Relevant bibliographies by topics / Hippocampal CA3

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Academic literature on the topic 'Hippocampal CA3'

Author: Grafiati
Published: 6 September 2023

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Journal articles on the topic "Hippocampal CA3"

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Ang, Mary Jasmin, Sueun Lee, Mai Wada, Poornima D. E. Weerasinghe-Mudiyanselage, Sung-Ho Kim, Taekyun Shin, Tae-Il Jeon, Seung-Soon Im, and Changjong Moon. "SREBP-1c Deficiency Affects Hippocampal Micromorphometry and Hippocampus-Dependent Memory Ability in Mice." International Journal of Molecular Sciences 22, no. 11 (June 5, 2021): 6103. http://dx.doi.org/10.3390/ijms22116103.

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Changes in structural and functional neuroplasticity have been implicated in various neurological disorders. Sterol regulatory element-binding protein (SREBP)-1c is a critical regulatory molecule of lipid homeostasis in the brain. Recently, our findings have shown the potential involvement of SREBP-1c deficiency in the alteration of novel modulatory molecules in the hippocampus and occurrence of schizophrenia-like behaviors in mice. However, the possible underlying mechanisms, related to neuronal plasticity in the hippocampus, are yet to be elucidated. In this study, we investigated the hippocampus-dependent memory function and neuronal architecture of hippocampal neurons in SREBP-1c knockout (KO) mice. During the passive avoidance test, SREBP-1c KO mice showed memory impairment. Based on Golgi staining, the dendritic complexity, length, and branch points were significantly decreased in the apical cornu ammonis (CA) 1, CA3, and dentate gyrus (DG) subregions of the hippocampi of SREBP-1c KO mice, compared with those of wild-type (WT) mice. Additionally, significant decreases in the dendritic diameters were detected in the CA3 and DG subregions, and spine density was also significantly decreased in the apical CA3 subregion of the hippocampi of KO mice, compared with that of WT mice. Alterations in the proportions of stubby and thin-shaped dendritic spines were observed in the apical subcompartments of CA1 and CA3 in the hippocampi of KO mice. Furthermore, the corresponding differential decreases in the levels of SREBP-1 expression in the hippocampal subregions (particularly, a significant decrease in the level in the CA3) were detected by immunofluorescence. This study suggests that the contributions of SREBP-1c to the structural plasticity of the mouse hippocampus may have underlain the behavioral alterations. These findings offer insights into the critical role of SREBP-1c in hippocampal functioning in mice.
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Świetlik, Dariusz, Jacek Białowąs, Janusz Moryś, Ilona Klejbor, and Aida Kusiak. "Computer Modeling of Alzheimer’s Disease—Simulations of Synaptic Plasticity and Memory in the CA3-CA1 Hippocampal Formation Microcircuit." Molecules 24, no. 10 (May 17, 2019): 1909. http://dx.doi.org/10.3390/molecules24101909.

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This paper aims to present computer modeling of synaptic plasticity and memory in the CA3-CA1 hippocampal formation microcircuit. The computer simulations showed a comparison of a pathological model in which Alzheimer’s disease (AD) was simulated by synaptic degradation in the hippocampus and control model (healthy) of CA3-CA1 networks with modification of weights for the memory. There were statistically higher spike values of both CA1 and CA3 pyramidal cells in the control model than in the pathological model (p = 0.0042 for CA1 and p = 0.0033 for CA3). A similar outcome was achieved for frequency (p = 0.0002 for CA1 and p = 0.0001 for CA3). The entropy of pyramidal cells of the healthy CA3 network seemed to be significantly higher than that of AD (p = 0.0304). We need to study a lot of physiological parameters and their combinations of the CA3-CA1 hippocampal formation microcircuit to understand AD. High statistically correlations were obtained between memory, spikes and synaptic deletion in both CA1 and CA3 cells.
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Świetlik, Dariusz, Jacek Białowąs, Janusz Moryś, Ilona Klejbor, and Aida Kusiak. "Effects of Inducing Gamma Oscillations in Hippocampal Subregions DG, CA3, and CA1 on the Potential Alleviation of Alzheimer’s Disease-Related Pathology: Computer Modeling and Simulations." Entropy 21, no. 6 (June 13, 2019): 587. http://dx.doi.org/10.3390/e21060587.

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The aim of this study was to evaluate the possibility of the gamma oscillation function (40–130 Hz) to reduce Alzheimer’s disease related pathology in a computer model of the hippocampal network dentate gyrus, CA3, and CA1 (DG-CA3-CA1) regions. Methods: Computer simulations were made for a pathological model in which Alzheimer’s disease was simulated by synaptic degradation in the hippocampus. Pathology modeling was based on sequentially turning off the connections with entorhinal cortex layer 2 (EC2) and the dentate gyrus on CA3 pyramidal neurons. Gamma induction modeling consisted of simulating the oscillation provided by the septo-hippocampal pathway with band frequencies from 40–130 Hz. Pathological models with and without gamma induction were compared with a control. Results: In the hippocampal regions of DG, CA3, and CA1, and jointly DG-CA3-CA1 and CA3-CA1, gamma induction resulted in a statistically significant improvement in terms of increased numbers of spikes, spikes per burst, and burst duration as compared with the model simulating Alzheimer’s disease (AD). The positive maximal Lyapunov exponent was negative in both the control model and the one with gamma induction as opposed to the pathological model where it was positive within the DG-CA3-CA1 region. Gamma induction resulted in decreased transfer entropy in accordance with the information flow in DG → CA3 and CA3 → CA1. Conclusions: The results of simulation studies show that inducing gamma oscillations in the hippocampus may reduce Alzheimer’s disease related pathology. Pathologically higher transfer entropy values after gamma induction returned to values comparable to the control model.
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Blom, Kim, Huiberdina L. Koek, Maarten H. T. Zwartbol, Rashid Ghaznawi, Hugo J. Kuijf, Theo D. Witkamp, Jeroen Hendrikse, Geert Jan Biessels, and Mirjam I. Geerlings. "Vascular Risk Factors of Hippocampal Subfield Volumes in Persons without Dementia: The Medea 7T Study." Journal of Alzheimer's Disease 77, no. 3 (September 29, 2020): 1223–39. http://dx.doi.org/10.3233/jad-200159.

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Background: Vascular risk factors have been associated with risk of Alzheimer’s disease (AD) and volume loss of the hippocampus, but the associations with subfields of the hippocampus are understudied. Knowing if vascular risk factors contribute to hippocampal subfield atrophy may improve our understanding of vascular contributions to neurodegenerative diseases. Objective: To investigate the associations between age, sex, and vascular risk factors with hippocampal subfields volumes on 7T MRI in older persons without dementia. Methods: From the Medea 7T study, 283 participants (67±9 years, 68% men) without dementia had 7T brain MRI and hippocampal subfield segmentation. Subfields were automatically segmented on the 3D T2-weighted 7T images with ASHS software. Using linear mixed models, we estimated adjusted associations of age, sex, and vascular risk factors with z-scores of volumes of the entorhinal cortex (ERC), subiculum (SUB), Cornu Ammonis (CA)1, CA2, CA3, CA4, and dentate gyrus (DG), and tail as multivariate correlated outcomes. Results: Increasing age was associated with smaller volumes in all subfields, except CA4/DG. Current smoking was associated with smaller ERC and SUB volumes; moderate alcohol use with smaller CA1 and CA4/DG, obesity with smaller volumes of ERC, SUB, CA2, CA3, and tail; and diabetes mellitus with smaller SUB volume. Sex, former smoking, and hypertension were not associated with subfield volumes. When formally tested, no risk factor affected the subfield volumes differentially. Conclusion: Several vascular risk factors were associated with smaller volumes of specific hippocampal subfields. However, no statistical evidence was found that subfields were differentially affected by these risk factors.
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Zapukhliak, O. S., O. V. Netsyk, and D. S. Isaev. "SYNCHRONIZATION OF EPILEPTIFORM ACTIVITY BETWEEN CA1 AND CA3 HIPPOCAMPAL FIELDS UNDER SYNAPTIC AND NON-SYNAPTIC CONDITIONS IN RAT BRAIN SLICES." Medical Science of Ukraine (MSU) 16, no. 1 (February 28, 2020): 3–7. http://dx.doi.org/10.32345/2664-4738.1.2020.01.

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Relevance. Over-synchronization of neuronal activity results in epileptic-like discharges that can lead to seizures and status epilepticus. Understanding mechanisms of neural net synchronization could provide new insights into the treatment of epileptic disorders. Objective: to compare the levels of synchronization between CA3 and CA1 hippocampal zones during epileptiform activity induced under synaptic and non-synaptic conditions. Materials and Methods. Transverse brain slices were obtained from 12-14 days old rats. For induction of epileptiform activity common pro-epileptic agents were used: bicuculline and 4-aminopiridine. Nonsynaptic epileptiform activity was induced by perfusion brain slices with low-Ca2+ and Cd2+-containing artificial cerebrospinal fluid (aCSF). Simultaneous extracellular recordings of field potentials were obtained from the CA3 and CA1 pyramidal cell layer with extracellular glass microelectrodes (2–3 MΩ). Signals were then low-pass filtered (kHz), amplified using a 2-channel differential amplifier M1800, digitized at 10 kHz using analog-to-digital converter. The level of synchronization between CA3 and CA1 was evaluated using cross-correlation analysis. Results: Perfusion hippocampal slices with bicuculline and 4-aminopyridine induced epileptiform activity with high level of synchronization between CA3 and CA1 hippocampal zones. Removing Ca2+ from extracellular solution as well as adding CdCl2 to the perfusion aCSF induced epileptiform activity that was not synchronized between hippocampal CA3 and CA1 fields. Conclusions: Synaptic interaction account for high level of CA3-CA1 synchronization induced by pro-epileptic agents bicuculline and 4-aminopiridine. Under non-synaptic conditions, local cellular interactions induce epileptiform activity with no synchronization between CA3 and CA1 hippocampal zones.
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Zapukhliak, Olha, Olga Netsyk, Artur Romanov, Oleksandr Maximyuk, Murat Oz, Gregory L. Holmes, Oleg Krishtal, and Dmytro Isaev. "Mecamylamine inhibits seizure-like activity in CA1-CA3 hippocampus through antagonism to nicotinic receptors." PLOS ONE 16, no. 3 (March 12, 2021): e0240074. http://dx.doi.org/10.1371/journal.pone.0240074.

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Cholinergic modulation of hippocampal network function is implicated in multiple behavioral and cognitive states. Activation of nicotinic and muscarinic acetylcholine receptors affects neuronal excitability, synaptic transmission and rhythmic oscillations in the hippocampus. In this work, we studied the ability of the cholinergic system to sustain hippocampal epileptiform activity independently from glutamate and GABA transmission. Simultaneous CA3 and CA1 field potential recordings were obtained during the perfusion of hippocampal slices with the aCSF containing AMPA, NMDA and GABA receptor antagonists. Under these conditions, spontaneous epileptiform discharges synchronous between CA3 and CA1 were recorded. Epileptiform discharges were blocked by addition of the calcium-channel blocker Cd2+ and disappeared in CA1 after a surgical cut between CA3 and CA1. Cholinergic antagonist mecamylamine abolished CA3-CA1 synchronous epileptiform discharges, while antagonists of α7 and α4β2 nAChRs, MLA and DhβE, had no effect. Our results suggest that activation of nicotinic acetylcholine receptors can sustain CA3-CA1 synchronous epileptiform activity independently from AMPA, NMDA and GABA transmission. In addition, mecamylamine, but not α7 and α4β2 nAChRs antagonists, reduced bicuculline-induced seizure-like activity. The ability of mecamylamine to decrease hippocampal network synchronization might be associated with its therapeutic effects in a wide variety of CNS disorders including addiction, depression and anxiety.
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Wu, Chiping, Marjan Nassiri Asl, Jesse Gillis, Frances K. Skinner, and Liang Zhang. "An In Vitro Model of Hippocampal Sharp Waves: Regional Initiation and Intracellular Correlates." Journal of Neurophysiology 94, no. 1 (July 2005): 741–53. http://dx.doi.org/10.1152/jn.00086.2005.

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During slow wave sleep and consummatory behaviors, electroencephalographic recordings from the rodent hippocampus reveal large amplitude potentials called sharp waves. The sharp waves originate from the CA3 circuitry and their generation is correlated with coherent discharges of CA3 pyramidal neurons and dependent on activities mediated by AMPA glutamate receptors. To model sharp waves in a relatively large hippocampal circuitry in vitro, we developed thick (1 mm) mouse hippocampal slices by separating the dentate gyrus from the CA2/CA1 areas while keeping the functional dentate gyrus-CA3-CA1 connections. We found that large amplitude (0.3–3 mV) sharp wave-like field potentials occurred spontaneously in the thick slices without extra ionic or pharmacological manipulation and they resemble closely electroencephalographic sharp waves with respect to waveform, regional initiation, pharmacological manipulations, and intracellular correlates. Through measuring tissue O2, K+, and synaptic and single cell activities, we verified that the sharp wave-like potentials are not a consequence of anoxia, nonspecific elevation of extracellular K+ and dissection-related tissue damage. Our data suggest that a subtle but crucial increase in the CA3 glutamatergic activity effectively recruits a population of neurons thus responsible for the generation of the sharp wave-like spontaneous field potentials in isolated hippocampal circuitry.
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Nwaubani, P., A. Colasanti, M. Cercignani, and A. Warner. "MRI Analysis: Optimization of parameters for diffusion MRI to enhance hippocampal subfield analysis and segmentation (Preliminary Data)." European Psychiatry 65, S1 (June 2022): S638. http://dx.doi.org/10.1192/j.eurpsy.2022.1637.

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Introduction The hippocampus is an important, complex limbic structure anatomically embedded in the medial temporal lobe of each cerebral cortex, which has been implicated in the pathogenesis of neuro-inflammatory disease conditions. Few studies have focused on the characterization of the MRI neuroimaging signatures of highly physio- pathologically relevant subfields of the hippocampus (CA1, CA4-DG, CA2/CA3, SLRM). Objectives Using self-guided manually segmented, Diffusion weighted and NODDI maps created from data obtained from the Human Connectome Project (HCP) we intend to test whether Diffusion MRI-based quantitative imaging parameters (MD, FA, ODI, ISOVF, ICVF), indicative of microstructural characteristics of major hippocampal subfields (CA1, CA2/CA3, CA4-DG and SLRM), correspond to predictions for animal literature and imaging-histology correlations. We will also explore the correlations between these parameters and age. Methods We used images from the Public connectome data (updated April 2018), exploring subjects with the 3T MRI sessions obtainable from the WU-Minn HCP Data section. For the purpose of this study, we selected and downloaded 10 preliminary imaging data (6 females and 4 males) based on age variability in the following ranges (26-30, 31-35 and 36+). We manually segmented, and computed quantitative parameters. Results Converging and consistent literature allude to decreasing volumes with increasing age. Analyzing the volumes from the diffusion maps (pilot data), this was also the case, with volumes computed from CA1 and DG-CA4 sub regions. IQT also allowed for better appreciation of neuroanatomical boundaries and land marks, hence allowing more regions to be easily manually segmented (addition of CA2/CA3). Conclusions Application to Neuroinflammatory imaging data. Disclosure No significant relationships.
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Stojanovic, Tamara, David Velarde Gamez, Gabor Jorrid Schuld, Daniel Bormann, Maureen Cabatic, Pavel Uhrin, Gert Lubec, and Francisco J. Monje. "Age-Dependent and Pathway-Specific Bimodal Action of Nicotine on Synaptic Plasticity in the Hippocampus of Mice Lacking the miR-132/212 Genes." Cells 11, no. 2 (January 13, 2022): 261. http://dx.doi.org/10.3390/cells11020261.

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Nicotine addiction develops predominantly during human adolescence through smoking. Self-administration experiments in rodents verify this biological preponderance to adolescence, suggesting evolutionary-conserved and age-defined mechanisms which influence the susceptibility to nicotine addiction. The hippocampus, a brain region linked to drug-related memory storage, undergoes major morpho-functional restructuring during adolescence and is strongly affected by nicotine stimulation. However, the signaling mechanisms shaping the effects of nicotine in young vs. adult brains remain unclear. MicroRNAs (miRNAs) emerged recently as modulators of brain neuroplasticity, learning and memory, and addiction. Nevertheless, the age-dependent interplay between miRNAs regulation and hippocampal nicotinergic signaling remains poorly explored. We here combined biophysical and pharmacological methods to examine the impact of miRNA-132/212 gene-deletion (miRNA-132/212−/−) and nicotine stimulation on synaptic functions in adolescent and mature adult mice at two hippocampal synaptic circuits: the medial perforant pathway (MPP) to dentate yrus (DG) synapses (MPP-DG) and CA3 Schaffer collaterals to CA1 synapses (CA3–CA1). Basal synaptic transmission and short-term (paired-pulse-induced) synaptic plasticity was unaltered in adolescent and adult miRNA-132/212−/− mice hippocampi, compared with wild-type controls. However, nicotine stimulation promoted CA3–CA1 synaptic potentiation in mature adult (not adolescent) wild-type and suppressed MPP-DG synaptic potentiation in miRNA-132/212−/− mice. Altered levels of CREB, Phospho-CREB, and acetylcholinesterase (AChE) expression were further detected in adult miRNA-132/212−/− mice hippocampi. These observations propose miRNAs as age-sensitive bimodal regulators of hippocampal nicotinergic signaling and, given the relevance of the hippocampus for drug-related memory storage, encourage further research on the influence of miRNAs 132 and 212 in nicotine addiction in the young and the adult brain.
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Daugherty, Ana M., Hillary D. Schwarb, Matthew D. J. McGarry, Curtis L. Johnson, and Neal J. Cohen. "Magnetic Resonance Elastography of Human Hippocampal Subfields: CA3-Dentate Gyrus Viscoelasticity Predicts Relational Memory Accuracy." Journal of Cognitive Neuroscience 32, no. 9 (September 2020): 1704–13. http://dx.doi.org/10.1162/jocn_a_01574.

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The hippocampus is necessary for binding and reconstituting information in relational memory. These essential memory functions are supported by the distinct cytoarchitecture of the hippocampal subfields. Magnetic resonance elastography is an emerging tool that provides sensitive estimates of microstructure vis-à-vis tissue mechanical properties. Here, we report the first in vivo study of human hippocampal subfield viscoelastic stiffness and damping ratio. Stiffness describes resistance of a viscoelastic tissue to a stress and is thought to reflect the relative composition of tissue at the microscale; damping ratio describes relative viscous-to-elastic behavior and is thought to generally reflect microstructural organization. Measures from the subiculum (combined with presubiculum and parasubiculum), cornu ammonis (CA) 1–2, and CA3-dentate gyrus (CA3-DG) were collected in a sample of healthy, cognitively normal men ( n = 20, age = 18–33 years). In line with known cytoarchitecture, the subiculum demonstrated the lowest damping ratio, followed by CA3-DG and then combined CA1–CA2. Moreover, damping ratio of the CA3-DG—potentially reflective of number of cells and their connections—predicted relational memory accuracy and alone replicated most of the variance in performance that was explained by the whole hippocampus. Stiffness did not differentiate the hippocampal subfields and was unrelated to task performance in this sample. Viscoelasticity measured with magnetic resonance elastography appears to be sensitive to microstructural properties relevant to specific memory function, even in healthy younger adults, and is a promising tool for future studies of hippocampal structure in aging and related diseases.
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Dissertations / Theses on the topic "Hippocampal CA3"

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Kyle, Colin T., and Colin T. Kyle. "Cytoarchitectonically-Driven MRI Atlas of the Hippocampus and the Behavioral Impact of Neural Recording Devices: Addressing Methodological Concerns for Studies of Age-Related Change in Hippocampal Subfields." Thesis, The University of Arizona, 2017. http://hdl.handle.net/10150/625684.

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The hippocampal formation forms a circuit of cytoarchitectonically distinct subregions, and substantial evidence suggests each region makes unique computational contributions that support spatial and episodic memory. With aging, hippocampal subfields undergo unique neurobiological alterations, and primate in vivo work making use of both MR imaging and chronic neural recording devices has important links to changes seen in nonprimate animal models with aging (Thome et al., 2016; Yassa et al., 2011a; Yassa et al., 2010). While MRI offers a noninvasive way to study the hippocampal subfields, identifying hippocampal subregions without using post mortem histology is a challenge. When different research labs attempted to identify the hippocampal subregions using a single subject’s MRI, researchers showed significant disagreement in where to label different subregions (Yushkevich et al., 2015a). Alternatively, chronic neural recording devices offer an invasive solution to studying hippocampal subfields. However, it is currently not clear whether the mechanical trauma and foreign body response produced by neural recording devices disrupts neural circuits critical for behavior. Here, my colleagues and I address these issues with in vivo primate research. Chapter I provides a general introduction to the hippocampal circuits and changes observed in aging. Chapter II presents novel methods for construction of a histology-driven MRI atlas of nonhuman primate hippocampus that addresses accurate identification of hippocampal subfields in MR images. Chapter III presents empirical work that examines whether chronic neural recording devices targeted at the hippocampus affect recognition memory. Finally, Chapter IV provides a general discussion of both works in the context of the broader literature.
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Becker, Nadine. "Imaging activity-dependent structural and functional plasticity of hippocampal CA3-CA1 synapses." Diss., lmu, 2008. http://nbn-resolving.de/urn:nbn:de:bvb:19-101290.

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Stevenson, Cassie Hayley. "Investigating the role of the hippocampal formation in episodic and spatial memory." Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/5632.

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This thesis aims to explore the two dominant functional roles of the hippocampal formation, in the relational encoding of episodic memory and the neural representation of allocentric space, using a combination of pharmaceutical manipulations and single-unit recording techniques in rodents. The first part of this thesis focuses on episodic-like memory, defined by the original episodic memory triad: ‘what-where-when’ (Tulving 1972), which enables the behavioural aspects of episodic memory to be tested in non-human animals. Permanent neurotoxic lesions of the hippocampus and it’s subregions were induced to assess their role in a putative episodic-like memory task developed by Eacott and Norman (2004). In view of the difficulties encountered in successfully demonstrating the temporal component of episodic-like memory in rats, this task tested integrated memory for ‘what-where-which’, where the temporal component (when) was replaced with another event specifier: context (on ‘which’ occasion). Disruption of the hippocampal circuitry led to a specific impairment in the integration of all three event components, whereas the associative recognition of any combination of these features in isolation was left intact. These results confirm the hippocampal dependence of this episodic-like memory task and further reveals the necessity of both CA3 and CA1, hypothetically due to the underlying autoassociative role of CA3 with CA1 functioning as the vital output pathway for this associated information and/or as a mismatch detector. There has been much debate over the inclusion of the temporal component and sceptics may argue that any such interpretations of task-dependence on episodic-like memory processing are invalid considering the requirement for temporal processing is absent. Due to the proposal that a temporal framework necessarily provides the foundation on which episodic memories are built, the second chapter focuses on the development of a suitable protocol in which integrated memory for the original ‘what-where-when’ episodic memory triad can be reliably tested. The other main function attributed to the hippocampus was brought to light by the fascinating revelation that it’s neurons selectively fire in different regions of an environment, termed ‘place cells’ (O’Keefe and Dostrovsky 1971). From the numerous publications resulting from this discovery it has emerged that place cells not only respond to the spatial features of the environment but are also sensitive to a multitude of non-spatial features. These characteristics support the logical assumption that the primary firing patterns of the hippocampus should underlie it’s main purported roles, leading to speculations that they reflect episodic memory processes. The second part of this thesis aims to examine the relationship between hippocampal cells and behaviour by extending the work of Ainge et al. (2007a), in which a subset of hippocampal place cells were found to encode both current and intended destination in a double Y-maze ‘win-stay’ task. The development of these ‘goal-sensitive’ cells were initially investigated during the learning phase of this task. An exciting pattern of results showed a strong positive correlation between the emergence of goal-sensitive firing and behavioural performance on the task, tempting speculations that these firing patterns may underlie spatial learning and future planning, necessary to support performance. To ensure these firing patterns were not a mere reflection of greater experience on the maze, a second study was conducted in which the task demands changed over set periods of days. A significant increase in the proportion of cells demonstrating goal-sensitive firing was revealed when the protocol shifted to incorporate the spatial memory demands of the ‘win-stay’ task, with all other parameters of the protocol remaining constant. These results support the theory that goal-sensitive firing patterns are specifically related to the learning and memory demands of the spatial task, not a result of increased exploration of the maze. The last of this series of studies assessed hippocampal-dependence of this task and revealed that bilateral hippocampal lesions induced an impairment in spatial ‘win-stay’ performance. Collectively, these experiments demonstrate that goal-sensitive firing of hippocampal cells emerge in line with behavioural performance in a hippocampal-dependent task and the emergence of these firing patterns are specific to the learning and memory demands of a spatial ‘win-stay’ protocol. The functional role of the hippocampus in allocentric spatial processing may thus underpin it’s function in episodic memory and potentially in the imagining and planning of future events, whereby the hippocampus provides a ‘space’ in which retrieved information can be integrated in a coherent context to support the fluent and flexible use of information. This hippocampal function would necessarily require visual information to be accessed, concerning the arrangement of landmarks and cues within the environment, in association with information regarding internal orientation and direction and this leads to the question assessed in the final part of this thesis of where this integration occurs. Based on anatomical evidence and the current literature, the postsubiculum, an input structure to the hippocampus, emerged as a potential site for the convergence of sensory cues into the internally generated head direction cell and place cell networks to enable hippocampal-dependent spatial processing. Thus, the effects of temporary pharmacological blockade of AMPARs and NMDARs in the postsubiculum were assessed on the encoding of spatial memory in an object recognition paradigm. The impairment revealed in the ability to recognise novel object-place configurations demonstrates a key role for NMDAR-dependent plasticity within the postsubiculum itself in the formation of allocentric spatial memory. In summary, the experimental results reported in this thesis further elucidate the critical role the hippocampal formation plays in spatial and episodic memory by combining evidence from cellular physiology and neuroanatomy to the behaving animal and extends these findings to discuss a more general role for the hippocampus in imagining both past and future events, in order to successfully navigate, learn and enable past experience to influence our intended future plans and decisions.
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Zhang, Pei. "Synaptic modifications in hippocampal CA3 pyramidal cells in an Alzheimer's mouse model." Thesis, Bordeaux, 2017. http://www.theses.fr/2017BORD0628/document.

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L'encodage de la mémoire dépend de changements durables dans l'activité des circuits synaptiques dans un ensemble de neurones interconnectés. La région CA3 de l'hippocampe reçoit des informations directement ou indirectement (à travers le gyrus denté - GD) en provenance des structures corticales. Des données théoriques et comportementales ont montré que la région CA3 est importante pour l'encodage de la mémoire épisodique, en particulier au stade initial de l'acquisition, en développant vraisemblablement une représentation instantanée d'un contexte. Les neurones pyramidaux CA3 reçoivent une variété de connections afférentes, parmi lesquelles les fibres moussues (FM), les axones des cellules du gyrus denté. Ces connections synaptiqes ont attiré une attention par leurs propriétés morphologiques et fonctionnelles uniques. Malgré les nombreuses études comportementales et computationnelle, les liens entre plasticité des circuits CA3 et encodage de la mémoire ne sont pas bien compris.Le cadre général de ce projet de thèse se situe dans l'étude des mécanismes synaptiques de l'encodage de la mémoire épisodique dans des conditions physiologiques ainsi que dans un modèle de souris de la maladie d'Alzheimer (MA). En effet, la MA se caractérise à un stade précoce par une mémoire épisodique altérée, qui peut être associée à une dysrégulation de la plasticité des circuits CA3.À l'aide de techniques d'enregistrement électrophysiologique, nous avons d'abord exploré les modifications dans les circuits CA3 peu de temps (quelques heures) après conditionnement de la peur contextuelle chez les souris adultes C57Bl6j. Nous avons observé une augmentation de la fréquence des IPSC spontanés accompagnée de changements mineurs dans le nombre de filopodia issus des boutons synaptiques des FM, tandis que les EPSCs et les plasticités à court terme de ces synapses ne sont pas modifiés. Cependant, cette augmentation n'est peut observée 24 heures après l'apprentissage contextuel. Nous avons également tenté de modéliser de manière simplifiée les réseaux neuronaux GD-CA3, afin d'étudier si et dans quelle mesure les interneurones locaux dans la région CA3 contribuent à la précision de l'encodage de la mémoire. [...]Dans l'ensemble ce travail a révélé que la transmission inhibitrice des circuits locaux CA3 de l'hippocampe pourrait être importante dans l'encodage de la mémoire épisodique. Dans le modèle murin de la MA avec déficit de mémoire, il y a une réduction de la transmission GABAergique et des courants médiés par les KAR réduits cellules pyramidales de CA3. Finalement, avons observé une modification transcriptionnelle d'un certain nombre de gènes dans CA3, à des stades précoces de développement de la pathologie dans notre modèle de MA. Notre étude pourrait contribuer à la compréhension des mécanismes pathologiques précoces de la MA, au niveau synaptique ainsi qu'au niveau transcriptionnel, et fournir des idées nouvelles sur les mécanismes sous-jacents au codage rapide de la mémoire contextuelle
Memory encoding is thought to proceed from durable changes in the activity of synaptic circuits to the storage of patterns of electrical events in a sparsely distributed ensemble of neurons. Located at the entry level of hippocampal circuitry, the CA3 region of hippocampus is thought to be important for episodic memory encoding, especially at the initial stage of acquisition, by presumably developing an instant representation of a context. CA3 pyramidal neurons receive a variety of diverse inputs, among which the mossy fiber (MF) inputs draw special attention for its peculiar structure and unique synaptic properties. However, the links between the plasticity of CA3 circuits and memory encoding are not well understood.This thesis project aimed to address the synaptic mechanisms of episodic memory encoding in physiological conditions as well as in a mouse model of Alzheimer's disease (AD).Using electrophysiological recording techniques, we first explored the changes in CA3 circuits shortly after one-trial contextual fear conditioning in adult C57Bl6j mice. We show that despite hardly any changes in filopodia number of MF terminals, an increase in spontaneous IPSC frequency can be registered, while the EPSCs and short-term plasticities of theses synapses are unaltered. However, this increase cannot be seen anymore 24 hours after the contextual learning. We also tried to do simplified computational modeling of the DG-CA3 neuronal networks, to investigate if and to what extent the local interneurons in CA3 region contribute to memory encoding precision.AD is characterized at an early stage by impaired episodic memory, which may involve dysregulation of the plasticity of CA3 circuits.In the next step, we searched for synaptic deficits in CA3 local circuit in the early stage of AD pathology, taking advantage of a familial AD mouse model: 6-month male APP/PS1 mice. We report that there is a reduction in spontaneous IPSC frequency in CA3 neurons together with decreased inhibitory charges of evoked events at MF-CA3 synapses, whereas the short-term plasticity of these synapses and intrinsic properties of CA3 neurons remain unaffected. Furthermore, there is a robust reduction in Kainate receptor (KAR) mediated currents at MF-CA3 synapses, and the same results can be obtained from PSKO mice too, suggesting that disturbed function of γ-secretase and NCad processing pathways might underlie the dysfunction of KARs at MF-CA3 synapses.Finally, to screen for changes on a transcriptome level, we performed RNA-seq with dissected CA3 tissue from APP/PS1 mice and found a list of up- and down-regulated genes at this early stage of AD. Moreover, we carried out ChIP-seq for a histone modification marker: H3K4me3, which has been shown to be directly related to one-trial contextual memory, and here we report that there is a concrete decrease in H3K4me3 levels at the promoter areas of various genes in CA3 neurons. However, these genes are not overlapping much with the down-regulated genes from RNA-seq result, suggesting that other epigenetic mechanisms might play more important roles in expressing early deficits in this AD mouse model.Taken together, we show that inhibitory innervations of hippocampal CA3 local circuits might be important for episodic memory encoding, and in early AD mouse model with memory deficits, there is reduced GABAergic transmission and reduced KAR-mediated currents in CA3 neurons, together with many active transcriptional regulations across the genome. Our study might contribute to the understanding of early AD pathologies at synaptic level as well as transcriptional level, and provide novel insights into the mechanisms underlying rapid encoding of contextual memory
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LICHERI, VALENTINA. "Modulation of Hyperpolarization-Activated Cation Currents (Ih) by Ethanol in Rat Hippocampal CA3 Pyramidal Neurons." Doctoral thesis, Università degli Studi di Cagliari, 2015. http://hdl.handle.net/11584/266622.

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It is well established that ethanol (EtOH), through the interaction with several membrane proteins, as well as intracellular pathways, is capable to modulate many neuronal function. Recent reports show that EtOH increases the firing rate of hippocampal GABAergic interneurons through the positive modulation of the hyperpolarization-activated cyclic nucleotide-gated (HCN) cation channels. This effect might be consistent with the increase of GABA release from presynaptic terminals observed in both CA1 and CA3 inhibitory synapses that leads the enhancement of the GABAergic system induced by EtOH. The activation of HCN produced an inward currents that are commonly called Ih. Ih play an important role for generating specific neuronal activities in different brain regions, including specific sub-regions of the hippocampal formation, such as CA1 and CA3 pyramidal neurons and hippocampal GABAergic interneurons. The main physiologic effect mediated by HCN-induced Ih is directed to the control of the neuronal resting membrane potential and action potential (AP) discharge as well as dampen synaptic integration. Since robust Ih are also present in CA3 glutamatergic neurons, I here investigated whether the action of EtOH in the control of CA3 excitability can be correlated with its possible direct interaction with these cation channels. For this purpose, patch-clamp experiments were performed in CA3 pyramidal neurons from hippocampal coronal slices obtained from male Sprague-Dawley rats. The data obtained demonstrated that EtOH is able to modulate Ih in biphasic manner depending on the concentrations used. Low EtOH concentrations enhanced Ih amplitude, while high reversibly reduced them. This biphasic action induced by EtOH reflects on firing rate and synaptic integration. In addition, in this reports it has been shown that EtOH modulates the function of HCN channels through interfering with the cAMP/AC/PKA intracellular pathways, an effect that is mimicked also by other endogenous compounds such as dopamine through D1 receptors activation. These data suggest that the HCN-mediated Ih currents in CA3 pyramidal neurons are sensitive to EtOH action, which at low or relevant concentrations is able to increase or reduce their function respectively. Altogether these data suggest a potential new mechanism of EtOH actions on hippocampal formation and may help to better understand the depressant central activity showed by this drug of abuse
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Canepari, Marco. "Intrinsic variability and short-term changes in synaptic transmission in the rat hippocampal CA3 region." Doctoral thesis, SISSA, 1999. http://hdl.handle.net/20.500.11767/4432.

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Kanak, Daniel James. "Influence of perforant path synaptic excitation on the initiation of hippocampal sharp-wave ripple activity in vitro." OpenSIUC, 2013. https://opensiuc.lib.siu.edu/dissertations/776.

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Sharp-wave ripples (SWR) generated in the CA3 subregion of the hippocampus (HC) during rest and sleep appear to coordinate memory consolidation to the neocortex (NC) by (1) reactivating small subsets of neurons (i.e. cell-assemblies) that encode recent waking experience and (2) propagating this information through the hippocampal formation. Although CA3 self-organizes SWRs in the absence of extrinsic inputs, cortical input to the HC conveyed by perforant path (PP) may influence SWR initiation nevertheless. Still, direct evidence that PP synaptic excitation can elicit SWRs is lacking, and it is unclear how this influence might compete or interact with self-organizing mechanisms. This dissertation tested the hypothesis that CA3's SWR pattern generator would self-organize its activity in the absence of PP input, but readily entrain to such input when present. Spontaneous SWRs (sSWR) occurred in slices prepared from the ventral portion of the mouse HC. Low-intensity electrical stimulation of PP afferents evoked short-latency field EPSPs in CA3 that were often followed by precisely timed evoked SWRs (eSWR). The network and single-cell characteristics of sSWRs and eSWRs were indistinguishable, indicative of a common patter generator. PP stimuli that followed sSWRs too closely usually failed to elicit eSWRs. Using a custom MATLAB/Simulink application to control PP stimulus timing during the ~250 ms sSWR refractory period revealed a statistically significant effect of stimulus delay (25, 50, 100, and 200 ms) on eSWR incidence, reaching a value of 0.72 (95% CI = [0.61, 0.81]) 200 ms after sSWR onset. In contrast, sSWR incidence at this time was much lower (95% CI = [0.015, 0.049]). Lesions targeting the direct PP input to CA3 substantially reduced eSWR incidence. In intact slices, eSWRs were readily evoked by stimulating the medial entorhinal cortex (MEC). In summary, PP input to CA3 from the MEC can initiate SWRs at times when self-organizing mechanisms generally cannot. Assuming sSWRs convey information to the NC, the ensuing refractory period might provide an opportunity for cortical feedback to reinforce the recently engaged cell-assembly. In the absence of such feedback, CA3 could revert to its default mode of self-organized replay.
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Dennis, Siobhan Dennis. "An investigation of the effects of oxygen glucose deprivation on glutamate receptor localisation within hippocampal CA3 pyramidal neurons." Thesis, University of Bristol, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.544384.

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Caiati, Maddalena Delma. "Activity-dependent regulation of GABA release at immature mossy fibers-CA3 synapses: role of the Prion protein." Doctoral thesis, SISSA, 2012. http://hdl.handle.net/20.500.11767/4719.

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In adulthood, mossy fibers (MFs), the axons of granule cells of the dentate gyrus (DG), release glutamate onto CA3 principal cells and interneurons. In contrast, during the first week of postnatal life MFs release -aminobutyric acid (GABA), which, at this early developmental stage exerts a depolarizing and excitatory action on targeted cells. The depolarizing action of GABA opens voltage-dependent calcium channels and NMDA receptors leading to calcium entry and activation of intracellular signaling pathways involved in several developmental processes, thus contributing to the refinement of neuronal connections and to the establishment of adult neuronal circuits. The release of GABA has been shown to be down regulated by several neurotransmitter receptors which would limit the enhanced excitability caused by the excitatory action of GABA. It is worth noting that the immature hippocampus exhibits spontaneous correlated activity, the so called giant depolarizing potentials or GDPs that act as coincident detector signals for enhancing synaptic activity, thus contributing to several developmental processes including synaptogenesis. GDPs render the immature hippocampus more prone to seizures. Here, I explored the molecular mechanisms underlying synaptic transmission and activity-dependent synaptic plasticity processes at immature GABAergic MF-CA3 synapses in wild-type rodents and in mice lacking the prion protein (Prnp0/0 mice). In the first paper, I studied the functional role of kainate receptors (KARs) in regulating GABA release from MF terminals. Presynaptic KARs regulate synaptic transmission in several brain areas and play a central role in modulating glutamate release at adult MF-CA3 synapses. I found that functional presynaptic GluK1 receptors are present on MF terminals where they down regulate GABA release. Thus, application of DNQX or UBP 302, a selective antagonist for GluK1 receptors, strongly increased the amplitude of MF-GABAA-mediated postsynaptic currents (GPSCs). This effect was associated with a decrease in failure rate and increase in PPR, indicating a presynaptic type of action. GluK1 receptors were found to be tonically activated by glutamate present in the extracellular space, since decreasing the extracellular concentration of glutamate with a glutamate scavenger system prevented their activation and mimicked the effects of KAR antagonists. The depressant effect of GluK1 on GABA release was dependent on pertussis toxin (PTx)-sensitive G protein-coupled kainate receptors since it was prevented when hippocampal slices were incubated in the presence of a solution containing PTx. This effect was presynaptic since application of UBP 302 to cells patched with an intracellular solution containing GDP S still potentiated synaptic responses. In addition, the depressant effect of GluK1 on GABA release was prevented by U73122, which selectively inhibits phospholipase C, downstream to G protein activation. Interestingly, U73122, enhanced the probability of GABA release, thus unveiling the ionotropic type of action of kainate receptors. In line with this, we found that GluK1 receptors enhanced MF excitability by directly depolarizing MF terminals via calcium-permeable cation channels. We also explored the possible involvement of GluK1 in spike time-dependent (STD) plasticity and we found that GluK1 dynamically regulate the direction of STD-plasticity, since the pharmacological block of this receptor shifted spike-time dependent potentiation into depression. The mechanisms underlying STD-LTD at immature MF-CA3 synapses have been investigated in detail in the second paper. STD-plasticity is a Hebbian form of learning which consists in bi-directional modifications of synaptic strength according to the temporal order of pre and postsynaptic spiking. Interestingly, we found that at immature mossy fibers (MF)-CA3 synapses, STD-LTD occurs regardless of the temporal order of stimulation (pre versus post or viceversa). However, as already mentioned, while STD-LTD induced by positive pairing (pre before post) could be shifted into STD-LTP after blocking presynaptic GluK1 receptors, STD-LTD induced by negative pairing (post before pre) relied on the activation of CB1 receptors. At P3 but not at P21, endocannabinoids released by the postsynaptic cell during spiking-induced membrane depolarization retrogradely activated CB1 receptors, probably expressed on MF terminals and persistently depressed GABA release in the rat hippocampus. Thus, bath application of selective CB1 receptor antagonists prevented STD-LTD. Pharmacological tools allow identifying anandamide as the endogenous ligand responsible of activity-dependent depressant effect. To further assess whether STD-LTD is dependent on the activation of CB1 receptors, similar experiments were performed on WT-littermates and CB1-KO mice. While in WT mice the pairing protocol produced a persistent depression of MF-GPSCs as in rats, in CB1-KO mice failed to induce LTD. Consistent with these data, in situ hybridization experiments revealed detectable levels of CB1 mRNA in the granule cell layer of P3 but not of P21mice. These experiments strongly suggest that at immature MF-CA3 synapses STD-LTD is mediated by CB1 receptors, probably transiently expressed, during a critical time window, on MF terminals. In the third paper, I studied synaptic transmission and activity dependent synaptic plasticity at immature MF-CA3 synapses in mice devoid of the prion protein (Prnp0/0). The prion protein (PrPC) is a conserved glycoprotein widely expressed in the brain and involved in several neuronal processes including neurotransmission. If converted to a conformationally altered form, PrPSc can cause neurodegenerative diseases, such as Creutzfeldt-Jakob disease in humans. Previous studies aimed at characterizing Prnp0/0 mice have revealed only mild behavioral changes, including an impaired spatial learning, accompanied by electrophysiological and biochemical alterations. Interestingly, PrPC is developmentally regulated and in the hippocampus its expression parallels the maturation of MF. Here, we tested the hypothesis that at immature (P3-P7) MF-CA3 synapses, PrPC interferes with synaptic plasticity processes. To this aim, the rising phase of Giant Depolarizing Potentials (GDPs), a hallmark of developmental networks, was used to stimulate granule cells in the dentate gyrus in such a way that GDPs were coincident with afferent inputs. In WT animals, the pairing procedure induced a persistent increase in amplitude of MF-GPSCs. In contrast, in Prnp0/0 mice, the same protocol produced a long-term depression (LTD). LTP was postsynaptic in origin and required the activation of cAMP-dependent PKA signaling while LTD was presynaptic and was reliant on G protein-coupled GluK1 receptor and protein lipase C downstream to G protein activation. In addition, at emerging CA3-CA1 synapses of PrPC-deficient mice, stimulation of Schaffer collateral failed to induce LTP, known to be PKA-dependent. Finally, we also found that LTD in Prnp0/0 mice was mediated by GluK1 receptors, since UBP 302 blocked its induction. These data suggest that in the immature hippocampus PrPC controls the direction of synaptic plasticity.
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Zhang, Pei [Verfasser], André [Akademischer Betreuer] Fischer, Helene [Gutachter] Marie, Lionel [Gutachter] Dahan, Yoon [Gutachter] Cho, and Christophe [Gutachter] Mulle. "Synaptic modifications in hippocampal CA3 pyramidal cells in an Alzheimer's mouse model / Pei Zhang ; Gutachter: Helene Marie, Lionel Dahan, Yoon Cho, Christophe Mulle ; Betreuer: André Fischer." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2018. http://d-nb.info/1153607174/34.

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Books on the topic "Hippocampal CA3"

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Ouanounou, Aviv. Modulation of synaptic transmission by exogenous calcium buffers in hippocampal CA1 neurons. Ottawa: National Library of Canada, 1996.

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Pawluski, Jodi Lynn. Primiparous rats, but not multiparous rats, exhibit dendritic atrophy in CA1 and CA3 pyramidal cells of the hippocampus. Ottawa: National Library of Canada, 2003.

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Breakwell, Nicholas Anthony. A1F[inferior 4]-induced synaptic plasticity in area CA1 of rat hippocampus. Birmingham: University of Birmingham, 1995.

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Wrong, Andrew D. Bimodal modulation of N-methyl-D-aspartate-induced currents in rat CA1 hippocampal neurons by kainate application. Ottawa: National Library of Canada, 2002.

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Jazayeri, Mehrdad. A theoretical investigation of the generation of a spontaneous slow rhythm in hippocampus Ca1. Ottawa: National Library of Canada, 2001.

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Dorri, Faramarz. Antisense deoxyoligonucleotide inhibitation of metabotropic glutamate receptor 5 synthesis in CA1 area of rat hippocampus. Ottawa: National Library of Canada, 1995.

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Donegan, Macayla. Coding of social novelty in the hippocampal Cornu Ammonis 2 region (CA2) and its disruption and rescue in a mouse model of schizophrenia. [New York, N.Y.?]: [publisher not identified], 2020.

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Song, Dong, and Theodore W. Berger. Hippocampal memory prosthesis. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780199674923.003.0055.

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Damage to the hippocampus and surrounding regions of the medial temporal lobe can result in a permanent loss of the ability to form new long-term memories. Hippocampal memory prosthesis is designed to restore this ability. The animal model described here is the memory-dependent, delayed nonmatch-to-sample (DNMS) task in rats, and the core of the prosthesis is a biomimetic multi-input, multi-output (MIMO) nonlinear dynamical model that predicts hippocampal output (CA1) signals based on input (CA3) signals. When hippocampal CA1 function is pharmacologically blocked, successful DNMS behavior is abolished. However, when MIMO model predictions are used to re-instate CA1 memory-related activities with electrical stimulation, successful DNMS behavior and long-term memory function are restored. The hippocampal memory prosthesis has been successfully implemented in rodents and nonhuman primates, but the current system requires major advances before it can approach a working prosthesis. Looking forward, a deeper knowledge of neural coding will provide further insights.
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Beninger, Richard J. Multiple memory systems. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198824091.003.0004.

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Multiple memory systems describes how memories can be declarative or non-declarative; incentive learning produces one type of non-declarative memory. Patients with bilateral hippocampal damage have declarative memory deficits (amnesia) but intact non-declarative memory; patients with striatal dysfunction, for example, Parkinson’s patients who lose striatal dopamine have impaired incentive learning but intact declarative memory. Rats with lesions of the fornix (hippocampal output pathway), but not lesions of the dorsal striatum, have impaired spatial (declarative) memory; rats with lesions of the dorsal striatum, but not fornix, have impaired stimulus–response memory that relies heavily on incentive learning. These memory systems possibly inhibit one another to control responding: in rats, a group that received fornix lesions and had impaired spatial learning did better on an incentive task; in humans, hippocampus damage was associated with improvement on an incentive learning task and striatal damage was associated with increased involvement of the hippocampus in a route-recognition task.
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Maren, Stephen. Neural Circuits for Context Processing in Aversive Learning and Memory. Edited by Israel Liberzon and Kerry J. Ressler. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190215422.003.0005.

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The nature and properties of emotional expression depend importantly on not only the stimuli that elicit emotional responses, but also the context in which those stimuli are experienced. Deficits in context processing have been associated with a variety of cognitive-emotional disorders, including post-traumatic stress disorder (PTSD). These deficits can be localized to specific neural circuits underlying context processing in the mammalian brain. In particular, the hippocampus has been implicated through numerous animal and human studies to be involved both in normal contextual memory formation, but also in discrimination of trauma-related cues. Decreased hippocampal functioning, as is observed in PTSD, is associated with increased generalization of fear and threat responses as well as deficits in extinction of fear. Understanding context processing offers the opportunity to further understand the biology of PTSD and to target new approaches to therapeutics.
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Book chapters on the topic "Hippocampal CA3"

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Graham, Bruce P., Vassilis Cutsuridis, and Russell Hunter. "Associative Memory Models of Hippocampal Areas CA1 and CA3." In Hippocampal Microcircuits, 459–94. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-0996-1_16.

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Migliore, Michele, Giorgio A. Ascoli, and David B. Jaffe. "CA3 Cells: Detailed and Simplified Pyramidal Cell Models." In Hippocampal Microcircuits, 353–74. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-0996-1_12.

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Sanjay, M., and Srinivasa B. Krothapalli. "Modelling Epileptic Activity in Hippocampal CA3." In Springer Series in Computational Neuroscience, 757–77. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-99103-0_22.

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Sanjay, M., and Srinivasa B. Krothapalli. "Correction to: Modelling Epileptic Activity in Hippocampal CA3." In Springer Series in Computational Neuroscience, C1. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-99103-0_26.

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Samura, Toshikazu, Motonobu Hattori, and Shun Ishizaki. "Sequence Disambiguation by Functionally Divided Hippocampal CA3 Model." In Neural Information Processing, 117–26. Berlin, Heidelberg: Springer Berlin Heidelberg, 2006. http://dx.doi.org/10.1007/11893028_14.

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Aitken, P. G., D. B. Jaffe, and J. V. Nadler. "Cholecystokinin and Epileptogenesis in the Hippocampal CA3 Region." In Physiology, Pharmacology and Development of Epileptogenic Phenomena, 103–6. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-46732-5_23.

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Granger, Richard, Makoto Taketani, and Gary Lynch. "Special Purpose Temporal Processing in Hippocampal Fields CA1 and CA3." In Neural Representation of Temporal Patterns, 183–95. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1919-5_8.

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Canepari, Marco, and Enrico Cherubini. "Dynamics of Transmitter Release at CA3 Hippocampal Excitatory Synapses." In Neural Circuits and Networks, 71–83. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-58955-3_5.

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Zheng, Chenguang, Qun Li, Yiyi Wang, and Tao Zhang. "Theta Phase Time-Delayed Modulating Low Gamma Amplitude in Hippocampal CA3–CA1 Network." In Advances in Cognitive Neurodynamics (V), 259–65. Singapore: Springer Singapore, 2016. http://dx.doi.org/10.1007/978-981-10-0207-6_36.

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Chitwood, Raymond A., Brenda J. Claiborne, and David B. Jaffe. "Modeling the Passive Properties of Nonpyramidal Neurons in Hippocampal Area CA3." In Computational Neuroscience, 59–64. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4757-9800-5_10.

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Conference papers on the topic "Hippocampal CA3"

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Shiva, Ashraya Samba, Mandar Gogate, Newton Howard, Bruce Graham, and Amir Hussain. "Complex-valued computational model of hippocampal CA3 recurrent collaterals." In 2017 IEEE 16th International Conference on Cognitive Informatics & Cognitive Computing (ICCI*CC). IEEE, 2017. http://dx.doi.org/10.1109/icci-cc.2017.8109745.

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Modak, Priyamvada, and V. Srinivasa Chakravarthy. "Izhikevich Models For Hippocampal Neurons And Its Sub-Region CA3." In 2018 Conference on Cognitive Computational Neuroscience. Brentwood, Tennessee, USA: Cognitive Computational Neuroscience, 2018. http://dx.doi.org/10.32470/ccn.2018.1189-0.

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Levy, William B., Kai S. Chang, and Andrew G. Howe. "Progressively introducing quantified biological complexity into a hippocampal CA3 model." In 2009 International Joint Conference on Neural Networks (IJCNN 2009 - Atlanta). IEEE, 2009. http://dx.doi.org/10.1109/ijcnn.2009.5178724.

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Song, Dong, Robert E. Hampson, Brian S. Robinson, Ioan Opris, Vasilis Z. Marmarelis, Sam A. Deadwyler, and Theodore W. Berger. "Nonlinear dynamical modeling of human hippocampal CA3-CA1 functional connectivity for memory prostheses." In 2015 7th International IEEE/EMBS Conference on Neural Engineering (NER). IEEE, 2015. http://dx.doi.org/10.1109/ner.2015.7146623.

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Wang, Peng, Xuewei Song, Xiyan Zhu, Jinlong Qiu, Shuaijun Yang, and Hui Zhao. "Study on Influencing Factors of Hippocampal Injury in Closed Head Impact Experiments of Rats Using Orthogonal Experimental Design Method." In WCX SAE World Congress Experience. 400 Commonwealth Drive, Warrendale, PA, United States: SAE International, 2023. http://dx.doi.org/10.4271/2023-01-0001.

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<div class="section abstract"><div class="htmlview paragraph">The hippocampus plays a crucial role in brain function and is one of the important areas of concern in closed head injury. Hippocampal injury is related to a variety of factors including the strength of mechanical load, animal age, and helmet material. To investigate the order of these factors on hippocampal injury, a three-factor, three-level experimental protocol was established using the L<sub>9</sub>(3<sup>4</sup>) orthogonal table. A closed head injury experiment regarding impact strength (0.3MPa, 0.5MPa, 0.7MPa), rat age (eight- week-old, ten-week-old, twelve-week-old), and helmet material (steel, plastic, rubber) were achieved by striking the rat's head with a pneumatic-driven impactor. The number of hippocampal CA3 cells was used as an evaluation indicator. The contribution of factors to the indicators and the confidence level were obtained by analysis of variance. The results showed that impact strength was the main factor affecting hippocampal injury (contribution of 89.2%, confidence level 0.01), rat age was a secondary factor (contribution of 8.9%, confidence level 0.05), and helmet material had no significant effect on hippocampal injury (contribution less than 1.9%). This paper provides a method to distinguish factors affecting hippocampal injury.</div></div>
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Obregón-Herrera, Armando. "Biophysical Properties of ATP-sensitive Potassium Channels in CA3 Hippocampal Neurons." In MEDICAL PHYSICS: Eighth Mexican Symposium on Medical Physics. AIP, 2004. http://dx.doi.org/10.1063/1.1811873.

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Koene, Randal A., and Michael E. Hasselmo. "A reversing buffer mechanism that enables instances of retrospective activity in hippocampal regions CA3 and CA1." In 2007 International Joint Conference on Neural Networks. IEEE, 2007. http://dx.doi.org/10.1109/ijcnn.2007.4371163.

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Dong Song, R. H. M. Chan, V. Z. Marmarelis, R. E. Hampson, S. A. Deadwyler, and T. W. Berger. "Estimation and statistical validation of event-invariant nonlinear dynamic models of hippocampal CA3-CA1 population activities." In 2011 33rd Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2011. http://dx.doi.org/10.1109/iembs.2011.6090903.

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Nejati, Alireza, and Charles P. Unsworth. "3-D Modeling of nitric oxide emission and vasodilation induced by CA3 hippocampal neurons." In 2011 33rd Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2011. http://dx.doi.org/10.1109/iembs.2011.6090160.

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Samura, Toshikazu, Yasuomi D. Sato, Yuji Ikegaya, Hatsuo Hayashi, and Takeshi Aihara. "Diverse background activities hidden in power-law spontaneous activity of hippocampal CA3 slice culture." In 2012 Joint 6th Intl. Conference on Soft Computing and Intelligent Systems (SCIS) and 13th Intl. Symposium on Advanced Intelligent Systems (ISIS). IEEE, 2012. http://dx.doi.org/10.1109/scis-isis.2012.6505225.

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