les synapses et montre que son altération contribue au développement de troubles neurologiquesProline-rich tyrosine kinase 2 (Pyk2) is a calcium-dependent non-receptor tyrosine kinase of the focal adhesion kinase (FAK) family, enriched in forebrain neurons. In this thesis, I studied Pyk2 in neuropathological conditions in vivo, using total or conditional knock-out mice. Pyk2 deficit in the hippocampus resulted in alterations of NMDA receptors, PSD-95 and dendritic spines. These defects were associated with an impairment of CA1 LTP and hippocampal-related learning thus confirming the crucial importance of Pyk2 in the expression of synaptic plasticity. Huntington’s and Alzheimer’s diseases were associated with decreased in total Pyk2 or its activated forms in hippocampus. Overexpression of Pyk2 using adeno-associated virus rescued synaptic properties and memory deficits. In parallel with this main project, we showed the efficacy of astrocytic delivery of BDNF (a known activator of Pyk2) in a mouse model of Alzheimer’s disease. Conversely, deletion of Pyk2 in the amygdala prevented spine alterations and development of depressive-like symptoms induced by chronic unpredictable stress. Finally, in the striatum, Pyk2 deficiency was not associated with the synaptic defects observed in other brain areas. However, it decreased locomotor response to acute cocaine injection without altering locomotor sensitization and conditioned place preference. This phenotype was recapitulated by deletion of Pyk2 in the nucleus accumbens or in D1 receptor-expressing neurons suggesting a specific role of Pyk2 in these neurons. Taken together this work supports an important role for Pyk2 in synapses and shows that its alteration contributes to the development of neurological disorders
29
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.
30
Jafari, Mehrnoosh. "Disease-associated modulation of adult hippocampal neurogenesis". Diss., Ludwig-Maximilians-Universität München, 2014. http://nbn-resolving.de/urn:nbn:de:bvb:19-174174.
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Adult neurogenesis has been the focus of over 1500 articles in the past 10 years. Evidence for the continuous production of new neurons in the adult brain has raised hopes for new therapeutic approaches. On the other hand, the generation of new neurons is modulated in several neurological diseases and disorders, suggesting the involvement of the adult neurogenesis in their pathogenesis. Therefore, a better understanding of the disease-associated modulation of adult neurogenesis is essential for determining the most effective therapeutic strategy.
The purpose of this doctoral project was to investigate long-term adult hippocampal neurogenesis changes in two disease models. BrdU labeling in combination with various cellular markers, and genetic fate-mapping approach were used to reach this goal.
In the first experiment, the impact of the BeAN strain of the Theiler’s virus on hippocampal cell proliferation and neuronal progenitors was evaluated in two mouse strains which differ in the disease course. It was shown that Theiler’s murine encephalomyelitis virus can exert delayed effects on the hippocampal neurogenesis with long-term changes evident 90 days following the infection. The hippocampal changes proved to depend on strain susceptibility and might have been affected by microglial cells.
In the second experiment, hippocampal neurogenesis was analyzed based on genetic fate mapping of transgenic animals in the amygdala-kindling model of epilepsy. The number of new granule neurons added to the dentate gyrus was increased in kindled animals. A prior seizure history proved to be sufficient to induce a long-term net effect on neuron addition and an ongoing occurrence of seizures did not further increase the number of new neurons. Hypertrophic astrocytes were observed in the kindled animals suggesting that seizures result in structural changes of astrocytes that could be detected long after the termination of the insults.
The results of the experiments indicated the importance of methodological considerations in chronic studies of neurogenesis.
31
Gutierrez, Rodriguez Ana. "Anatomical Characterization of the Type-1 cannabinoid receptors in specific brain cell populations of mutant mice". Thesis, Bordeaux, 2016. http://www.theses.fr/2016BORD0236/document.
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Dans cette thèse l’expression du récepteur CB1 dans l’hippocampe de souris mutantes ré-exprimant spécifiquement le gène spécifiquement dans certains types cellulaires du cerveau tels que : les neurones glutamatergiques du télencéphale dorsal, et les neurones GABAergiques a été analysé. De plus, dans le but de connaître la distribution anatomique exacte des récepteurs CB1 astrogliaux par rapport aux synapses excitatrices et inhibitrices, j’ai étudié l’expression des récepteurs CB1 dans les astrocytes de souris exprimant le récepteur CB1 seulement dans les astrocytes et une souris mutante ciblée pour exprimer la protéine cytoplasmique hrGFP diffusible dans les cellules astrogliales, ce qui permet une meilleure détection des prolongements astrocytaires. Les conclusions de ce travail de thèse sont les suivantes : la distance la plus commune entre le récepteur CB1 astroglial et la synapse la plus proche est de 400 à 800 nm. La majorité des synapses entourées par des astrocytes immunopositifs pour le récepteur CB1 dans l’hippocampe, est de nature excitatrice. Les souris mutantes ré-exprimant le récepteur CB1 caractérisées dans ce travail de thèse montrent : 1) l’expression du récepteur CB1 dans différents types cellulaires, 2) la réexpression est limitée à une population neuronale particulière ou aux astrocytes, 3) les niveaux endogènes de récepteurs CB1 sont maintenus dans les différents types cellulaires ré-exprimant le récepteur CB1. De façon générale, ces résultats nous montrent que les souris mutantes ré-exprimant le récepteur CB1 sont d’excellents outils pour l’étude fonctionnelle et translationnelle sur le rôle de ce récepteur dans le cerveau sain ou pathologiqueThe Cannabinoid Type I receptor protein (CB1) expression in the hippocampus of rescue mice modified to express the gene exclusively in specific brain cell types: such as dorsal telencephalic glutamatergic neurons, or GABAergic neurons have been analyzed. Furthermore, aiming at knowing the exact anatomical distribution of the astroglial CB1 receptors with respect to the excitatory and inhibitory synapses, the CB1 receptor expression in astrocytes of mouse expressing CB1 receptor only in astrocytes and mutant mouse expressing the protein hrGFP into astrocytes (that allows for better detection of the astrocytic processes) have been also investigated. The results showed that the majority of the hippocampal synapses surrounded by CB1 receptor immunopositive astrocytes in the 400-800 nm range are of excitatory nature. Moreover, the CB1 receptor rescue mutant mice characterized in this Doctoral Thesis have proven 1) to express CB1 receptors in specific brain cell types; 2) the re-expression is limited to the particular brain cell populations; 3) the endogenous levels of CB1 receptors are maintained in the brain cell types re-expressing the receptor. Which makes this mutant mice excellent tools for functional and translational investigations on the role of the CB1 receptors in the normal and diseased brain
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Dissanayake, Watuthanthrige Dilshani Nadira. "Sensory gating in the hippocampus and the medial prefrontal cortex". Thesis, University of Nottingham, 2008. http://eprints.nottingham.ac.uk/29088/.
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Sensory gating is a mechanism by which irrelevant sensory information is filtered in the brain, enabling efficient information processing. The auditory conditioning-test paradigm, an index of sensory gating, measures the reduction in the auditory-evoked response (AER) produced by a test stimulus following an initial conditioning stimulus. Schizophrenic patients demonstrate a lack of attenuation of the test response measured in the P50 component of the cortical auditory-evoked potential. The N2/N40 auditory-evoked potential recorded from rat hippocampus is considered homologous to the human P50 wave. Altered glutamatergic neurotransmission and the endocannabinoid system have been implicated in the pathogenesis of schizophrenia with structural and functional abnormalities in the hippocampus and the medial prefrontal cortex (mPFC). The current study examined sensory gating using auditory conditioning-test paradigm in the dentate gyrus (DG) and the CA3 region of the hippocampus and in the medial prefrontal cortex (mPFC) before and after administration of N-Methyl- D-Aspartate (NMDA) receptor antagonist phencyclidine (PCP; 1 mg/kg, i.p) or the cannabinoid agonist WIN55,212-2 (1.2mg/kg, i.p). Electrophysiological recordings were conducted in Lister hooded rats, under isoflurane anaesthesia, during the presentation of paired auditory stimuli. Extracellular action potential spikes and local field potentials (LFPs) were recorded simultaneously using multi-electrode arrays and the effects of acute administration of PCP (1 mg/kg, i.p) or WIN55,212-2 (1.2mg/kg, i.p) was determined. Gating of the N2 wave was assessed by measuring the ratio of the Test to Conditioning response amplitude (T/C ratio); T/C ratio ≤ 50% was indicative of gating. Robust auditory-evoked potentials were recorded from the hippocampal CA3 and DG regions and the mPFC; some rats demonstrated auditory gating while others failed to. In rats that demonstrated gating of N2, mPFC showed higher T/C ratios and shorter conditioning response latencies compared to DG and CA3. PCP disrupted auditory gating in all three areas with a significant increase in test response amplitudes in the gating rats. PCP had no effect on T/C ratios in the non-gating rats. The atypical antipsychotic clozapine (5mg/kg, i.p) prevented PCP induced disruption of gating in the CA3, DG and mPFC. WIN55,212-2 disrupted auditory gating with a significant increase in test response amplitudes in the gating rats. WIN55,212-2 had no effect on T/C ratios in the non-gating rats. The cannabinoid receptor (CB1) antagonist SR141716A (1mg/kg, i.p) prevented WIN55,212-2 induced disruption of gating. Neither clozapine nor SR141716A had any effects on the non-gating rats. Both PCP and WIN55,212- 2 disrupted gating of the single-unit responses in the CA3, DG and mPFC, effects which were prevented by the pre- administration of clozapine or SR141716A. The non-gating rats may model some inhibitory deficits observed in schizophrenic patients. Administration of PCP disrupted auditory gating which was prevented by clozapine; similar deficits are observed in schizophrenic patients. Furthermore, cannabinoid receptor activation disrupted auditory gating which was prevented by CB1 receptor antagonism, suggesting the endocannabinoid system as a potential target for future clinical research in the treatment in schizophrenia.
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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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Billwiller, Francesca. "Activation du gyrus dentelé par le noyau supramammillaire au cours du sommeil paradoxal chez le rongeur : étude neuroanatomique et fonctionnelle". Thesis, Lyon, 2016. http://www.theses.fr/2016LYSE1025/document.
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Ce travail s'inscrit dans l'étude du réseau neuronal responsable de l'activation corticale au cours du sommeil paradoxal (SP) chez le rongeur. Dans la première partie de ma thèse, j'ai participé à la démonstration que cette activation est limitée à quelques structures limbiques déterminantes pour l'apprentissage, dont le gyrus dentelé de l'hippocampe (GD). Nous avons ensuite montré que l'activation du GD en SP est due à une projection issue du noyau supramammillaire (Sum). J'ai ensuite montré en combinant l'hybridation in situ d'un marqueur des neurones glutamatergiques et GABAergiques et l'immunohistochimie du FOS que les neurones du Sum latéral actifs en SP sont à la fois glutamatergiques et GABAergiques (GLU/GABA). Enfin, j'ai montré que l'augmentation du nombre de neurones FOS+ dans le GD dorsal en SP est abolie après la lésion neurochimique du Sum. De plus, la lésion du Sum induit une nette réduction de la densité de fibres glutamatergiques dans le GD dorsal. Ces résultats indiquent que les neurones du GD dorsal sont activés en SP par les neurones GLU/GABA du Sum latéral. Le deuxième objectif de ma thèse a été de déterminer la fonction de cette voie en SP. Ainsi j'ai utilisé la technique d'optogénétique afin d'inactiver ou activer les fibres GLU/GABA provenant du Sum localisées dans le GD dorsal au cours du SP. Nos résultats montrent que l'activation de ces fibres en SP induit une augmentation de la fréquence et de la puissance du thêta enregistré dans le GD. Ces résultats indiquent que la voie Sum-GD dorsal contrôle le thêta hippocampique et soutiennent l'hypothèse d'un rôle de cette voie dans les processus de consolidation mnésique prenant place au cours du SPDuring my PhD I studied the neuronal network responsible for cortical activation during paradoxical sleep (PS) in rodents. In the first part of my thesis, I participated to the demonstration that this activation is limited to a few limbic structures involved in learning, including the dentate gyrus of the hippocampus (DG). Then, we showed that the activation of DG during PS is due to a projection from the supramammillary nucleus (Sum). Besides, by combining the in situ hybridization of markers of GABAergic and glutamatergic neurons and FOS immunohistochemistry, I demonstrated that lateral Sum neurons active in SP are both glutamatergic and GABAergic (GLU/GABA). Finally, I showed that the increasing number of FOS+ neurons in the dorsal DG during PS is abolished by the neurochemical lesion of the Sum. In addition, the Sum lesion induces a clear reduction of the density of glutamatergic fibers in the dorsal DG. These results indicate that during PS, dorsal DG neurons are activated by GLU/GABA neurons located in the lateral Sum. The second aim of my thesis was to determine the function of this pathway during PS. To realize that, I inactivated or activated by optogenetics the Sum GLU/GABA fibers located in the dorsal GD during SP. Our results show that the activation of these fibers during SP induces an increase in the theta frequency and power recorded in the dorsal DG. These results indicate that the Sum-dorsal DG-pathway modulates the hippocampal theta and supports the hypothesis of a role of this pathway in the memory consolidation process during SP
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Hulme, Sarah R., i n/a. "Heterosynaptic metaplasticity in area CA1 of the hippocampus". University of Otago. Department of Psychology, 2009. http://adt.otago.ac.nz./public/adt-NZDU20090818.161738.
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Long-term potentiation (LTP) is an activity-dependent increase in the efficacy of synaptic transmission. In concert with long-term depression (LTD), this synaptic plasticity likely underlies some types of learning and memory. It has been suggested that for LTP/LTD to act as effective memory storage mechanisms, homeostatic regulation is required. This need for plasticity regulation is incorporated into the Bienenstock, Cooper and Munro (BCM) theory by a threshold determining LTD/LTP induction, which is altered by the previous history of activity (Bienenstock et al., 1982). The present work aimed to test key predictions of the BCM model. This was done using field and intracellular recordings in area CA1 of hippocampal slices from young, adult male Sprague-Dawley rats. The first prediction tested was that following a strong, high-frequency priming stimulation all synapses on primed cells will show inhibition of subsequent LTP and facilitation of LTD induction (heterosynaptic metaplasticity). This was confirmed using two independent Schaffer collateral pathways to the same CA1 pyramidal cells. Following priming stimulation to one pathway, LTP induction was heterosynaptically inhibited and LTD facilitated. To more fully investigate whether all synapses show metaplastic changes, the priming stimulation was given in a different dendritic compartment, in stratum oriens, prior to LTP induction in stratum radiatum. This experiment supported the conclusion that all synapses show inhibited LTP following priming. A second prediction of the BCM model is that metaplasticity induction is determined by the history of cell firing. To investigate this, cells were hyperpolarized during priming to completely prevent somatic action potentials. Under these conditions inhibitory priming of LTP was still observed, and thus somatic action potentials are not critical for the induction of the effect. The next aim was to determine the mechanism underlying heterosynaptic metaplasticity. One way in which plasticity induction can be altered is through changes in gamma-aminobutyric acid (GABA)-mediated inhibition of pyramidal cells. For this reason, it was tested whether blocking all GABAergic inhibition, for the duration of the experiment, would prevent priming of LTP. However, priming inhibited subsequent LTP and it was concluded that GABAergic changes do not underlie either the induction, or expression, of the metaplastic state. Proposed revisions to the BCM model predict that postsynaptic elevations in intracellular Ca�⁺ determine the induction of metaplasticity. There are many potential sources for postsynaptic Ca�⁺ elevations, including entry through N-methyl-D-asparate receptors (NMDARs) or voltage-dependent calcium channels (VDCCs), or release from intracellular stores. Results of the present work demonstrate that the inhibition of LTP is dependent on the release of Ca�⁺ from intracellular stores during priming; however this release is not triggered by Ca�⁺ entry through NMDARs or VDCCs, or via activation of metabotropic glutamate receptors. Overall, the present results show that, in accordance with the BCM model, a high level of prior activity induces a cell-wide metaplastic state, such that LTD is facilitated and LTP is inhibited. In contrast to predictions of the BCM model, this is not mediated by cell-firing during priming. Instead the release of Ca�⁺ from intracellular stores is critical for induction of the metaplastic state.
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Johansson, Sara. "Characterization of hippocampal slice cultures as model systems for neurodegenerative processes in Alzheimer's disease /". Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-541-0/.
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Sloan, Hazel L. "Operant analysis of cognitive behaviours dependent upon prefrontal and hippocampal systems of the brain". Thesis, Cardiff University, 2005. http://orca.cf.ac.uk/55988/.
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The hippocampus and the prefrontal cortex are two areas of the brain that are fundamental for a wide range of cognitive processes. Studies of both human patients who have incurred damage to these regions, and animals with circumscribed lesions, have led to a variety of theories concerning their contributions to cognitive behaviours. The hippocampus and the prefrontal cortex are connected anatomically, but the behavioural sequelae of experimental lesions have been shown to be dissociable. This thesis investigates the roles of the hippocampus and the prefrontal cortex in the rat, with a focus on delayed matching working memory tasks. Chapter 4 reports on a study which demonstrated a delay-dependent deficit on retention of delayed matching to position (DMTP) in the Skinner box following prefrontal lesions hippocampal lesions left performance intact. Neither lesion impaired the ability to switch between matching and non-matching rules. Chapter 5 describes an experiment which revealed that neither area was involved in postoperative acquisition of DMTP. Next, rats with lesions of the two main hippocampal pathways were assessed on retention of DMTP in Chapter 6. Lesions of the fornix revealed a delay-independent deficit, whereas entorhinal cortex lesions were without effect. Chapter 7 investigated recognition memory using a spontaneous novelty preference task. None of the lesions impaired performance on this task up to a 2 hour delay, however hippocampal lesions showed an impairment when a spatial component was included. Furthermore, there was a suggestion of both prefrontal and hippocampal involvement when memory for relative recency was assessed. Finally, Chapter 8 investigated a novel task in the Skinner box which combined both rules within one session. This task revealed a surprising pattern of results, with hippocampal lesions producing a dramatic impairment, whilst prefrontal lesions were without effect. Additionally, water maze data provided ample support for a hippocampal role in spatial memory.
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Gutnikov, Sergei A. "Behavioural studies of the NMDA system in rats". Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.294382.
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Ferrigan, Leanne M. "Synaptic interactions between cholinergic and GABAergic systems of the hippocampus". Thesis, University of Glasgow, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.410010.
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Bubner, Manja [Verfasser]. "Langzeittherapie mit Lithium bei bipolar-affektiv erkrankten Patienten in Remission: Tesla-Kernspinspektroskopie, auf hippocampale Gedächtnisleistungen sowie auf das Hypothalamus-Hypophysen-Nebennierenrinden-System : Funktionelle Auswirkungen auf neurochemische Metabolite des Hippocampus in der 3 / Manja Bubner". Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2006. http://d-nb.info/1021818550/34.
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Cannon, Richard L. "The Effect of Trimethyltin on the Cholinergic System of the Rat Hippocampus". Digital Commons @ East Tennessee State University, 1992. https://dc.etsu.edu/etd/2650.
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Trimethyltin (TMT) is a neurotoxin occurring in the environment. Exposure to (TMT) is known to destroy specific neuronal components of the hippocampus in the rat and to cause clinical symptoms in exposed humans, including mnemonic deficits, that indicate hippocampal involvement. In addition to hippocampal cell loss TMT causes significant increases in cholinergic markers such as acetylcholinesterase (AChE) stain density and choline acetyltransferase (ChAT) activity in the hippocampus of rats. However, despite these observations the effect of TMT on hippocampal cholinergic system has not been investigated in detail. The purpose of the present study was to elucidate more fully the consequences of TMT administration on the rat cholinergic system. To this end the effects of increasing doses of TMT and time after TMT administration on choline acetyltransferase (ChAT) activity as well as TMT's effect on cholinergic muscarinic receptors was examined. Results indicate that 4 and 6 mg/kg doses of TMT measurable neuropathological effects on pyramidal cells of the hippocampus. ChAT activity was increased in the hippocampus as a result of the 6 mg/kg dose. Six mg/kg TMT was observed to affect morphology differentially over time, with the various sub-fields examined being affected at different time intervals. The effect of time on increased ChAT activity after TMT-treatment was observed in the dentate gyrus prior to the CA1 region. The effect of 6 mg/kg TMT on muscarinic receptor distribution over time is first observed in CA1 and CA3c then CA3a-b of the subtype M$\sb2$. The subtype M$\sb1$ receptors are also affected in these regions but at later time intervals. The total distribution of muscarinic receptors is reduced in regions CA1 and CA3c. This is observed at similar time intervals as for M$\sb1$ receptors. The conclusions made as a result of these findings are: (1) That TMT's effect on ChAT activity and morphology of the rat hippocampus is both dose and time dependent; (2) That adverse effects of TMT on ChAT activity and morphology in sub-regions of the hippocampus are observed at different time intervals; and (3) That the distribution of the muscarinic receptors examined are affected by TMT in a regional manner dependent upon the time following administration of TMT.
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Griffiths, Martin Huw. "#beta#-Amyloidosis and the cholinergic system in ageing and Alzheimer's disease". Thesis, University of Newcastle Upon Tyne, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.263021.
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Ponomarenko, Alexei. "High frequency oscillations in hippocampus and amygdala modulation by ascending systems /". [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=968526209.
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McDonald, Robert James. "Interactions among learning and memory systems : amygdala, dorsal striatum, and hippocampus". Thesis, McGill University, 1994. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=28491.
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This series of experiments used the multiple learning and memory systems hypothesis of the mammalian nervous system to investigate the possibility that the amygdala, dorsal striatum, and hippocampal systems might, in certain situations, interact to produce behavior in the normal animal. Using variations of the conditioned-cue preference (CCP) task, evidence is presented showing that context-specific information acquired by the hippocampus interferes with acquisition of amygdala-based stimulus-reward learning. It was also demonstrated that there are amygdala-, dorsal striatum-, and hippocampus-based forms of place learning and that cue ambiguity and movement are important factors determining which of these learning and memory systems gain behavioral control in place learning situations. These findings provide evidence for interactions among learning and memory systems and implicate the amygdala and dorsal striatum in some types of non-hippocampal based place learning using distal cues.
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Bui, Loc. "Estimating the parameters of a vesicular storage and release system in rat hippocampus". Thesis, McGill University, 2011. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=103562.
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During high frequency stimulation, synaptic efficacy decreases due to the depletion of the readily releasable pool (RRP), and its replenishment is vital in maintaining synaptic transmission. According to the 'mobilization by liberation' model, stimulation and subsequent calcium accumulation frees vesicles from their cytoskeletal constraints, leading to the replenishment of the RRP. Additionally, okadaic acid (a phosphotase inhibitor) and staurosporine (a protein kinase inhibitor) have been shown to affect vesicular mobility. In this thesis, the 'mobilization by liberation' model is tested by evaluating how the dynamics of the vesicular system change with stimulation, calcium, temperature, and compounds which affect vesicular mobility. The parameters of a vesicular storage and release model were estimated using the excitatory post-synaptic currents recorded from rat hippocampal CA1 neurons. The fractional release increases with calcium, whereas the replenishment rate is calcium-independent. During long, high frequency stimulation, the fractional release remains constant and the replenishment rate decreases markedly and rapidly. Thus, stimulation induced changes of vesicular dynamics are not determined by calcium accumulation. Agents that affect vesicular mobility did not influence the replenishment rate, and these compounds were ineffective in influencing how the replenishment rate decreases with stimulation. Therefore, the replenishment of the RRP is unlikely to be associated with vesicular movement. The replenishment rate decreases during stimulation at low temperatures (< 22C), and it increases at high temperatures (> 28C). After prolonged stimulation, the replenishment rate recovers rapidly, to a steady-state level that is above its pre-stimulation estimate. The recovery of synaptic efficacy is thus an unreliable index of the replenishment rate. In conclusion, our results do not support the 'mobilization by liberation' model in excitatory synapses of the rat hippocampus, and future studies should clarify the underlying biophysical process of vesicular replenishment.Lors de la stimulation à haute fréquence, l'efficacité synaptique diminue en raison de l'appauvrissement du 'readily releasable pool' (RRP), et le remplissage est essentiel au maintien de la transmission synaptique. Selon le modèle de la 'mobilization by liberation', la stimulation et l'accumulation subséquente de calcium libèrent les vésicules de leurs contraintes au cytosquelette, menant à un remplissage accéléré du RRP. La mobilité vésiculaire est également modulée par la phosphorylation, et l'acide okadaïque (un inhibiteur de phosphatase) mène à une augmentation du trafique vésiculaire. Inversement, la staurosporine (un inhibiteur de protéine kinase) limite le mouvement vésiculaire. Selon la tradition, le taux de remplissage est estimé à partir de l'efficacité synaptique suivant l'épuisement du RRP. Dans cette thèse, le modèle de la 'mobilization by liberation' est testé en évaluant comment les dynamiques vésiculaires changent avec la stimulation, la calcium, la température, et des composés qui affectent la mobilité vésiculaire. Les paramètres du système de stockage et de relâchement vésiculaire étaient estimés à partir des enregistrements des courants post-synaptiques excitateurs des neurones CA1 de l'hippocampe de rat. Le relâchement fractionnel augmente avec la calcium, alors que le taux de remplissage est calcium-indépendant. Pendant de longues stimulations à haute fréquence, le relâchement fractionnel demeure constant et le taux de remplissage diminue de façon marquée et rapide. Ainsi les changements dans la dynamique vésiculaires induits par la stimulation ne sont pas déterminés par l'accumulation de calcium. Les agents qui affectent la mobilité vésiculaire n'influencent pas le taux de remplissage, et ces composés n'ont pas d'effet sur la diminution du taux de remplissage lors de la stimulation. Ainsi, le remplissage du RRP n'est vraisemblablement pas associé au mouvement vésiculaire. Le taux de remplissage diminue durant la stimulation à faibles températures (< 22C), et augmente à des températures plus élevées (> 28C). Suite à une stimulation prolongée, le taux de remplissage reprend rapidement, à un niveau stable, qui est supérieur à l'estimé de pré-stimulation. La reprise de l'efficacité synaptique est ainsi un indice incertain du taux de remplissage. En conclusion, nos résultats éliminent le modèle de la 'mobilization by liberation', et des études futures devront clarifiées les processus biophysiques sous-jacents au remplissage vésiculaire.
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Woodhall, Gavin Lawrence. "The role of glutamate receptors at the CA3/CA1 Schaffer collateral/commissural synapse of rat hippocampus". Thesis, University of Southampton, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.295902.
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Subramanian, Shanmugam Suresh Kannan. "Genetic regulation of adult hippocampal neurogenesis: A Systems genetics approach using BXD recombinant inbred mouse strains". Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2012. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-88637.
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Adult hippocampal neurogenesis is regulated at various levels and by various factors. Genetic influence is an important key determinant of adult neurogenesis and exerts its effects at all levels. In vivo studies have suggested that adult hippocampal neurogenesis is highly variable and heritable among different laboratory strains of mice. To dissect the genetic effect from other contributing factors, it is necessary to study adult neurogenesis under highly controlled environment conditions. We extracted adult hippocampal precursor cells (AHPCs) from 20 strains of the BXD set of recombinant inbred mice, cultured them and studied the effect of genetic background on neurogenesis.
The BXD panel consists of mouse lines derived from an intercross between inbred parentals C57BL/6J and DBA/2J. Both of the parentals are fully sequenced and all the strains are well characterized in terms of genotypic and phenotypic characteristics. This allows us to use advanced genetic techniques to identify novel genomic loci and gene-gene interactions important in adult neurogenesis. Comparison of the AHPCs from 20 BXD strains, with respect to cell proliferation and neuronal and astrocytic differentiation in vitro, revealed a large variation for these traits across the strains. Proliferation, as measured by BrdU incorporation, showed over two- fold differences between the extremes.
Similar differences were observed for neurogenic (4-fold) and astrogenic differentiation (2-fold). These three traits all showed strong heritability values indicating that the differences were mainly attributed to the genetic component. QTL mapping, with these phenotypic data, revealed that there was no major contribution from single loci controlling these traits. Instead, we found many loci with smaller effects associated with these traits. Gene expression profiling using RNA samples from proliferating cultures of the 20 BXD mice strains yielded two cis eQTL candidates that directly regulated proliferation, LRP6 and Chchd8. LRP6 is well known as a co-receptor of Wnt signaling, but the function of Chchd8 is not known. Further experimentation, using over expression and gene silencing demonstrated that LRP6 negatively regulates AHPCs proliferation. Thus, from this study using a system genetics approach, we were able to identify, LRP6 as a novel regulator of adult hippocampal neurogenesis.
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Riel, Els van. "Dysregulation of the HPA-axis implications for serotonin responses in the hippocampus /". [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2004. http://dare.uva.nl/document/73464.
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Arleo, Angelo. "Spatial learning and navigation in neuro-mimetic systems : modeling the rat hippocampus /". [S.l.] : [s.n.], 2000. http://library.epfl.ch/theses/?nr=2312.
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Kibler, Andrew B. "EPILEPTIFORM PROPAGATION IN THE HIPPOCAMPUS AND A RECORDING ARRAY SYSTEM FOR IN-VITRO ANALYSIS". Case Western Reserve University School of Graduate Studies / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=case1303323835.
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