Relevant bibliographies by topics / Synapses

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Synapses'

Author: Grafiati
Published: 4 June 2021
Last updated: 19 October 2024

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Journal articles on the topic "Synapses"

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Feng, Bo, Andiara E. Freitas, Lilach Gorodetski, Jingyi Wang, Runyi Tian, Yeo Rang Lee, Akumbir S. Grewal, and Yimin Zou. "Planar cell polarity signaling components are a direct target of β-amyloid–associated degeneration of glutamatergic synapses." Science Advances 7, no. 34 (August 2021): eabh2307. http://dx.doi.org/10.1126/sciadv.abh2307.

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The signaling pathway directly controlling the maintenance of adult glutamatergic synapses has not been well understood. Planar cell polarity (PCP) signaling components were recently shown to play essential roles in the formation of glutamatergic synapses. Here, we show that they are localized in the adult synapses and are essential for their maintenance. Synapse loss at early stages of Alzheimer’s disease is thought to be induced by β-amyloid (Aβ) pathology. We found that oligomeric Aβ binds to Celsr3 and assists Vangl2 in disassembling synapses. Moreover, a Wnt receptor and regulator of PCP signaling, Ryk, is also required for Aβ-induced synapse loss. In the 5XFAD mouse model of Alzheimer’s disease, Ryk conditional knockout or a function-blocking monoclonal Ryk antibody protected synapses and preserved cognitive function. We propose that tipping of the fine balance of Wnt/PCP signaling components in glutamatergic synapses may cause synapse degeneration in neurodegenerative disorders with Aβ pathology.
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Dejanovic, Borislav, Tiffany Wu, Ming-Chi Tsai, David Graykowski, Vineela D. Gandham, Christopher M. Rose, Corey E. Bakalarski, et al. "Complement C1q-dependent excitatory and inhibitory synapse elimination by astrocytes and microglia in Alzheimer’s disease mouse models." Nature Aging 2, no. 9 (September 20, 2022): 837–50. http://dx.doi.org/10.1038/s43587-022-00281-1.

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AbstractMicroglia and complement can mediate neurodegeneration in Alzheimer’s disease (AD). By integrative multi-omics analysis, here we show that astrocytic and microglial proteins are increased in TauP301S synapse fractions with age and in a C1q-dependent manner. In addition to microglia, we identified that astrocytes contribute substantially to synapse elimination in TauP301S hippocampi. Notably, we found relatively more excitatory synapse marker proteins in astrocytic lysosomes, whereas microglial lysosomes contained more inhibitory synapse material. C1q deletion reduced astrocyte–synapse association and decreased astrocytic and microglial synapses engulfment in TauP301S mice and rescued synapse density. Finally, in an AD mouse model that combines β-amyloid and Tau pathologies, deletion of the AD risk gene Trem2 impaired microglial phagocytosis of synapses, whereas astrocytes engulfed more inhibitory synapses around plaques. Together, our data reveal that astrocytes contact and eliminate synapses in a C1q-dependent manner and thereby contribute to pathological synapse loss and that astrocytic phagocytosis can compensate for microglial dysfunction.
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Amano, Ryota, Mitsuyuki Nakao, Kazumichi Matsumiya, and Fumikazu Miwakeichi. "A computational model to explore how temporal stimulation patterns affect synapse plasticity." PLOS ONE 17, no. 9 (September 23, 2022): e0275059. http://dx.doi.org/10.1371/journal.pone.0275059.

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Plasticity-related proteins (PRPs), which are synthesized in a synapse activation-dependent manner, are shared by multiple synapses to a limited spatial extent for a specific period. In addition, stimulated synapses can utilize shared PRPs through synaptic tagging and capture (STC). In particular, the phenomenon by which short-lived early long-term potentiation is transformed into long-lived late long-term potentiation using shared PRPs is called “late-associativity,” which is the underlying principle of “cluster plasticity.” We hypothesized that the competitive capture of PRPs by multiple synapses modulates late-associativity and affects the fate of each synapse in terms of whether it is integrated into a synapse cluster. We tested our hypothesis by developing a computational model to simulate STC, late-associativity, and the competitive capture of PRPs. The experimental results obtained using the model revealed that the number of competing synapses, timing of stimulation to each synapse, and basal PRP level in the dendritic compartment altered the effective temporal window of STC and influenced the conditions under which late-associativity occurs. Furthermore, it is suggested that the competitive capture of PRPs results in the selection of synapses to be integrated into a synapse cluster via late-associativity.
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Grant, Seth G. N. "Synapse diversity and synaptome architecture in human genetic disorders." Human Molecular Genetics 28, R2 (July 26, 2019): R219—R225. http://dx.doi.org/10.1093/hmg/ddz178.

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Abstract Over 130 brain diseases are caused by mutations that disrupt genes encoding the proteome of excitatory synapses. These include neurological and psychiatric disorders with early and late onset such as autism, schizophrenia and depression and many other rarer conditions. The proteome of synapses is highly complex with over 1000 conserved proteins which are differentially expressed generating a vast, potentially unlimited, number of synapse types. The diversity of synapses and their location in the brain are described by the synaptome. A recent study has mapped the synaptome across the mouse brain, revealing that synapse diversity is distributed into an anatomical architecture observed at scales from individual dendrites to the whole systems level. The synaptome architecture is built from the hierarchical expression and assembly of proteins into complexes and supercomplexes which are distributed into different synapses. Mutations in synapse proteins change the synaptome architecture leading to behavioral phenotypes. Mutations in the mechanisms regulating the hierarchical assembly of the synaptome, including transcription and proteostasis, may also change synapse diversity and synaptome architecture. The logic of synaptome hierarchical assembly provides a mechanistic framework that explains how diverse genetic disorders can converge on synapses in different brain circuits to produce behavioral phenotypes.
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Wang, Yizhi, Congchao Wang, Petter Ranefall, Gerard Joey Broussard, Yinxue Wang, Guilai Shi, Boyu Lyu, et al. "SynQuant: an automatic tool to quantify synapses from microscopy images." Bioinformatics 36, no. 5 (October 9, 2019): 1599–606. http://dx.doi.org/10.1093/bioinformatics/btz760.

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Abstract Motivation Synapses are essential to neural signal transmission. Therefore, quantification of synapses and related neurites from images is vital to gain insights into the underlying pathways of brain functionality and diseases. Despite the wide availability of synaptic punctum imaging data, several issues are impeding satisfactory quantification of these structures by current tools. First, the antibodies used for labeling synapses are not perfectly specific to synapses. These antibodies may exist in neurites or other cell compartments. Second, the brightness of different neurites and synaptic puncta is heterogeneous due to the variation of antibody concentration and synapse-intrinsic differences. Third, images often have low signal to noise ratio due to constraints of experiment facilities and availability of sensitive antibodies. These issues make the detection of synapses challenging and necessitates developing a new tool to easily and accurately quantify synapses. Results We present an automatic probability-principled synapse detection algorithm and integrate it into our synapse quantification tool SynQuant. Derived from the theory of order statistics, our method controls the false discovery rate and improves the power of detecting synapses. SynQuant is unsupervised, works for both 2D and 3D data, and can handle multiple staining channels. Through extensive experiments on one synthetic and three real datasets with ground truth annotation or manually labeling, SynQuant was demonstrated to outperform peer specialized unsupervised synapse detection tools as well as generic spot detection methods. Availability and implementation Java source code, Fiji plug-in, and test data are available at https://github.com/yu-lab-vt/SynQuant. Supplementary information Supplementary data are available at Bioinformatics online.
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Mamiya, Akira, and Farzan Nadim. "Target-Specific Short-Term Dynamics Are Important for the Function of Synapses in an Oscillatory Neural Network." Journal of Neurophysiology 94, no. 4 (October 2005): 2590–602. http://dx.doi.org/10.1152/jn.00110.2005.

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Short-term dynamics such as facilitation and depression are present in most synapses and are often target-specific even for synapses from the same type of neuron. We examine the dynamics and possible functions of two synapses from the same presynaptic neuron in the rhythmically active pyloric network of the spiny lobster. Using simultaneous recordings, we show that the synapses from the lateral pyloric (LP) neuron to the pyloric dilator (PD; a member of the pyloric pacemaker ensemble) and the pyloric constrictor (PY) neurons both show short-term depression. However, the postsynaptic potentials produced by the LP-to-PD synapse are larger in amplitude, depress less, and recover faster than those produced by the LP-to-PY synapse. The main function of the LP-to-PD synapse is to slow down the pyloric rhythm. However, in some cases, it slows down the rhythm only when it is fast and has no effect or to speeds up when it is slow. In contrast, the LP-to-PY synapse functions to delay the activity of the PY neuron; this delay increases as the cycle period becomes longer. Using a computational model, we show that the short-term dynamics of synaptic depression observed for each of these synapses are tailored to their individual functions and that replacing the dynamics of either synapse with the other would disrupt these functions. Together, the experimental and modeling results suggest that the target-specific features of short-term synaptic depression are functionally important for synapses efferent from the same presynaptic neuron.
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Bloom, Ona, Emma Evergren, Nikolay Tomilin, Ole Kjaerulff, Peter Löw, Lennart Brodin, Vincent A. Pieribone, Paul Greengard, and Oleg Shupliakov. "Colocalization of synapsin and actin during synaptic vesicle recycling." Journal of Cell Biology 161, no. 4 (May 19, 2003): 737–47. http://dx.doi.org/10.1083/jcb.200212140.

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It has been hypothesized that in the mature nerve terminal, interactions between synapsin and actin regulate the clustering of synaptic vesicles and the availability of vesicles for release during synaptic activity. Here, we have used immunogold electron microscopy to examine the subcellular localization of actin and synapsin in the giant synapse in lamprey at different states of synaptic activity. In agreement with earlier observations, in synapses at rest, synapsin immunoreactivity was preferentially localized to a portion of the vesicle cluster distal to the active zone. During synaptic activity, however, synapsin was detected in the pool of vesicles proximal to the active zone. In addition, actin and synapsin were found colocalized in a dynamic filamentous cytomatrix at the sites of synaptic vesicle recycling, endocytic zones. Synapsin immunolabeling was not associated with clathrin-coated intermediates but was found on vesicles that appeared to be recycling back to the cluster. Disruption of synapsin function by microinjection of antisynapsin antibodies resulted in a prominent reduction of the cytomatrix at endocytic zones of active synapses. Our data suggest that in addition to its known function in clustering of vesicles in the reserve pool, synapsin migrates from the synaptic vesicle cluster and participates in the organization of the actin-rich cytomatrix in the endocytic zone during synaptic activity.
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Stevens-Sostre, Whitney A., and Mrinalini Hoon. "Cellular and Molecular Mechanisms Regulating Retinal Synapse Development." Annual Review of Vision Science 10, no. 1 (September 15, 2024): 377–402. http://dx.doi.org/10.1146/annurev-vision-102122-105721.

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Synapse formation within the retinal circuit ensures that distinct neuronal types can communicate efficiently to process visual signals. Synapses thus form the core of the visual computations performed by the retinal circuit. Retinal synapses are diverse but can be broadly categorized into multipartner ribbon synapses and 1:1 conventional synapses. In this article, we review our current understanding of the cellular and molecular mechanisms that regulate the functional establishment of mammalian retinal synapses, including the role of adhesion proteins, synaptic proteins, extracellular matrix and cytoskeletal-associated proteins, and activity-dependent cues. We outline future directions and areas of research that will expand our knowledge of these mechanisms. Understanding the regulators moderating synapse formation and function not only reveals the integrated developmental processes that establish retinal circuits, but also divulges the identity of mechanisms that could be engaged during disease and degeneration.
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Uchigashima, Motokazu, Toshihisa Ohtsuka, Kazuto Kobayashi, and Masahiko Watanabe. "Dopamine synapse is a neuroligin-2–mediated contact between dopaminergic presynaptic and GABAergic postsynaptic structures." Proceedings of the National Academy of Sciences 113, no. 15 (March 25, 2016): 4206–11. http://dx.doi.org/10.1073/pnas.1514074113.

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Midbrain dopamine neurons project densely to the striatum and form so-called dopamine synapses on medium spiny neurons (MSNs), principal neurons in the striatum. Because dopamine receptors are widely expressed away from dopamine synapses, it remains unclear how dopamine synapses are involved in dopaminergic transmission. Here we demonstrate that dopamine synapses are contacts formed between dopaminergic presynaptic and GABAergic postsynaptic structures. The presynaptic structure expressed tyrosine hydroxylase, vesicular monoamine transporter-2, and plasmalemmal dopamine transporter, which are essential for dopamine synthesis, vesicular filling, and recycling, but was below the detection threshold for molecules involving GABA synthesis and vesicular filling or for GABA itself. In contrast, the postsynaptic structure of dopamine synapses expressed GABAergic molecules, including postsynaptic adhesion molecule neuroligin-2, postsynaptic scaffolding molecule gephyrin, and GABAA receptor α1, without any specific clustering of dopamine receptors. Of these, neuroligin-2 promoted presynaptic differentiation in axons of midbrain dopamine neurons and striatal GABAergic neurons in culture. After neuroligin-2 knockdown in the striatum, a significant decrease of dopamine synapses coupled with a reciprocal increase of GABAergic synapses was observed on MSN dendrites. This finding suggests that neuroligin-2 controls striatal synapse formation by giving competitive advantage to heterologous dopamine synapses over conventional GABAergic synapses. Considering that MSN dendrites are preferential targets of dopamine synapses and express high levels of dopamine receptors, dopamine synapse formation may serve to increase the specificity and potency of dopaminergic modulation of striatal outputs by anchoring dopamine release sites to dopamine-sensing targets.
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Staple, Julie K., Florence Morgenthaler, and Stefan Catsicas. "Presynaptic Heterogeneity: Vive la difference." Physiology 15, no. 1 (February 2000): 45–49. http://dx.doi.org/10.1152/physiologyonline.2000.15.1.45.

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Since individual synapses of the same neuron may have different molecular composition, an important question in neurobiology is how the properties of individual synapses are established and maintained. Recent technical advances allow assay of activity at individual synapses and investigation of the relationship between function and molecular composition at the synapse.
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Dissertations / Theses on the topic "Synapses"

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Evergren, Emma. "Coordination of endocytosis at the synaptic periactive zone /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-683-2/.

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Ho, Shu Xian. "Silent synapses and postnatal development of the mouse cerebellar cortex." Thesis, Aix-Marseille, 2018. http://www.theses.fr/2018AIXM0604/document.

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Dans le cortex cérébelleux, au premier chef impliqué dans l’apprentissage moteur, chaque neurone de Purkinje reçoit des centaines de milliers d'entrées provenant de cellules granulaires. Etonnement, il a été suggéré qu'une grande majorité de ces connexions (synapses) sont silencieuses, c’est-à-dire qu’elles ne transmettent pas d’information détectable. Les propriétés et le rôle de ces synapses silencieuses restent mystérieux. Jouent-elles le rôle d’une réserve ou sont-elles le produit de l’apprentissage cérébelleux ? En combinant l’enregistrement électrique de la transmission synaptique et la cartographie des entrées synaptiques dans des tranches aigües de cervelet de souris, nous avons étudié l'évolution du pourcentage des synapses qui sont silencieuses entre deux âges : avant le sevrage et une fois que l’agilité d’adulte est acquise. Nous avons observé que le pourcentage de synapses qui sont silencieuses reste remarquablement stable malgré l’augmentation du nombre total de synapses
In the cerebellar cortex, primarily involved in motor learning, any Purkinje neuron receives hundreds of thousands of inputs from granule cells. Disturbingly, it has been suggested that the vast majority of these connections (synapses) are silent, that is to say they do not transmit any detectable information. The properties and the role of these silent synapses remains mysterious. Do they serve as a reserve pool for additional information storage or are they a byproduct of cerebellar learning? Combining the electrical recording of synaptic transmission and the mapping of synaptic inputs in acute cerebellar slices from mice, we have studied how the percentage of synapses which are silent changes between two postnatal ages: before weaning and once adult agility is acquired. Our main finding is that the percentage of synapses which are silent remains remarkably stable despite the increase in the total number of synapses
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Couchman, Kiri. "Receptors and Synapses in the MSO." Diss., lmu, 2011. http://nbn-resolving.de/urn:nbn:de:bvb:19-130529.

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Tan, Scott H. (Scott Howard). "Epitaxial SiGe synapses for neuromorphic arrays." Thesis, Massachusetts Institute of Technology, 2018. http://hdl.handle.net/1721.1/118687.

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Thesis: S.M., Massachusetts Institute of Technology, Department of Mechanical Engineering, 2018.
Cataloged from PDF version of thesis.
Includes bibliographical references (pages 59-68).
Intelligent machines could help to facilitate language translation, maximize attentive learning, and optimize medical care. However, hardware to train and deploy Al systems are power-hungry and too slow for many applications. Neuromorphic arrays could potentially offer better efficiency compared to conventional hardware by storing high-precision analog weights between digital processors. However, neuromorphic arrays have not experimentally demonstrated learning accuracy comparable to conventional hardware due to irreproducibility associated with existing artificial synapses. Large variation arises in conventional devices due to the stochastic nature of metal movement through an amorphous synapse. Hence, passive arrays have only been demonstrated as small-scale systems. In this thesis, I developed single-crystalline Silicon-Germanium (SiGe) artificial synapses that have suitable properties for large-scale neurormorphic arrays. In contrast to amorphous films, epitaxially-grown SiGe can confine metal filaments within widened threading dislocations for uniform conductance update thresholds. Metal confinement reduces temporal variation to as low as 1%, which is the lowest variation reported to date, to the extent of the author's knowledge. Dislocations are selectively etched to allow for high ON/OFF ratio, good retention, many cycles of endurance, and linear conductance change. Simulations accounting for non-ideal device properties suggest that SiGe synapses in passive crossbar arrays could perform supervised learning for handwriting digit recognition with up to 95.1% accuracy. Hence, SiGe synapses demonstrate great promise for large-scale neuromorphic arrays.
by Scott H. Tan.
S.M.
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Wang, Xin-hao. "Modulation of developing synapses by neurotrophin /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 1998. http://wwwlib.umi.com/cr/ucsd/fullcit?p9834974.

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

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High frequency repetitive stimulation of an excitatory input in the hippocampus results in a post-tetanic potentiation (PTP) of short duration (about 3 min) that can be followed by a long-term synaptic potentiation (LTP) of the same excitatory input (Schwartzkroin and Wester, 1975; Andersen et al., 1977). It has been reported that this tetanus-induced LTP cannot be elicited in a Ca²⁺-free medium and is therefore a Ca²⁺-dependent process (Dunwiddie et al., 1978; Dunwiddie and Lynch, 1979; Wigstrӧm et al., 1979). Whether the induction of LTP is directly dependent upon Ca²⁺, or whether, Ca²⁺ is required because synaptic transmission is needed to initiate certain postsynaptic process(es) (a postsynaptic depolarization, for instance) leading to LTP, is unknown. Recent studies from this laboratory showed that both short-term potentiation (STP; with a duration resembling PTP) and LTP can be associatively induced if activation of a test input co-occured with either a tetanic stimulation of separate excitatory inputs or a sufficient depolarization of the postsynaptic neurone (Sastry et al., 1985). In this study, experiments were performed to investigate (1) whether associative STP could be induced when activation of the test input preceded or followed the onset of the conditioning train and (2) whether LTP could be induced in the absence of Ca²⁺ in the extracellular medium if sufficient depolarizations of the presynaptic terminals and postsynaptic neurones were provided. All experiments were performed using the transversely sectioned hippocampal slice preparation. Test stimuli were delivered via an electrode located in the stratum radiatum while the conditioning tetani (100 Hz, 10 pulses per train) were delivered via another electrode located in the recorded from the apical dendritic area of CA₁ neurones. After the initial control stimulation period, 5 conditioning tetani were given at a frequency of 0.2 Hz. The test stimuli either preceded (-) or followed ( + ) the onset of each conditioning train by 0 to 100 ms. When the test stimulus followed the onset of each conditioning train, there was significant STP of the test EPSP up to a conditioning-test interval of +80 ms. When the test stimulus preceded the onset of each conditioning train, there was significant STP of the test EPSP up to a conditioning-test interval of -50 ms. Conditioning tetani that were given without co-activation of the test input resulted in a subsequent depression of the test EPSP. It is suggested that either the test or the conditioning input can initiate some postsynaptic process(es) which can in turn affect the activated presynaptic terminals to increase transmitter release or alter the subsynaptic dendritic properties. For studying the possibility of the induction of LTP in the absence of Ca²⁺ in the extracellular medium, population EPSPs were recorded from apical dendritic area of CA₁ neurones in response to stratum radiatum stimulation. After the control stimulation period, slices were exposed either to Ca²⁺-containing or Ca²⁺-free (with Mn²⁺ and Mg²⁺ replacing Ca²⁺) medium, with the concentration of KC1 at 10 to 80 mM. Long-term potentiation of the population EPSPs was observed following the exposure to high K⁺ in Ca²⁺-free media. Following a brief period of potentiation initially, population EPSPs often exhibited a tendency toward depression after exposure to high K⁺ in Ca²⁺-containing media. LTP induced by high K⁺ in Ca²⁺-free medium could also be observed when a fixed number of axons were being activated, indicating that a recruitment of presynaptic fibres cannot entirely account for the potentiation. LTP of the depolarizing commands were paired with activation of the stratum radiatum while the slices were exposed to Ca²⁺ -free medium (normal concentration of KC1). These results suggest that extracellular Ca²⁺, synaptic transmission and thus subsynaptic receptor activation are not necessary for the induction of LTP as long as sufficient depolarizations of the presynaptic terminals and postsynaptic neurones are provided.
Medicine, Faculty of
Anesthesiology, Pharmacology and Therapeutics, Department of
Graduate
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Javalet, Charlotte. "Rôle des exosomes comme nouvelle voie de communication entre les neurones." Thesis, Université Grenoble Alpes (ComUE), 2016. http://www.theses.fr/2016GREAV028/document.

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Les exosomes sont des vésicules d’origine endosomale sécrétées par les cellules dans leur environnement après fusion à la membrane plasmique des endosomes multivésiculés. Les exosomes représentent un nouveau mode de communication entre les cellules en permettant un transfert direct de protéines, de lipides et d’ARN. L’objectif de ma thèse était d’étudier le rôle des exosomes dans la communication entre les neurones. Précédemment, le laboratoire a montré que les neurones sécrètent des exosomes de manière régulée par l’activité synaptique. Nous avons observé que les exosomes neuronaux ne sont endocytés que par les neurones. Après avoir montré qu’ils ne contiennent que des ARN courts, nous avons réalisé un séquençage complet de leurs microARN et observé que ces microARN étaient sélectivement exportés dans les exosomes. Nos observations suggèrent que les microARN contenus dans les exosomes peuvent modifier la physiologie des neurones receveurs. Nos résultats renforcent l’hypothèse du rôle des exosomes dans la communication entre les neurones via le transfert de microARN
Exosomes are vesicles of endocytic origin released by cells into their environment following fusion of multivesicular endosomes with the plasma membrane. Exosomes represent a novel mechanism of cell communication allowing direct transfer of proteins, lipids and RNA. The goal of my PhD thesis was to study that exosomes represent a novel way of interneuronal communication. Our team has previously reported that neurons release exosomes in a way tightly regulated by synaptic activity. We observed that exosomes released by neurons are only endocytosed by neurons. We found that exosomes contain only small RNA and did a deep sequencing of all their microRNA. MicroRNA are selectively exported into exosomes. It seems that exosomal microRNA can modify the physiology of receiving neurons. Our results strengthen the hypothesis of the role of exosomes in the interneuronal communication by the way of microARN transfert
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Chen, Yu. "Regulation of EphA4-dependent signaling at synapses /." View abstract or full-text, 2007. http://library.ust.hk/cgi/db/thesis.pl?BICH%202007%20CHEN.

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Gray, Gregory Clark. "Ultrastructure of the retinal synapses in cubozoans /." Electronic version (PDF), 2007. http://dl.uncw.edu/etd/2007-3/grayg/gregorygray.pdf.

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Sun, Yu. "Recruitment of synaptic vesicles to developing synapses." Thesis, University of British Columbia, 2011. http://hdl.handle.net/2429/36445.

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Synapse formation begins with the recognition of appropriate targets and formation of incipient contacts, and culminates with the recruitment of pre- and postsynaptic proteins to points of cell-cell contact. It is still unclear how cell-cell contact translates into the recruitment of synaptic proteins. Previous studies have shown that the cadherin/β-catenin cell adhesion complex plays an important role in localizing synaptic vesicles to developing synapses. This dissertation discusses work elucidating the transduction pathway that is activated following cell-cell contact, leading to the recruitment and retention of synaptic vesicles to presynaptic compartments. Using rat and mouse primary hippocampal cultures as a model system, we have demonstrated that β-catenin mediates the localization of synaptic vesicles to synapses through its recruitment of the PDZ scaffold protein, scribble, and it’s subsequent recruitment of the Rac/Cdc42 guanine nucleotide exchange factor, β-pix. We further demonstrate that β-pix enhances actin polymerization at these discrete sites, which is important for the “trapping” of synaptic vesicles as they translocate along the axon. We have demonstrated that cadherin, β-catenin, scribble, and β-pix form a complex at developing synapses using immunohistochemistry coupled with immunoprecipitation assays using synaptosomal fractions. Knockdown of β-catenin, scribble or β-pix using RNA interference (RNAi) disrupts the appropriate localization of synaptic vesicles at synapses. We have ordered this pathway and have shown that β-catenin is important for the recruitment and clustering of scribble to synapses, but that scribble knockdown does not affect β-catenin localization. We have also demonstrated that scribble knockdown disrupts the clustering of β-pix at synaptic sites. This complex has shown to control vesicle localization through β-pix-mediated enhancement of actin polymerization at these discrete sites. Indeed, β-pix knockdown results in decreased actin polymerization at synapses. Importantly, restoring actin polymerization at synapses through cortactin overexpression rescues the mislocalization of synaptic vesicles. This work provides novel insights into the molecular and cellular mechanisms underlying the development presynaptic compartments.
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Books on the topic "Synapses"

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Maxwell, Cowan W., Südhof Thomas C, Stevens Charles F. 1934-, and Howard Hughes Medical Institute, eds. Synapses. Baltimore: Johns Hopkins University Press, 2001.

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Apolloni, Bruno, and Franz Kurfess, eds. From Synapses to Rules. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-0705-5.

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Nägerl, U. Valentin, and Antoine Triller, eds. Nanoscale Imaging of Synapses. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-9179-8.

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Heckman, James J. Schools, skills, and synapses. Cambridge, MA: National Bureau of Economic Research, 2008.

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S, Faber Donald, and Human Frontier Science Program, eds. Central synapses: Quantal mechanisms and plasticity. Strasbourg: Human Frontier Science Program, 1998.

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1966-, Hensch Takao K., and Fagiolini Michela, eds. Excitatory-inhibitory balance: Synapses, circuits, systems. New York: Kluwer Academic/Plenum, 2004.

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Huganir, Richard, and Holly Cline. Abstracts of papers presented at the 2007 meeting on synapses: From molecules to circuits & behavior : April 18-April 22, 2006. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory, 2007.

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Meeting on Synapses (2011 Cold Spring Harbor Laboratory). Abstracts of papers presented at the 2011 meeting on synapses: From molecules to circuits & behavior, April 12-April 16, 2011. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory, 2011.

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1933-, Shepherd Gordon M., Black Ira B, and Killackey Herbert P, eds. Synapses, circuits, and the beginnings of memory. Cambridge, Mass: MIT Press, 1986.

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Komissarov, I. V. Mekhanizmy khimicheskoĭ chuvstvitelʹnosti sinapticheskikh membran. Kiev: Nauk. dumka, 1986.

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Book chapters on the topic "Synapses"

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Heppner, John B., David B. Richman, Steven E. Naranjo, Dale Habeck, Christopher Asaro, Jean-Luc Boevé, Johann Baumgärtner, et al. "Synapse, pl., synapses." In Encyclopedia of Entomology, 3669. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6359-6_4510.

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van Putten, Michel J. A. M. "Synapses." In Dynamics of Neural Networks, 27–43. Berlin, Heidelberg: Springer Berlin Heidelberg, 2020. http://dx.doi.org/10.1007/978-3-662-61184-5_2.

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Bolling, Danielle. "Synapses." In Encyclopedia of Autism Spectrum Disorders, 3057–58. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1698-3_585.

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Sabah, Nassir H. "Synapses." In Neuromuscular Fundamentals, 185–230. First edition. | Boca Raton : CRC Press, 2021.: CRC Press, 2020. http://dx.doi.org/10.1201/9781003024798-6.

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Tranquillo, Joseph V. "Synapses." In Quantitative Neurophysiology, 77–87. Cham: Springer International Publishing, 2009. http://dx.doi.org/10.1007/978-3-031-01628-8_6.

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Bolling, Danielle. "Synapses." In Encyclopedia of Autism Spectrum Disorders, 4722. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-319-91280-6_585.

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Rothman, Jason S. "Modeling Synapses." In Encyclopedia of Computational Neuroscience, 1738–50. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4614-6675-8_240.

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Börgers, Christoph. "Chemical Synapses." In An Introduction to Modeling Neuronal Dynamics, 153–64. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-51171-9_20.

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Krstić, Radivoj V. "Synapses. Classification." In General Histology of the Mammal, 344–45. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70420-8_168.

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Rothman, Jason S. "Modeling Synapses." In Encyclopedia of Computational Neuroscience, 1–15. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-7320-6_240-1.

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Conference papers on the topic "Synapses"

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Li, Dingwei, Yitong Chen, Huihui Ren, Yingjie Tang, Yan Wang, Qi Huan, and Bowen Zhu. "Optoelectronic Synapses Based on Inorganic-Organic Hybrid Phototransistors." In 2024 31st International Workshop on Active-Matrix Flatpanel Displays and Devices (AM-FPD), 173–74. IEEE, 2024. http://dx.doi.org/10.23919/am-fpd61635.2024.10615854.

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Dias, Lília M. S., Lianshe Fu, Elias Towe, Rute A. S. Ferreira, and Paulo S. B. André. "Luminescent Waveguides with Synaptic Properties for Photonic Artificial Neural Networks." In CLEO: Applications and Technology, JTu2A.12. Washington, D.C.: Optica Publishing Group, 2024. http://dx.doi.org/10.1364/cleo_at.2024.jtu2a.12.

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We replicate biological neurons and synapses, transmitting 0.2 Hz impulses through luminescent waveguides with adjustable features. This breakthrough has significant implications for neuromorphic engineering, providing valuable insights into neural networks technological applications and signal transmission.
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Oommen, Roshni, and Aswathi R. Nair. "Performance comparison of ZnO and ZnON based optoelectronic synapses." In 2024 IEEE International Conference on Electronics, Computing and Communication Technologies (CONECCT), 1–6. IEEE, 2024. http://dx.doi.org/10.1109/conecct62155.2024.10677191.

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Krishnamoorthy, Ashok V., Gökçe Yayla, Gary C. Marsden, and Sadik Esener. "Free-space optoelectronic neural system prototype." In OSA Annual Meeting. Washington, D.C.: Optica Publishing Group, 1992. http://dx.doi.org/10.1364/oam.1992.mqq2.

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We have previously designed a freespace optoelectronic neural system1 based on the D-STOP architecture.2 The neural architecture minimizes the number of required light transmitters and provides full connectivity between neurons, flexible functionality neurons and synapses, low signal timing skew, and accurate electronic fan-in with dendritic processing capability. Neural signals are encoded by using a combination of pulse-width modulating optical neurons and pulse-amplitude modulating electronic synapses. The neural system prototype consists of a 16-node input layer, a four-neuron hidden layer, and a single neuron output layer. The input layer consists of a 4 × 4 array of PLZT modulators. An 8 × 8 synapse scalable prototype of the neural chip and the space-invariant optical interconnection system have been fabricated. The image of the modulator array is distributed optically to the 64 synapses of the four hidden layer neurons, which are electrically connected to the output neuron. One differencing dendrite per four synapses is used. Measured synapse and dendrite unit characteristics exhibit high linearity with low power consumption. Test results allow a 100 ns minimum pulse width for neural outputs.
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Najem, Joseph S., Graham J. Taylor, Charles P. Collier, and Stephen A. Sarles. "Synapse-Inspired Variable Conductance in Biomembranes: A Preliminary Study." In ASME 2017 Conference on Smart Materials, Adaptive Structures and Intelligent Systems. American Society of Mechanical Engineers, 2017. http://dx.doi.org/10.1115/smasis2017-3820.

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Memristors are solid-state devices that exhibit voltage-controlled conductance. This tunable functionality enables the implementation of biologically-inspired synaptic functions in solid-state neuromorphic computing systems. However, while memristors are meant to emulate an intricate signal transduction process performed by soft biomolecular structures, they are commonly constructed from silicon- or polymer-based materials. As a result, the volatility, intricate design, and high-energy resistance switching in memristive devices, usually, leads to energy consumption in memristors that is several orders of magnitude higher than in natural synapses. Additionally, solid-state memristors fail to achieve the coupled dynamics and selectivity of synaptic ion exchange that are believed to be necessary for initiating both short- and long-term potentiation (STP and LTP) in neural synapses, as well as paired-pulse facilitation (PPF) in the presynaptic terminal. LTP is a phenomenon mostly responsible for driving synaptic learning and memory, features that enable signal transduction between neurons to be history-dependent and adaptable. In contrast, current memristive devices rely on engineered external programming parameters to imitate LTP. Because of these fundamental differences, we believe a biomolecular approach offers untapped potential for constructing synapse-like systems. Here, we report on a synthetic biomembrane system with biomolecule-regulated (alamethicin) variable ion conductance that emulates vital operational principals of biological synapse. The proposed system consists of a synthetic droplet interface bilayer (DIB) assembled at the conjoining interface of two monolayer-encased aqueous droplets in oil. The droplets contain voltage-activated alamethicin (Alm) peptides, capable of creating conductive pathways for ion transport through the impermeable lipid membrane. The insertion of the peptides and formation of transmembrane ion channels is achieved at externally applied potentials higher than ∼70 m V. Just like in biological synapses, where the incorporation of additional receptors is responsible for changing the synaptic weight (i.e. conductance), we demonstrate that the weight of our synaptic mimic may be changed by controlling the number of alamethicin ion channels created in a synthetic lipid membrane. More alamethicin peptides are incorporated by increasing the post-threshold external potential, thus leading to higher conductance levels for ion transport. The current-voltage responses of the alamethicin-based synapse also exhibit significant “pinched” hysteresis — a characteristic of memristors that is fundamental to mimicking synapse plasticity. We demonstrate the system’s capability of exhibiting STP/PPF behaviors in response to high-frequency 50 ms, 150 mV voltage pulses. We also present and discuss an analytical model for an alamethicin-based memristor, classifying that later as a “generic memristor”.
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Fadare, Anuoluwapo Grace, Yashika S. Kamte, Manish N. Chandwani, and Lauren A. O'Donnell. "Pediatric Neurotropic Infection Alters Synaptic Development in the Developing Brain." In 28th Annual Rowan-Virtua Research Day. Rowan University Libraries, 2024. http://dx.doi.org/10.31986/issn.2689-0690_rdw.stratford_research_day.173_2024.

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Many neurotropic viruses cause more significant pathology in younger hosts as their brains are still developing. This experiment asked how central nervous system (CNS) viral-infections affect the development of synapses in the pediatric brain during infection and post-infection. Synaptogenesis is at its peak in pediatric mice (10 days old) and we hypothesized that a neurotropic infection could disrupt synaptic proteins. We used a transgenic mouse model where measles virus (MV) infects only mature neurons, leading us to question whether synapses were impacted. We examined synaptic markers in the cerebellum and hippocampus in MV-infected and uninfected mice 9 days and 90 days post-infection through western blot analysis. We found differential downregulation of pre-synaptic proteins (synapsins 1, 2 and 3) during infection, which was dependent on the brain region and the time point examined. This highlights the short and long-term consequences of a pediatric infection on neurodevelopment and potential dysregulation of synaptogenesis.
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Carro-Perez, I., H. G. Gonzalez-Hernandez, and C. Sanchez-Lopez. "High-frequency memristive synapses." In 2017 IEEE 8th Latin-American Symposium on Circuits & Systems (LASCAS). IEEE, 2017. http://dx.doi.org/10.1109/lascas.2017.7948077.

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Gholipour, B., P. Bastock, K. Khan, C. Craig, D. W. Hewak, N. I. Zheludev, and C. Soci. "Chalcogenide Microfiber Photonic Synapses." In CLEO: Applications and Technology. Washington, D.C.: OSA, 2014. http://dx.doi.org/10.1364/cleo_at.2014.jw2a.32.

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lubrano, claudia, ugo bruno, chiara ausilio, and francesca santoro. "Engineer neuromimetic artificial synapses." In Neuromorphic Materials, Devices, Circuits and Systems. València: FUNDACIO DE LA COMUNITAT VALENCIANA SCITO, 2023. http://dx.doi.org/10.29363/nanoge.neumatdecas.2023.023.

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Koch, Christof. "Synapses that compute motion." In OSA Annual Meeting. Washington, D.C.: Optica Publishing Group, 1987. http://dx.doi.org/10.1364/oam.1987.mt2.

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Direction selective ganglion cells in the vertebrate retina respond differentially to the direction of a moving stimulus. Extracellular recordings in the rabbit retina [Barlow and Levick (1965)] indicate that the mechanism underlying this nonlinear operation involves inhibition vetoing excitation in the null direction. In the preferred direction, inhibition arrives too late to block excitation. Torre and Poggio (1978) proposed that this veto operation is mediated by the nonlinear interaction between excitation and inhibition with a reversal potential close to the resting potential of the cell (silent or shunting inhibition).
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Reports on the topic "Synapses"

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Heckman, James. Schools, Skills, and Synapses. Cambridge, MA: National Bureau of Economic Research, June 2008. http://dx.doi.org/10.3386/w14064.

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Mueller, Paul. Hardware Implementation of Neuron Nets and Synapses. Fort Belvoir, VA: Defense Technical Information Center, May 1991. http://dx.doi.org/10.21236/ada237704.

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Brown, Thomas H. Self-Organization of Hebbian Synapses on Hippocampal Neurons. Fort Belvoir, VA: Defense Technical Information Center, September 1995. http://dx.doi.org/10.21236/ada299559.

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Brown, Thomas H. Self-Organization of Hebbian Synapses on Hippocampal Neurons. Fort Belvoir, VA: Defense Technical Information Center, January 1996. http://dx.doi.org/10.21236/ada309810.

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White, Marvin H., Chun-Yu M. Chen, Margaret French, and Amit Banerjee. Electrically Modifiable Nonvolatile SONOS Synapses for Electronic Neural Networks. Fort Belvoir, VA: Defense Technical Information Center, September 1992. http://dx.doi.org/10.21236/ada258318.

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Johnston, Daniel. Heterosynaptic Modulation of Long-Term Potentiation at Mossy Fiber Synapses in Hippocampus. Fort Belvoir, VA: Defense Technical Information Center, May 1991. http://dx.doi.org/10.21236/ada238027.

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Artun, Omer B., Harel Z. Shouval, and Leon N. Cooper. The Effect of Dynamic Synapses on Spatio-temporal Receptive Fields in Visual Cortex. Fort Belvoir, VA: Defense Technical Information Center, December 1997. http://dx.doi.org/10.21236/ada333497.

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Bonci, Antonello. Plasticity of GABAergic Synapses in the Ventral Tegmental Area During Withdrawal from In Vivo Ethanol Administration. Fort Belvoir, VA: Defense Technical Information Center, July 2002. http://dx.doi.org/10.21236/ada407409.

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Terrian, David M. Presynaptic Modulation of the Hippocampal Mossy Fiber Synapse. Fort Belvoir, VA: Defense Technical Information Center, October 1991. http://dx.doi.org/10.21236/ada243381.

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Terrian, David M. Presynaptic Modulation of the Hippocampal Mossy Fiber Synapse. Fort Belvoir, VA: Defense Technical Information Center, September 1990. http://dx.doi.org/10.21236/ada229105.

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