Relevant bibliographies by topics / Synapse activity

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

Academic literature on the topic 'Synapse activity'

Author: Grafiati
Published: 19 October 2024

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Journal articles on the topic "Synapse activity"

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Hu, Xiaoge, Jian-hong Luo, and Junyu Xu. "The Interplay between Synaptic Activity and Neuroligin Function in the CNS." BioMed Research International 2015 (2015): 1–13. http://dx.doi.org/10.1155/2015/498957.

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Neuroligins (NLs) are postsynaptic transmembrane cell-adhesion proteins that play a key role in the regulation of excitatory and inhibitory synapses. Previousin vitroandin vivostudies have suggested that NLs contribute to synapse formation and synaptic transmission. Consistent with their localization, NL1 and NL3 selectively affect excitatory synapses, whereas NL2 specifically affects inhibitory synapses. Deletions or mutations in NL genes have been found in patients with autism spectrum disorders or mental retardations, and mice harboring the reported NL deletions or mutations exhibit autism-related behaviors and synapse dysfunction. Conversely, synaptic activity can regulate the phosphorylation, expression, and cleavage of NLs, which, in turn, can influence synaptic activity. Thus, in clinical research, identifying the relationship between NLs and synapse function is critical. In this review, we primarily discuss how NLs and synaptic activity influence each other.
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Pettem, Katherine L., Daisaku Yokomaku, Hideto Takahashi, Yuan Ge, and Ann Marie Craig. "Interaction between autism-linked MDGAs and neuroligins suppresses inhibitory synapse development." Journal of Cell Biology 200, no. 3 (January 28, 2013): 321–36. http://dx.doi.org/10.1083/jcb.201206028.

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Rare variants in MDGAs (MAM domain–containing glycosylphosphatidylinositol anchors), including multiple protein-truncating deletions, are linked to autism and schizophrenia, but the function of these genes is poorly understood. Here, we show that MDGA1 and MDGA2 bound to neuroligin-2 inhibitory synapse–organizing protein, also implicated in neurodevelopmental disorders. MDGA1 inhibited the synapse-promoting activity of neuroligin-2, without altering neuroligin-2 surface trafficking, by inhibiting interaction of neuroligin-2 with neurexin. MDGA binding and suppression of synaptogenic activity was selective for neuroligin-2 and not neuroligin-1 excitatory synapse organizer. Overexpression of MDGA1 in cultured rat hippocampal neurons reduced inhibitory synapse density without altering excitatory synapse density. Furthermore, RNAi-mediated knockdown of MDGA1 selectively increased inhibitory but not excitatory synapse density. These results identify MDGA1 as one of few identified negative regulators of synapse development with a unique selectivity for inhibitory synapses. These results also place MDGAs in the neurexin–neuroligin synaptic pathway implicated in neurodevelopmental disorders and support the idea that an imbalance between inhibitory and excitatory synapses may contribute to these disorders.
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Ko, Jaewon, Gilberto J. Soler-Llavina, Marc V. Fuccillo, Robert C. Malenka, and Thomas C. Südhof. "Neuroligins/LRRTMs prevent activity- and Ca2+/calmodulin-dependent synapse elimination in cultured neurons." Journal of Cell Biology 194, no. 2 (July 25, 2011): 323–34. http://dx.doi.org/10.1083/jcb.201101072.

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Neuroligins (NLs) and leucine-rich repeat transmembrane proteins (LRRTMs) are postsynaptic cell adhesion molecules that bind to presynaptic neurexins. In this paper, we show that short hairpin ribonucleic acid–mediated knockdowns (KDs) of LRRTM1, LRRTM2, and/or NL-3, alone or together as double or triple KDs (TKDs) in cultured hippocampal neurons, did not decrease synapse numbers. In neurons cultured from NL-1 knockout mice, however, TKD of LRRTMs and NL-3 induced an ∼40% loss of excitatory but not inhibitory synapses. Strikingly, synapse loss triggered by the LRRTM/NL deficiency was abrogated by chronic blockade of synaptic activity as well as by chronic inhibition of Ca2+ influx or Ca2+/calmodulin (CaM) kinases. Furthermore, postsynaptic KD of CaM prevented synapse loss in a cell-autonomous manner, an effect that was reversed by CaM rescue. Our results suggest that two neurexin ligands, LRRTMs and NLs, act redundantly to maintain excitatory synapses and that synapse elimination caused by the absence of NLs and LRRTMs is promoted by synaptic activity and mediated by a postsynaptic Ca2+/CaM-dependent signaling pathway.
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Gaidarova, Svetlana, JianWu Li, Laura G. Corral, Emilia Glezer, Peter H. Schafer, Weilin Xie, Antonia Lopez-Girona, Bruce D. Cheson, and Brydon Bennett. "Lenalidomide Alone and in Combination with Rituximab Enhances NK Cell Immune Synapse Formation in Chronic Lymphocytic Leukemia (CLL) Cells in Vitro through Activation of Rho and Rac1 GTPases." Blood 114, no. 22 (November 20, 2009): 3441. http://dx.doi.org/10.1182/blood.v114.22.3441.3441.

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Abstract Abstract 3441 Poster Board III-329 Background CLL is characterized by the progressive accumulation of monoclonal B lymphocytes. One theory to explain how CLL cells avoid elimination through immune surveillance mechanisms is through a defect in the ability of T-cells to form immunological synapses with antigen-presenting tumor B-cells (Ramsay et al JCI 2008). Lenalidomide is an immunomodulatory agent with clinical activity in the treatment of B-cell malignancies. Recent laboratory studies showed that lenalidomide not only stimulates T- and natural killer (NK)-cell-mediated ADCC, it also restores the T-cell-mediated ability to form immunological synapses with CLL tumor cells. Since NK cells also exert cytotoxicity through immune synapse formation, here we explore how lenalidomide affects NK-cell-mediated cytotoxicity mechanisms and whether this activity is altered in the presence of rituximab since published studies showed that lenalidomide-pretreated B-cells have a down-regulated surface CD20 expression. Further, we investigated the molecular events associated with immune synapse formation and the effect of lenalidomide. Methods Immune synapse formation was assessed in NK cells (from healthy donors PBMCs) co-cultured with either B-CLL cells derived from pts or with K562 cells (positive control). Cells were fixed and the ability to form synapses was assessed via immunohistochemisty co-staining for either F-actin and CD2, or F-actin and perforin (a cytolytic protein found in NK cells). Synapse formation was visualized by microscopy and measured via relative mean fluorescent intensity. Activity of RhoA, Rac1, Cdc42 were measured using Rho GTPases assay kits. Inhibition of lenalidomide-mediated immune synapse activity was assayed using the cell permeable Rho inhibitor C3 (0.5 mM). Flow cytometry was used to measure changes in surface CD20 and CD54 (ICAM-1) expression in B-CLL samples from 3 pts after treatment with lenalidomide. Results Lenalidomide induced the formation of immunological synapses between NK cells and primary B-CLL cells (p<.01) or the K562 cell line. Lenalidomide activated NK cells regardless of the presence of target cells, as measured by F-actin and perforin staining. RhoA and Rac1 were activated at the immunological synapse in the presence of lenalidomide. Inhibition of RhoA by the C3 inhibitor blocked F-actin localization, as well as perforin accumulation induced by lenalidomide at cell-cell contact sites, indicating inhibition of immune synapses and the associated cytolytic activity. This was also observed with Rac1 inhibition, but to a lesser degree than with RhoA inhibition. Functionality of formed synapses was confirmed by co-localization of F-actin and perforin at the synapse sites. 3 CLL pt samples treated ex vivo with lenalidomide demonstrated variable changes in CD20 expression: a 20-30% decrease in CD20 expression was observed in 2 B-CLL pt samples, whereas CD20 levels remained unchanged in the third. In the presence of rituximab, lenalidomide-induced synapse formation between NK cells and B-cells from CLL patients was further enhanced. This was accompanied by upregulation of costimulatory and adhesion molecule CD54 on B-CLL cells suggesting increased antigen presentation, which might contribute to the increased synapse formation. Conclusion Lenalidomide can directly activate NK-cell-mediated anti-tumor activity through enhanced formation of immune synapses via the regulation of Rho and Rac1 GTPases and the cytoskeleton. Despite some down-modulation of CD20 expression in lenalidomide-pretreated B-CLL cells, the immune synapse activity increases when lenalidomide is combined with rituximab suggesting that combining lenalidomide and anti-CD20 antibodies warrants exploration in the CLL clinical setting. Disclosures Gaidarova: Celgene: Employment, Equity Ownership. Li:Celgene: Employment. Corral:Celgene: Employment. Glezer:Celgene: Employment, Equity Ownership. Schafer:Celgene: Employment. Xie:Celgene: Employment. Lopez-Girona:Celgene: Employment.
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Moss, Brenda L., Abby D. Fuller, Christie L. Sahley, and Brian D. Burrell. "Serotonin Modulates Axo-Axonal Coupling Between Neurons Critical for Learning in the Leech." Journal of Neurophysiology 94, no. 4 (October 2005): 2575–89. http://dx.doi.org/10.1152/jn.00322.2005.

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S cells form a chain of electrically coupled neurons that extends the length of the leech CNS and plays a critical role in sensitization during whole-body shortening. This process requires serotonin, which acts in part by altering the pattern of activity in the S-cell network. Serotonin-containing axons and varicosities were observed in Faivre's nerve where the S-to-S-cell electrical synapses are located. To determine whether serotonin modulates these synapses, S-cell action-potential (AP) propagation was studied in a two-ganglion chain containing one electrical synapse. Suction electrodes were placed on the cut ends of the connectives to stimulate one S cell while recording the other, coupled S cell's APs. A third electrode, placed en passant, recorded the APs near the electrical synapse before they propagated through it. Low concentrations of the gap junction inhibitor octanol increased AP latency across the two-ganglion chain, and this effect was localized to the region of axon containing the electrical synapse. At higher concentrations, APs failed to propagate across the synapse. Serotonin also increased AP latency across the electrical synapse, suggesting that serotonin reduced coupling between S cells. This effect was independent of the direction of propagation and increased with the number of electrical synapses in progressively longer chains. Furthermore, serotonin modulated instantaneous AP frequency when APs were initiated in separate S cells and in a computational model of S-cell activity after mechanosensory input. Thus serotonergic modulation of S-cell electrical synapses may contribute to changes in the pattern of activity in the S-cell network.
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Wei, Wei, and Xiao-Jing Wang. "Downstream Effect of Ramping Neuronal Activity through Synapses with Short-Term Plasticity." Neural Computation 28, no. 4 (April 2016): 652–66. http://dx.doi.org/10.1162/neco_a_00818.

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Ramping neuronal activity refers to spiking activity with a rate that increases quasi-linearly over time. It has been observed in multiple cortical areas and is correlated with evidence accumulation processes or timing. In this work, we investigated the downstream effect of ramping neuronal activity through synapses that display short-term facilitation (STF) or depression (STD). We obtained an analytical result for a synapse driven by deterministic linear ramping input that exhibits pure STF or STD and numerically investigated the general case when a synapse displays both STF and STD. We show that the analytical deterministic solution gives an accurate description of the averaging synaptic activation of many inputs converging onto a postsynaptic neuron, even when fluctuations in the ramping input are strong. Activation of a synapse with STF shows an initial cubical increase with time, followed by a linear ramping similar to a synapse without STF. Activation of a synapse with STD grows in time to a maximum before falling and reaching a plateau, and this steady state is independent of the slope of the ramping input. For a synapse displaying both STF and STD, an increase in the depression time constant from a value much smaller than the facilitation time constant [Formula: see text] to a value much larger than [Formula: see text] leads to a transition from facilitation dominance to depression dominance. Therefore, our work provides insights into the impact of ramping neuronal activity on downstream neurons through synapses that display short-term plasticity. In a perceptual decision-making process, ramping activity has been observed in the parietal and prefrontal cortices, with a slope that decreases with task difficulty. Our work predicts that neurons downstream from such a decision circuit could instead display a firing plateau independent of the task difficulty, provided that the synaptic connection is endowed with short-term depression.
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Liu, Kang K. L., Michael F. Hagan, and John E. Lisman. "Gradation (approx. 10 size states) of synaptic strength by quantal addition of structural modules." Philosophical Transactions of the Royal Society B: Biological Sciences 372, no. 1715 (March 5, 2017): 20160328. http://dx.doi.org/10.1098/rstb.2016.0328.

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Memory storage involves activity-dependent strengthening of synaptic transmission, a process termed long-term potentiation (LTP). The late phase of LTP is thought to encode long-term memory and involves structural processes that enlarge the synapse. Hence, understanding how synapse size is graded provides fundamental information about the information storage capability of synapses. Recent work using electron microscopy (EM) to quantify synapse dimensions has suggested that synapses may structurally encode as many as 26 functionally distinct states, which correspond to a series of proportionally spaced synapse sizes. Other recent evidence using super-resolution microscopy has revealed that synapses are composed of stereotyped nanoclusters of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors and scaffolding proteins; furthermore, synapse size varies linearly with the number of nanoclusters. Here we have sought to develop a model of synapse structure and growth that is consistent with both the EM and super-resolution data. We argue that synapses are composed of modules consisting of matrix material and potentially one nanocluster. LTP induction can add a trans-synaptic nanocluster to a module, thereby converting a silent module to an AMPA functional module. LTP can also add modules by a linear process, thereby producing an approximately 10-fold gradation in synapse size and strength. This article is part of the themed issue ‘Integrating Hebbian and homeostatic plasticity’.
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Zhao, Qing-Tai, Fengben Xi, Yi Han, Andreas Grenmyr, Jin Hee Bae, and Detlev Gruetzmacher. "Ferroelectric Devices for Neuromorphic Computing." ECS Meeting Abstracts MA2022-02, no. 32 (October 9, 2022): 1183. http://dx.doi.org/10.1149/ma2022-02321183mtgabs.

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Neuromorphic computing inspired by the neural network systems of the human brain enables energy efficient computing for big-data processing. A neural network is formed by thousands or even millions of neurons which are connected by even a higher number of synapses. Neurons communicate with each other through the connected synapses. The main responsibility of synapses is to transfer information from the pre-synaptic to the postsynaptic neurons. Synapses can memorize and process the information simultaneously. The plasticity of a synapse to strengthen or weaken their activity over time make it capable of learning and computing. Thus, artificial synapses which can emulate functionalities and the plasticity of bio-synapses form the backbones of neuromorphic computing. Alternative artificial synapses have been successfully demonstrated. The classical two-terminal memristor devices, like resistive random access memory (ReRAM), phase change memory (PCM) and ferroelectric tunnel junctions (FTJs) with one terminal connected to the pre-synaptic neuron and another connected with the post-synaptic neuron, own advantages of simple structure, easy processing with high density, and capability of integration with CMOS. However, signal processing and learning cannot be performed simultaneously in 2-terminal devices, thus limiting their synaptic functionalities. Ferroelectric field effect transistors (FeFET) which uses ferroelectric as the gate oxide are the most interesting three-terminal artificial synapse devices, in which the gate or the source is connected to the pre-synaptic neuron while the drain is used for the terminal of the post-synaptic neuron , thus can perform signal transmission and learning simultaneously. However, traps at the channel interface can degrade the device performance causing low endurance. Focuses of those abovementioned devices have been mainly put on the homosynaptic plasticity, which is input specific, meaning that the plasticity occurs only at the synapse with a pre-synaptic activation . The homosynaptic plasticity has a drawback of positive feedback loop: when a synapse is potentiated, the probability of the synapse to be further potentiated is increased. Similarly, when a synapse is depressed the probability of the synapse of being further depressed is higher. Therefore, synaptic weights tend to be either strengthened to the maximum value or weakened to zero, causing the system to be unstable. In contrast, heterosynaptic plasticity can be induced at any synapse at the same time after episodes of strong postsynaptic activity, avoiding the positive feedback problem and stabilize the activity of the post-synaptic neuron. To address the above challenges we proposed a very simple 4-terminal synapse structure based on gated Schottky diodes on silicon (FEMOD) with a ferroelectric layer. The conductance of the Schottky diode is modulated by the polarization of the ferroelectric layer. With this simple synapse structure we can achieve multiple hetero-synaptic functions, including excitatory/ inhibitory post-synaptic current (EPSC/IPSC), paired-pulse facilitation/depression (PPF/PPD), long-term potentiation/depression (LTP/LTD), as well as biological neuron-like spike-timing-dependent plasticity (STDP) characteristics. The modulatory synapse can modify the weight of another synapse with a very low voltage. Furthermore, logic gates, like AND and NAND which are highly desired for in-memory computing can be realized with such simple structure. Figure 1
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Wilson, Emily S., and Karen Newell-Litwa. "Stem cell models of human synapse development and degeneration." Molecular Biology of the Cell 29, no. 24 (November 26, 2018): 2913–21. http://dx.doi.org/10.1091/mbc.e18-04-0222.

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Many brain disorders exhibit altered synapse formation in development or synapse loss with age. To understand the complexities of human synapse development and degeneration, scientists now engineer neurons and brain organoids from human-induced pluripotent stem cells (hIPSC). These hIPSC-derived brain models develop both excitatory and inhibitory synapses and functional synaptic activity. In this review, we address the ability of hIPSC-derived brain models to recapitulate synapse development and insights gained into the molecular mechanisms underlying synaptic alterations in neuronal disorders. We also discuss the potential for more accurate human brain models to advance our understanding of synapse development, degeneration, and therapeutic responses.
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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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Dissertations / Theses on the topic "Synapse activity"

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Ghezali, Grégory. "Control of synaptic transmission by astroglial connexin 30 : molecular basis, activity-dependence and physiological implication." Thesis, Paris 6, 2016. http://www.theses.fr/2016PA066423/document.

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Les astrocytes périsynaptiques participent activement, au côté des neurones, dans le traitement de l’information cérébrale. Une propriété essentielle des astrocytes est d’exprimer un niveau élevé de protéines appelées connexines (Cxs), et formant les sous-unités des jonctions communicantes. Étonnamment, bien qu’il ait été suggéré très tôt que la Cx30 astrocytaire soit impliquée dans des processus cognitifs, son rôle exact dans la neurophysiologie demeure cependant encore mal connu. Nous avons récemment révélé que la Cx30, via une fonction non-canal inédite, contrôle la force et la plasticité de la transmission synaptique glutamatergique de l’hippocampe en régulant les niveaux synaptiques de glutamate par le biais du transport astrocytaire du glutamate. Cependant, les mécanismes moléculaire et cellulaire impliqués dans ce contrôle, ainsi que sa régulation dynamique par l’activité neuronale et son impact in vivo dans un contexte physiologique restaient inconnus. Dans le cadre de cette problématique, j’ai démontré durant ma thèse que: 1) La Cx30 induit la maturation morphologique des astrocytes de l’hippocampe par l’intermédiaire de la modulation d’une voie de signalisation dépendante de la laminine et régulant la polarisation cellulaire ; 2) l’expression de la Cx30, sa localisation perisynaptique, ainsi que ses fonctions sont modulées par l’activité neuronale ; 3) Le contrôle de la couverture astrocytaire des synapses du noyau supraoptique de l’hypothalamus par la Cx30 fixe les niveaux plasmatiques de base de la neurohormone ocytocine et ainsi favorise la mise en place de comportements sociaux adaptés. Dans l’ensemble, ces résultats éclairent les régulations des Cxs astrocytaires par l’activité neuronale et leur rôle dans le développement postnatal des réseaux neurogliaux, ainsi que dans le contrôle des interactions structurelles astrocytes-synapses à l’origine de processus comportementaux
Perisynaptic astrocytes are active partners of neurons in cerebral information processing. A key property of astrocytes is to express high levels of the gap junction forming proteins, the connexins (Cxs). Strikingly, astroglial Cx30 was suggested early on to be involved in cognitive processes; however, its specific role in neurophysiology has yet been unexplored. We recently reveal that Cx30, through an unconventional non-channel function, controls hippocampal glutamatergic synaptic strength and plasticity by directly setting synaptic glutamate levels through astroglial glutamate clearance. Yet the cellular and molecular mechanisms involved in such control, its dynamic regulation by activity and its impact in vivo in a physiological context were unknown. To answer these questions, I demonstrated during my PhD that: 1) Cx30 drives the morphological maturation of hippocampal astrocytes via the modulation of a laminin signaling pathway regulating cell polarization; 2) Cx30 expression, perisynaptic localization and functions are modulated by neuronal activity; 3) Cx30-mediated control of astrocyte synapse coverage in the supraoptic nucleus of the hypothalamus sets basal plasmatic level of the neurohormone oxytocin and hence promotes appropriate oxytocin-based social abilities. Taken together, these data shed new light on astroglial Cxs activity-dependent regulations and roles in the postnatal development of neuroglial networks, as well as in astrocyte-synapse structural interactions mediating behavioral processes
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Mardinly, Alan Robert. "Regulation of Synapse Development by Activity Dependent Transcription in Inhibitory Neurons." Thesis, Harvard University, 2013. http://dissertations.umi.com/gsas.harvard:10739.

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Neuronal activity and subsequent calcium influx activates a signaling cascade that causes transcription factors in the nucleus to rapidly induce an early-response program of gene expression. This early-response program is composed of transcriptional regulators that in turn induce transcription of late-response genes, which are enriched for regulators of synaptic development and plasticity that act locally at the synapse.
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Brown, Rosalind. "Role of activity in neuromuscular synaptic degeneration : insights from Wlds mice." Thesis, University of Edinburgh, 2012. http://hdl.handle.net/1842/6523.

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The nervous system is a dynamic structure. Both during development and in the adult, synapses display activity-dependent plasticity which can modify their structure and function. In the neonate, activity influences the stability of functional connections between the muscle and nerve. In adults, the process of neurotransmitter release and the structure of the postsynaptic muscle can also be altered by external stimuli such as exercise. It is important to understand this plasticity of the neuromuscular system, the ways in which it can be modified, and its relationship to the maintenance or degeneration of synapses. After injury, peripheral nerve undergoes Wallerian Degeneration, during which the connections between axons and muscle fibres are lost, followed by the fragmentation of the nerve itself. The primary goal of this thesis was to determine whether activity modulates this process; that is, whether enhancing or reducing neuromuscular activity creates a susceptibility to degeneration or alternatively provides any protection against it. Developing greater understanding of this process is essential in relation to neurodegenerative disorders in which the benefits of activity, in the form of exercise, are controversial. Using Wlds mice, in which synaptic degeneration occurs approximately ten times more slowly than normal after nerve injury, I investigated the influence of both decreased (tetrodotoxin induced paralysis) and increased (voluntary wheel running) activity in vivo on this process. Paralysis prior to axotomy resulted in a significant increase in the rate of synapse degeneration. Using a novel method of repeatedly visualising degenerating synapses and axons in vivo I also established that this effect was specific to the synapse, as it did not affect the degeneration of axons. In contrast, voluntary wheel running had no effect on the rate of either axonal or neuromuscular synapse degeneration, but induced a slight modification of neuromuscular transmission. To provide a more stringent test I developed a novel assay based on overnight, ex vivo incubation of nerve-muscle preparations at 32°C. I first demonstrated that this procedure separates the different degeneration time courses for neuromuscular synapse degeneration in wild-type and Wlds preparations. I then extended the study to investigate further ways of modulating synaptic degeneration. First, I tested the effects of electrical stimulation. Intermittent high frequency (100Hz) stimulation reduced the level of protection. Finally, I tested the effects of NAMPT enzymatic inhibitor FK866 on synaptic degeneration. Interestingly, the synaptic protection observed in Wlds muscles was enhanced in the presence of FK866. The results of my findings are relevant to understanding the plasticity of synapses and its relationship to degeneration. Together, these studies highlight the potential of genetic and epigenetic factors, including activity, to regulate neuromuscular synapse degeneration. My study also provides proof of concept for a novel organotypic culture system in which to identify pharmacological modulators of synaptic degeneration that could form part of a second-line screen for neuroprotective compounds or phenotypes. My findings may be viewed in the wide context of neurodegenerative disease, since synaptic use or disuse is widely thought to influence susceptibility, onset and progression in such disorders.
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Xiao, Wei. "Class 5 semaphorins mediate synapse elimination and activity-dependent synaptic plasticity in hippocampal neurons." Thesis, University of British Columbia, 2017. http://hdl.handle.net/2429/60340.

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Although autism spectrum disorders (ASDs) have long been known to have a strong heritability, the genetic basis of these disorders has remained largely elusive. Hundreds of genes have been linked to ASDs, but most of them only contribute a small increase in risk. In 2009, a genome-wide association study identified Semaphorin 5A (SEMA5A) as a novel autism susceptibility gene. Sema5A is a member of the Semaphorin family consisting of secreted and membrane-associated proteins characterized by the Sema domain. Although initially identified as axon guidance cues, Semaphorins have been found to play numerous key roles in the development and function of the nervous system. Here, I provide evidence that Sema5A, along with Sema5B, regulates dendritic morphology and excitatory synaptic elimination in hippocampal neurons. The overexpression of Sema5A/Sema5B negatively impacted dendrite complexity and reduced excitatory synapse density without affecting inhibitory synapses, in contrast the knockdown of Sema5A/Sema5B increased excitatory synapse density. I also investigated the relationship between Sema5A/Sema5B and activity-dependent plasticity including long-term potentiation (LTP) and long-term depression (LTD), which are cellular models of learning and memory. It was demonstrated that the overexpression of Sema5A/Sema5B attenuated the LTP-mediated increase of synapse density, whereas the knockdown of Sema5A/Sema5B blocked the LTD-mediated decrease of synapse density. Furthermore, soluble Sema5A treatment altered the surface expression of the AMPA receptor subunit GluA1 with total level of GluA1 unchanged. Finally, I examined the signaling mechanisms of Sema5A-mediated synapse elimination and plasticity. I found that in vitro Sema5A signalled through two members (Plexin A1 and Plexin A2) of the Plexin family, which are known as the neuronal receptors for the Semaphorin family. Moreover, TAG-1, a cell adhesion molecule also known as Contactin-2, was necessary for the function of Sema5A and Sema5B. Lastly I found that ALLN, an inhibitor of protease calpain, significantly rescued Sema5A-mediated synapse elimination, suggesting that calpain was downstream of Sema5A signaling in hippocampal neurons. Thus, my data revealed a new role for class 5 Semaphorins in synapse density and plasticity, and may therefore provide insights into the critical roles of Sema5A in the general mechanisms of circuit formation and the specific etiology of ASDs.
Medicine, Faculty of
Graduate
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Jay, Taylor Reagan. "The TREM2 Receptor Directs Microglial Activity in Neurodegeneration and Neurodevelopment." Case Western Reserve University School of Graduate Studies / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=case1560181547156823.

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Ataman, Bulent. "The Molecular Mechanisms of Activity-Dependent Wingless (Wg)/Wnt Signaling at a Drosophila Glutamatergic Synapse: a Dissertation." eScholarship@UMMS, 2008. https://escholarship.umassmed.edu/gsbs_diss/353.

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Synaptic plasticity, the ability of synapses to change in strength, underlies complex brain functions such as learning and memory, yet little is known about the precise molecular mechanisms and downstream signaling pathways involved. The major goal of my doctoral thesis was to understand these molecular mechanisms and cellular processes underlying synaptic plasticity using the Drosophilalarval neuromuscular junction (NMJ) as a model system. My work centered on a signaling pathway, the Wg/Wnt signaling pathway, which was found to be crucial for activity-driven synapse formation. The Wg/Wnt family of secreted proteins, besides its well-characterized roles in embryonic patterning, cell growth and cancer, is beginning to be recognized as a pivotal player during synaptic differentiation and plasticity in the brain. At the DrosophilaNMJ, the Wnt-1 homolog Wingless (Wg) is secreted from presynaptic terminals and binds to Frizzled-2 (DFz2) receptors in the postsynaptic muscle. Perturbations in Wg signaling lead to poorly differentiated NMJs, containing synaptic sites that lack both neurotransmitter release sites and postsynaptic structures. In collaboration with other members of the Budnik lab, I set out to unravel the mechanisms by which Wg regulates synapse differentiation. We identified a novel transduction pathway that provides communication between the postsynaptic membrane and the nucleus, and which is responsible for proper synapse development. In this novel Frizzled Nuclear Import (FNI) pathway, the DFz2 receptor is internalized and transported towards the nucleus. The C-terminus of DFz2 is subsequently cleaved and imported into the postsynaptic nucleus for potential transcriptional regulation of synapse development (Mathews, Ataman, et al. Science (2005) 310:1344). My studies also centered on the genetic analysis of Glutamate Receptor (GluR) Interacting Protein (dGRIP), which in mammals has been suggested to regulate the localization of GluRs and more recently, synapse development. I generated mutations in the gene, transgenic strains carrying a dGRIP-RNAi and fluorescently tagged dGRIP, and antibodies against the protein. Remarkably, I found dgrip mutants had synaptic phenotypes that closely resembled those in mutations altering the FNI pathway. Through the genetic analysis of dgrip and components of the FNI pathway, immunoprecipitation studies, electron microscopy, in vivotrafficking assays, time-lapse imaging, and yeast two-hybrid assays, I demonstrated that dGRIP had a hitherto unknown role as an essential component of the FNI pathway. dGRIP was found in trafficking vesicles that contain internalized DFz2. Further, DFz2 and dGRIP likely interact directly. Through the use of pulse chase experiments I found that dGRIP is required for the transport of DFz2 from the synapse to the nucleus. These studies thus provided a molecular mechanism by which the Wnt receptor, DFz2, is trafficked from the postsynaptic membrane to the nucleus during synapse development and implicated dGRIP as an essential component of the FNI pathway (Ataman et al. PNAS (2006) 103:7841). In the final part of my dissertation, I concentrated on understanding the mechanisms by which neuronal activity regulates synapse formation, and the role of the Wnt pathway in this process. I found that acute changes in patterned activity lead to rapid modifications in synaptic structure and function, resulting in the formation of undifferentiated synaptic sites and to the potentiation of spontaneous neurotransmitter release. I also found that these rapid modifications required a bidirectional Wg transduction pathway. Evoked activity induced Wg release from synaptic sites, which stimulated both the postsynaptic FNI pathway, as well as an alternative presynaptic Wg pathway involving GSK-3ß/Shaggy. I suggest that the concurrent activation of these alternative pathways by the same ligand is employed as a mechanism for the simultaneous and coordinated assembly of the pre- and postsynaptic apparatus during activity-dependent synapse remodeling (Ataman et al. Neuron (2008) in press). In summary, my thesis work identified and characterized a previously unrecognized synaptic Wg/Wnt transduction pathway. Further, it established a mechanistic link between activity-dependent synaptic plasticity and bidirectional Wg/Wnt signaling. These findings provide novel mechanistic insight into synaptic plasticity.
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Sjölin, Hanna. "Regulation of NK cell activity : studies of DAP12-associated receptors in immune synapse formation and in responses to cytomegalovirus infection /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-985-8/.

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Louçã, Mathilde. "Functional impacts of Huntingtin lowering on the synaptic maturation and activity of neuronal networks derived from human induced pluripotent stem cells." Electronic Thesis or Diss., université Paris-Saclay, 2024. http://www.theses.fr/2024UPASL054.

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La maladie de Huntington (MH) est une maladie neurodégénérative causée par la mutation de la Huntingtine (HTT). La réduction de l'expression de la HTT mutante est une piste thérapeutique évidente en cours d’exploration chez les patients. Le ciblage de la HTT mutante s’accompagne cependant le plus souvent d’une réduction concomitante de la HTT non mutée. Les conséquences de la perte de cette protéine sur la santé des neurones restent mal connues.Mon travail de thèse traite cette question en utilisant des modèles in vitro de réseaux neuronaux humains différenciés à partir de cellules souches induites à la pluripotence. Mes travaux démontrent que la perte de HTT induit des anomalies de développement et d’homéostasie de ces réseaux. Mes résultats suggèrent que les thérapies ciblant indifféremment la HTT mutante et non mutante pourraient compromettre la santé des circuits neuronaux ciblés
Huntington's disease (HD) is a neurodegenerative disorder caused by a mutation in the Huntingtin gene (HTT). Reducing the expression of mutant HTT is an obvious therapeutic approach explored in patients. However, targeting mutant HTT often leads to a simultaneous reduction in non-mutant HTT. The consequences of losing this protein on neuronal health remain poorly understood.My doctoral work addresses this question using in vitro models of human neuronal networks differentiated from induced pluripotent stem cells. My research demonstrates that HTT loss induces developmental and homeostatic abnormalities in these networks. My results suggest that therapies targeting both mutant and non-mutant HTT indiscriminately could compromise the health of targeted neuronal circuits
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McMahon, Catherine. "The mechanisms underlying normal spike activity of the primary afferent synapse in the cochlea and its dysfunction : an investigation of the possible mechanisms of peripheral tinnitus and auditory neuropathy." University of Western Australia. School of Biomedical and Chemical Sciences, 2004. http://theses.library.uwa.edu.au/adt-WU2003.0034.

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[Truncated abstract] One of the problems in researching tinnitus is that it has often been assumed that the physiological mechanisms underlying the tinnitus percept cannot be objectively measured. Nonetheless, it is generally accepted that the percept results from altered spontaneous neural activity at some site along the auditory pathway, although it is still debated whether it is produced by: synchronisation of activity of adjacent neurones; a change in the temporal pattern of activity of individual neurones; or an increase in the spontaneous firing rate per se. Similarly, it is possible that the recently coined “auditory neuropathy” is produced by under-firing of the primary afferent synapse, although several other mechanisms can also produce the symptoms described by this disorder (normal cochlear mechanical function but absent, or abnormal, synchronous neural firing arising from the cochlea and auditory brainstem, known as the auditory brainstem response, or ABR). Despite an absent ABR, some subjects can detect pure tones at near-normal levels, although their ability to integrate complex sounds, such as speech, is severely degraded in comparison with the pure-tone audiogram. The aim of the following study was to investigate the normal mechanisms underlying neural firing at the primary afferent synapse, and its regulation, to determine the possible mechanisms underlying over-firing (tinnitus) or under-firing (auditory neuropathy) of primary afferent neurones.
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Katona, Linda. "The role of cell-type selective synaptic connections in rhythmic neuronal network activity in the hippocampus." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:cebe42e9-4040-486b-8ff4-fa1bf642bea0.

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Books on the topic "Synapse activity"

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Mamalyga, L. M., ed. Simulation of Neural Networks Based on Self-Assembly of Reaction-Diffusion Electrical Synapses and their Nonlinear Electrophysiological Activity, 164 p. [in Russian]. Moscow: Moscow Pedagogical State University, Department of Biology & Chemistry, 2012.

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Baldi, Elisabetta, and Corrado Bucherelli. Neuroscience. Florence: Firenze University Press, 2017. http://dx.doi.org/10.36253/978-88-6453-638-5.

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This bibliographic material is patrimony of our Laboratory of the Behavior Physiology. This research unit originated in 1972 by will of Aldo Giachetti (until 1990) and with the beginning of the activity of Corrado Bucherelli. In the early 1980s, with Carlo Ambrogi Lorenzini (until 2004), the cataloging became more capillary and systematic, to continue to this day. All the researchers who worked in our laboratory contributed to this collection (Giovanna Tassoni 1986-2000, Benedetto Sacchetti 1996-2002 and Elisabetta Baldi from 1991). The study of learning, memory and behavior requires to follow a broad spectrum of neuroscience topics, ranging from neuronal biochemistry to neuropsychology. The Authors’ idea of publishing this collection comes from believing that a such website, though not exhaustive, might be a useful and targeted tool for the selection of bibliographic material in the field of behavioral neuroscience. The bibliographic references present at the publication (29500), accompanied by a brief comment highlighting the contents, are organized in relation to the topics (represented by the 99 themes) constituting the publication itself. The intersection of several references will point out the topics that represent them simultaneously. Concerning neurotransmitters and neuromodulators, references to agonists, antagonists or molecules interfering with the activity of these synapses have been inserted in the pages of the implicated neurotransmitter (e.g. acetylcholine). The pages including topics that could have been dealt with separately (e.g. active and passive avoidance) are introduced by a short explanatory note. The comment of each publication highlights the animal species used. Each comment is intended to indicate the content rather than the experimental results of paper. This choice comes from wanting to provide the reader with a more objective and less speculative comment.
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Grant, Seth G. N. Synaptic Mechanisms of Psychotic Disorders. Edited by Dennis S. Charney, Eric J. Nestler, Pamela Sklar, and Joseph D. Buxbaum. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190681425.003.0017.

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Synapses are the hallmark of the neuroanatomy of the brain. The million billion synapses of the human brain connect the nerve cells into the networks that underpin all behavior. The molecular anatomy of synapses is also remarkably complicated with ~2000 proteins in the synapse proteome. The proteins are physically organized into a hierarchy of molecular machines that control synapse biology. These proteins integrate and compute the information in patterns of nerve cell activity. Mutations in hundreds of genes that encode synaptic proteins contribute to over one hundred brain diseases, including common mental disorders. The synapse proteome is of fundamental importance to mental illness.
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Flavell, Steven Willem. Regulation of synapse development by the activity-regulated transcription factor MEF2. 2009.

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Sturgill, James Fitzhugh. Activity-dependent regulation of synapse structure and function: Roles of PSD-95 and the metabolic sensor, AMPK. 2010.

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Bay, Mihee J., and Bruce K. Shapiro. Attention Deficit-Hyperactivity Disorder. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0060.

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Attention deficit hyperactivity disorder (ADHD) is the most common neurobehavioral disorder in children and is characterized by developmentally inappropriate levels of attention and/or activity level. The current diagnostic criteria are summarized in the recently updated DSM-5. Although the neurobiology of ADHD is not completely understood, dysfunction in the fronto-striatal network and catecholaminergic system is likely implicated in pathophysiology of ADHD although recent studies suggest involvement of other neural substrates as well. Stimulants have been the mainstay of pharmacotherapy for ADHD due to its role in increasing available catecholamines in the synapse. However, treatment approach should be multimodal.
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Beninger, Richard J. Neuroanatomy and dopamine systems. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198824091.003.0011.

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Neuroanatomy and dopamine systems explains how sensory signals ascend the central nervous system via a series of nuclei; axons detecting specific elements converge onto higher-order neurons that respond to particular stimulus features. Assemblies of feature-detection cells in the cerebral cortex detect complex stimuli such as faces. These cell assemblies project to motor nuclei of the dorsal and ventral striatum where they terminate on dendritic spines of efferent medium spiny neurons. Dopaminergic projections from ventral mesencephalic nuclei terminate on the same spines. Individual corticostriatal afferents contact relatively few medium spiny neurons and individual dopaminergic neurons contact a far larger number. Stimuli activate specific subsets of corticostriatal synapses. Synaptic activity that is closely followed by a rewarding stimulus, that produces a burst of action potentials in dopaminergic neurons, is modified so that those specific corticostriatal synapses acquire an increased ability to elicit approach and other responses in the future, i.e., incentive learning.
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Beninger, Richard J. Mechanisms of dopamine-mediated incentive learning. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198824091.003.0012.

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Mechanisms of dopamine-mediated incentive learning explains how sensory events, resulting from an animal’s movement and the environment, activate cortical glutamatergic projections to dendritic spines of striatal medium spiny neurons to initiate a wave of phosphorylation. If no rewarding stimulus is encountered, a subsequent wave of phosphatase activity undoes the phosphorylation. If a rewarding stimulus is encountered, dopamine initiates a cascade of events in D1 receptor-expressing medium spiny neurons that may prevent the phosphatase effects and work synergistically with signaling events produced by glutamate. As a result, corticostriatal synapses have a greater impact on response systems; this may be part of the mechanism of incentive learning. Dopamine acting on dendritic spines of D2 receptor-expressing medium spiny neurons may prevent synaptic strengthening by inhibiting adenosine signaling; these synapses may be weakened through mechanisms involving endocannabinoids. When dopamine concentrations drop, e.g. during negative prediction errors, the opposite may occur, producing inverse incentive learning.
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Book chapters on the topic "Synapse activity"

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Palm, Daniel, and Frank Entschladen. "Neoneurogenesis and the Neuro-Neoplastic Synapse." In Neuronal Activity in Tumor Tissue, 91–98. Basel: KARGER, 2007. http://dx.doi.org/10.1159/000100049.

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Zänker, Kurt S. "The Neuro-Neoplastic Synapse: Does it Exist?" In Neuronal Activity in Tumor Tissue, 154–61. Basel: KARGER, 2007. http://dx.doi.org/10.1159/000100075.

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Ulbricht, Carolin, Ruth Leben, Yu Cao, Raluca A. Niesner, and Anja E. Hauser. "Combined FRET-FLIM and NAD(P)H FLIM to Analyze B Cell Receptor Signaling Induced Metabolic Activity of Germinal Center B Cells In Vivo." In The Immune Synapse, 91–111. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-3135-5_6.

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Barber, Michael J., and Jeff W. Lichtman. "Resolving the Paradoxical Effect of Activity on Synapse Elimination." In Computational Neuroscience, 131–35. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-4831-7_22.

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Gorman, Julia, Konstantin Holzhausen, Joyce Reimer, and Jørgen Riseth. "Realizing Synaptic Signal Transmission During Astrocyte-Neuron Interactions within the EMI Framework." In Computational Physiology, 65–78. Cham: Springer Nature Switzerland, 2023. http://dx.doi.org/10.1007/978-3-031-25374-4_5.

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AbstractThe tripartite synapse or “neural threesome” refers to the interplay in the synapse between neighbouring neurons, the synaptic cleft, and the surrounding glial cells. Despite extensive research, the effects of glial cells, such as astrocytes, on signal transduction between neurons are not fully understood. The Kirchhoff-Nernst- Planck (KNP) and Extracellular-Membrane-Intracellular (EMI) models constitute a promising framework for modeling these kinds of systems. However, they lack the neurotransmitter-related mechanisms that are necessary to bridge signal transduction across the synaptic cleft. Here, we propose an extension to the KNP-EMI model by a spatio-temporal diffusion-based description of the most prominent neurotransmitter, glutamate, that allows for investigation of the contribution of astrocytes to the functionality of the synapse. We validate our model by showing that the presence of an astrocyte in the domain affects the glutamate flux across the postsynaptic terminal, as observed physiologically. The proposed extension offers a sufficiently simple way of integrating synaptic glutamate dynamics into the KNP-EMI framework. It introduces the relevant interactions between electrical activity and diffusion processes at the tripartite synapse that are necessary to assess how astrocytes might contribute to the functionality of the synapse. This work has implications for future studies involving glial mechanisms and other charged species within the KNP-EMI framework.
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Bera, Sujoy, Gonca Bayraktar, Katarzyna M. Grochowska, Michelle Melgarejo da Rosa, and Michael R. Kreutz. "Activity Dependent Protein Transport from the Synapse to the Nucleus." In Dendrites, 111–24. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-56050-0_5.

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Borodinsky, Laura N., and Nicholas C. Spitzer. "Mechanisms of Synapse Formation: Activity-Dependent Selection of Neurotransmitters and Receptors." In Co-Existence and Co-Release of Classical Neurotransmitters, 1–12. Boston, MA: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-09622-3_3.

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Graham, Bruce. "Multiple Forms of Activity-Dependent Plasticity Enhance Information Transfer at a Dynamic Synapse." In Artificial Neural Networks — ICANN 2002, 45–50. Berlin, Heidelberg: Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/3-540-46084-5_8.

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Farsi, Zohreh, and Andrew Woehler. "Imaging Activity-Dependent Signaling Dynamics at the Neuronal Synapse Using FRET-Based Biosensors." In Methods in Molecular Biology, 261–75. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-6688-2_18.

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Varfolomeev, Sergey, Viktor Bykov, and Svetlana Tsybenova. "Kinetic modelling of processes in the cholinergic synapse. Mechanisms of functioning and control methods." In ORGANOPHOSPHORUS NEUROTOXINS, 127–39. ru: Publishing Center RIOR, 2020. http://dx.doi.org/10.29039/22_127-139.

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The kinetic model describing the dynamics of synaptic “discharge” taking into account the kinetics of the injection of the neurotransmitter into the synaptic cleft, the pH-dependence of catalytic activity of the enzyme and diffusion withdrawal of protons is proposed and studied. In the framework of the kinetic model, the functioning of the cholinergic synapse is considered. The results of mathematical modeling of changes in the level of acetylcholine, induced pH impulse, the influence of the frequency of impulse transfer and inhibition of acetylcholinesterase are presented. Physico-chemical explanation for a number of important physiological phenomena, such as neuromuscular paralysis, the molecular mechanism of neurological memory, actions of nerve poisons and toxins and Alzheimer’s disease is given.
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Conference papers on the topic "Synapse activity"

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Tsai, Chiou-Tsun, Norihiro Watanabe, and Maksim Mamonkin. "313 Enhancing anti-cancer activity of therapeutic T-cells with a synapse-stabilizing receptor." In SITC 38th Annual Meeting (SITC 2023) Abstracts. BMJ Publishing Group Ltd, 2023. http://dx.doi.org/10.1136/jitc-2023-sitc2023.0313.

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Danaei, Farzaneh, Fariba Bahrami, and Mahyar Janahmadi. "Alzheimer's disease can cause epileptic seizure activity in a CA3-CA1 tripartite synapse: A computational study." In 2014 22nd Iranian Conference on Electrical Engineering (ICEE). IEEE, 2014. http://dx.doi.org/10.1109/iraniancee.2014.6999870.

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Mejias, J. F., J. J. Torres, Joaquín Marro, Pedro L. Garrido, and Pablo I. Hurtado. "Memory and pattern storage in neural networks with activity dependent synapses." In MODELING AND SIMULATION OF NEW MATERIALS: Proceedings of Modeling and Simulation of New Materials: Tenth Granada Lectures. AIP, 2009. http://dx.doi.org/10.1063/1.3082323.

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Sergeeva, Svetlana. "ELECTRICAL SYNAPSES ON NERVE BRANCHES FORM THE REVERBERATION ACTIVITY OF A NEURON." In XVIII INTERNATIONAL INTERDISCIPLINARY CONGRESS NEUROSCIENCE FOR MEDICINE AND PSYCHOLOGY. LCC MAKS Press, 2022. http://dx.doi.org/10.29003/m2922.sudak.ns2022-18/305.

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Ibanez, Jorge, Haley Houke, Michaela Meehl, Jennifer Ocasio, Nikhil Hebbar, Paulina Velasquez, Suzanne Baker, and Giedre Krenciute. "231 Dysfunctional immune synapses restrain anti-DIPG activity of CAR T cells." In SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.0231.

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Werner, T., D. Garbin, E. Vianello, O. Bichler, D. Cattaert, B. Yvert, B. De Salvo, and L. Perniola. "Real-time decoding of brain activity by embedded Spiking Neural Networks using OxRAM synapses." In 2016 IEEE International Symposium on Circuits and Systems (ISCAS). IEEE, 2016. http://dx.doi.org/10.1109/iscas.2016.7539048.

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Yuniati, Anis, and Retno Dwi Astuti. "Neural Network Synchronization of the Morris-Lecar Neuron Model Coupled with Short-Term Plasticity (STP)." In The 6th International Conference on Science and Engineering. Switzerland: Trans Tech Publications Ltd, 2024. http://dx.doi.org/10.4028/p-ymnn4n.

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This study used the Morris-Lecar (ML) neuron model coupled with Short-Term Plasticity (STP) to simulate neuronal connectivity and synaptic patterns. We analyze this neural network synchronization activity, examined the post-synaptic conductance patterns in the modelled neural network, investigated the dynamics of the neural network membrane potentials in the synchronous state, and analyze the Short-Term Plasticity (STP) synaptic transmission patterns by varying the inter-neuron connection probability for both inhibitory (pi) and excitatory (pe). This computational-based study was executed using Brian2 Simulator. The results revealed that the higher the connection probability, the more connections and synapses are formed. The greater value of pe, the more synchronous the neural network activity. In contrast, the higher value of pi, the less synchronous the neural network activity. A synchronous neural network implies that the spikes occur coincidentally, where coincidental spikes lead to easily detectable membrane potentials and postsynaptic conductance. Furthermore, spikes affect the release of neurotransmitters, thereby affecting synaptic transmission patterns. We further determined the frequency of this neural network synchronization.
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Badica, C., M. Teodorescu, C. Spahiu, A. Badica, and C. Fox. "Integrating role activity diagrams and hybrid IDEF for business process modeling using MDA." In Seventh International Symposium on Symbolic and Numeric Algorithms for Scientific Computing (SYNASC'05). IEEE, 2005. http://dx.doi.org/10.1109/synasc.2005.40.

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Gabrielli, Ângelo, Camila Sousa Bragunce Alves, Bruna Oliveira Bicalho, and Débora Pimenta Alves. "Benefits and Challenges of Cannabis Use in the Treatment of Refractory Epilepsy." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.239.

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Introduction: Refractory epilepsy (RE) is a disease that causes continuous and debilitating seizures. Due to the ineffectiveness of antiepileptic therapies, there is a growing interest in drugs made with cannabidiol (CBD), a substance extracted from Cannabis. Objective: To point out benefits and challenges of the use of CBD in the treatment of RE. Methods: Literature review performed at PubMed, with the descriptors Epilepsy, Drug Therapy and Cannabis. Results: It is suggested that CBD is mediated by cannabinoid receptors coupled to protein G, by blockade of NMDA receptors, by GABAergic modulation, glutamatergic synapses and / or mechanisms involving noncannabinoid receptors. CBD can also oppose the actions of exogenous and endogenous cannabinoid agonists, due to the negative allosteric modulation. The benefits of CBD are: great therapeutic diversity, safety and tolerability, rare and mild side effects, low risk of drug interactions, and milder cognitive effects, when compared to other antiepileptic drugs. Despite the benefits, CBD has adverse effects such as drowsiness, appetite reduction, diarrhea, increased activity of liver enzymes and interaction with substances metabolized by cytochrome P450. Still, the inefficient regulation generates variation in the composition of the marketed drugs, which can lead to Δ9 - tetrahydrocannabinol (THC) intoxication. Conclusions: Thus, it is essential that the scientific community remains open to investigate the effects of CBD, given the advantages of its use for treating RE.
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Tsukimata, Márcio Yutaka, Bianca Lumi Inomata da Silva, and Jennison Alves Guimarães. "Açaí: potential anticonvulsant agent." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.064.

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Background: Convulsion is an involuntary contraction of skeletal muscles. When considering vulnerable populations exposed to the mentioned pathophysiological situation, it is recognized that many of them will not have access to the indicated pharmacological treatment. Therefore, the ingestion of açai, Euterpe oleracea (EO) attenuates the problem, acting as an anticonvulsant. Objectives: evaluate the EO as an anticonvulsant agent. Design and setting: It is a bibliographic research and the data collection was done from the PubMed and Scielo databases. Methods: The descriptor used was “Euterpe oleracea” and the inclusion criteria adopted were: articles published in the last five years, available in full and publications related to epilepsy. Results: The EO acts on the GABAergic system when interacting occurs with the GABA receptor of cortical neurons and, above all, of astrocytes in an inhibitory mechanism for the uptake of the neurotransmitter GABA, that accumulates in the synaptic cleft, preventing the exaggerated neurotransmission that causes convulsions. In pentylenetetrazol-induced seizure (PTZ), EO showed some results similar to diazepam: reduced duration of tonic-clonic convulsion and increased latencies for the first myoclonic spasm and for the first generalized tonic-clonic seizure. Conclusions: Studies suggest that EO can be classified as an anticonvulsant, considering its inhibitory activity during synapses. Furthermore, the consumption of EO is more viable at a socioeconomic level compared to traditional drug treatments.
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