Gotowa bibliografia na temat „Inhibitory synapse”

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Artykuły w czasopismach na temat "Inhibitory synapse"

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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 (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 w
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Dejanovic, Borislav, Tiffany Wu, Ming-Chi Tsai, 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 (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
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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-
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Suckow, Arthur T., Davide Comoletti, Megan A. Waldrop та ін. "Expression of Neurexin, Neuroligin, and Their Cytoplasmic Binding Partners in the Pancreatic β-Cells and the Involvement of Neuroligin in Insulin Secretion". Endocrinology 149, № 12 (2008): 6006–17. http://dx.doi.org/10.1210/en.2008-0274.

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The composition of the β-cell exocytic machinery is very similar to that of neuronal synapses, and the developmental pathway of β-cells and neurons substantially overlap. β-Cells secrete γ-aminobutyric acid and express proteins that, in the brain, are specific markers of inhibitory synapses. Recently, neuronal coculture experiments have identified three families of synaptic cell-surface molecules (neurexins, neuroligins, and SynCAM) that drive synapse formation in vitro and that control the differentiation of nascent synapses into either excitatory or inhibitory fully mature nerve terminals. T
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Jasinska, Malgorzata, Ewa Siucinska, Ewa Jasek, Jan A. Litwin, Elzbieta Pyza, and Malgorzata Kossut. "Effect of Associative Learning on Memory Spine Formation in Mouse Barrel Cortex." Neural Plasticity 2016 (2016): 1–11. http://dx.doi.org/10.1155/2016/9828517.

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Associative fear learning, in which stimulation of whiskers is paired with mild electric shock to the tail, modifies the barrel cortex, the functional representation of sensory receptors involved in the conditioning, by inducing formation of new inhibitory synapses on single-synapse spines of the cognate barrel hollows and thus producing double-synapse spines. In the barrel cortex of conditioned, pseudoconditioned, and untreated mice, we analyzed the number and morphological features of dendritic spines at various maturation and stability levels: sER-free spines, spines containing smooth endop
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Overstreet, Linda S., and Gary L. Westbrook. "Synapse Density Regulates Independence at Unitary Inhibitory Synapses." Journal of Neuroscience 23, no. 7 (2003): 2618–26. http://dx.doi.org/10.1523/jneurosci.23-07-02618.2003.

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Hines, Pamela J. "Inhibitory synapse specificity." Science 363, no. 6425 (2019): 360.6–361. http://dx.doi.org/10.1126/science.363.6425.360-f.

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Jasinska, Malgorzata, Ewa Siucinska, Stansislaw Glazewski, Elzbieta Pyza, and And Kossut. "Characterization and plasticity of the double synapse spines in the barrel cortex of the mouse." Acta Neurobiologiae Experimentalis 66, no. 2 (2006): 99–104. http://dx.doi.org/10.55782/ane-2006-1595.

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The somatosensory barrel cortex of rodents and its afferent pathway from the facial vibrissae is a very useful model for studying neuronal plasticity. Dendritic spines are the most labile elements of synaptic circuitry and the most likely substrate of experience-dependent alterations in neuronal circuits in cerebral cortex. We characterized morphologically and numerically a specific population of spines, i.e. double synapse spines, which have two different inputs – one excitatory and the other inhibitory, in the B2 barrel of mouse somatosensory cortex. We also described changes in mor
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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 (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
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Barreira da Silva, Rosa, Claudine Graf, and Christian Münz. "Cytoskeletal stabilization of inhibitory interactions in immunologic synapses of mature human dendritic cells with natural killer cells." Blood 118, no. 25 (2011): 6487–98. http://dx.doi.org/10.1182/blood-2011-07-366328.

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Abstract Human mature dendritic cells (DCs) can efficiently stimulate natural killer (NK)–cell responses without being targeted by their cytotoxicity. To understand this important regulatory crosstalk, we characterized the development of the immunologic synapse between mature DCs and resting NK cells. Conjugates between these 2 innate leukocyte populations formed rapidly, persisted for prolonged time periods and matured with DC-derived f-actin polymerization at the synapse. Polarization of IL-12 and IL-12R to the synapse coincided with f-actin polymerization, while other activating and inhibit
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Rozprawy doktorskie na temat "Inhibitory synapse"

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Berry, Kalen P. (Kalen Paul). "Visualizing inhibitory and excitatory synapse dynamics In vivo." Thesis, Massachusetts Institute of Technology, 2018. http://hdl.handle.net/1721.1/117876.

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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Biology, June 2018.<br>Cataloged from PDF version of thesis. Page 75 blank.<br>Includes bibliographical references (pages 66-74).<br>Structural plasticity is one of the physical manifestations of circuit rewiring in the brain. Once thought to be relegated solely to developmental time periods, we now know that even in the mature brain inhibitory or excitatory connections can be made and broken, modifying the information flow within a circuit by enabling or removing specific information channels. However, the properties of inhi
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Sheehan, D. "Membrane dynamics of neuroligin 2 at the inhibitory synapse." Thesis, University College London (University of London), 2015. http://discovery.ucl.ac.uk/1470159/.

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Recent innovations in live-cell imaging have demonstrated that the synapse undergoes constant remodelling and reorganisation. One well characterised aspect of this process is the lateral mobility of neurotransmitter gated receptors, which enables their dynamic exchange between synaptic and extrasynaptic populations. Regulation of this process, primarily via transient receptor-scaffold interactions, determines receptor number at the synapse and thus directly shapes the strength of synaptic neurotransmission. Neuroligins (NLs) are trans-synaptic proteins that project across the synaptic cleft an
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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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Dietrich, Craig Julius. "Endogenous acidification of the inhibitory synapse proton amplification of GABAA-mediated neurotransmission /." Connect to Electronic Thesis (CONTENTdm), 2009. http://worldcat.org/oclc/457179973/viewonline.

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Dobie, Frederick Andrew. "Molecular and cellular mechanisms of inhibitory synapse formation in developing rat hippocampal neurons." Thesis, University of British Columbia, 2012. http://hdl.handle.net/2429/41933.

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The proper functioning of the brain and central nervous system (CNS) requires the precise formation of synapses between neurons. The two main neurotransmitter systems for fast synaptic communication in the CNS are excitatory glutamate and inhibitory gamma-aminobutyric acid. A growing body of evidence has begun to uncover several shared and divergent rules for the establishment of each of these two types of synapses. At the molecular level, a number of key proteins have been shown to be involved in the initial formation and subsequent development of synaptic connection, including cell adhesion
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Pettem, Katherine Laura. "New synaptic organizing proteins and their roles in excitatory and inhibitory synapse development." Thesis, University of British Columbia, 2012. http://hdl.handle.net/2429/42478.

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Merlaud, Zaha. "Nouveaux mécanismes de régulation de la synapse GABAergique inhibitrice de l’hippocampe : implication de la voie de signalisation WNK et de l’état de conformation des récepteurs GABA-A." Electronic Thesis or Diss., Sorbonne université, 2024. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2024SORUS301.pdf.

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Le récepteur ionotrope de l'acide γ-aminobutyrique (GABAAR), perméable aux ions chlorures, est le principal récepteur neurotransmetteur médiateur de l'inhibition dans le cerveau des mammifères. La transmission GABAergique est soumise à une régulation complexe et multifactorielle. Non seulement façonnée par le cycle d'ouverture du GABAAR, qui dicte le passage entre ses conformations au repos, ouverte et désensibilisée, mais aussi par l'homéostasie des ions chlorure, laquelle détermine la polarité et l'efficacité de la transmission GABAergique, la transmission GABAergique repose aussi fortement
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Ramos, Mariana. "Unraveling the impact of IL1RAPL1 mutations on synapse formation : towards potential therapies for intellectual disability." Thesis, Sorbonne Paris Cité, 2015. http://www.theses.fr/2015PA05T036/document.

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L’intégrité des synapses neuronales est primordiale pour le développement et le maintien des capacités cognitives. Des mutations dans des gènes codant pour des protéines synaptiques ont été trouvées chez des patients atteints de déficience intellectuelle (DI), qui est une maladie neurodéveloppementale ayant des conséquences sur les fonctions intellectuelles et adaptatives. Ce travail de thèse porte sur l’étude de l’un de ces gènes, IL1RAPL1, dont les mutations sont responsables d’une forme non-syndromique de DI liée au chromosome X, et sur le rôle de la protéine IL1RAPL1 dans la formation et l
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Salvatico, Charlotte. "Mécanisme de diffusion-capture dans les synapses inhibitrices : suivi en molécule unique à haute densité et aspects thermodynamiques." Thesis, Paris 6, 2015. http://www.theses.fr/2015PA066736/document.

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La synapse est une structure macromoléculaire dont les composants sont renouvelés en permanence alors que l’assemblage est quasi-stable. A l’échelle mésoscopique, les récepteurs aux neurotransmetteurs (RN) sont accumulés dans le compartiment post-synaptique (PSD). Cette accumulation résulte de la diffusion latérale des RNs dans la membrane neuronale et de leurs immobilisations transitoires dans la PSD. Les protéines d’échafaudage (PE) localisées sous la membrane post-synaptique constituent des sites de capture en interagissant avec les RNs. Mon travail de thèse s’inscrit dans le cadre d’une co
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Mosser, Coralie-Anne. "Implication des cellules microgliales dans le développement des réseaux synaptiques du néocortex somatosensoriel Microglial BDNF promotes the functional maturation of thalamocortical synaptic networks Microglia and prenatal inflammation regulate local and horizontal wiring of inhibitory circuits." Thesis, Sorbonne Paris Cité, 2018. https://wo.app.u-paris.fr/cgi-bin/WebObjects/TheseWeb.woa/wa/show?t=2167&f=13404.

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La microglie désigne l'ensemble des macrophages résidents du système nerveux central (SNC). Longtemps considérées comme étant actives uniquement en conditions pathologiques, les cellules microgliales sont pourtant essentielles à l'activité physiologique du SNC. En particulier, pendant la formation du SNC, elles régulent apoptose et survie neuronales, et interagissent directement avec les synapses en les éliminant, en promouvant leur formation ou en régulant leur activité. Toutefois, les mécanismes microgliaux impliqués dans la mise en place et la maturation fonctionnelle des circuits corticaux
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Książki na temat "Inhibitory synapse"

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

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Cherubini, Enrico, ed. Building up the inhibitory synapse. Frontiers Media SA, 2013. http://dx.doi.org/10.3389/978-2-88919-097-3.

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Woodin, Melanie A., and Arianna Maffei. Inhibitory Synaptic Plasticity. Springer, 2014.

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Woodin, Melanie A., and Arianna Maffei. Inhibitory Synaptic Plasticity. Springer, 2011.

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Hensch, Takao K. Excitatory-Inhibitory Balance: "Synapses, Circuits, Systems". Springer, 2012.

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(Editor), Takao K. Hensch, and Michela Fagiolini (Editor), eds. Excitatory-Inhibitory Balance: Synapses, Circuits, Systems. Springer, 2003.

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Fagiolini, Michela, and Takao K. Hensch. Excitatory-Inhibitory Balance: Synapses, Circuits, Systems. Springer London, Limited, 2012.

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(Compiler), Michael, and Irene Ash (Compiler), eds. Handbook of Corrosion Inhibitors (Synapse Chemical Library). Synapse Information Resources, Inc., 2000.

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Stafstrom, Carl E. Disorders Caused by Botulinum Toxin and Tetanus Toxin. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0156.

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Anaerobic organisms of the genus Clostridia (C) can cause significant human disease. Exotoxins secreted by C botulinum and C tetani cause botulism and tetanus, respectively (summarized in Table 156.1). Botulinum neurotoxin causes neuromuscular blockade by interfering with vesicular acetylcholine release, leading to cholinergic blockade at the neuromuscular junctions of skeletal muscle, and consequently, symmetric flaccid paralysis. Tetanus toxin prevents release of inhibitory neurotransmitters at central synapses, leading to overactivity of motor neurons and muscle rigidity and spasms. This ch
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Noebels, Jeffrey L., Massimo Avoli, Michael A. Rogawski, Annamaria Vezzani, and Antonio V. Delgado-Escueta, eds. Jasper's Basic Mechanisms of the Epilepsies. 5th ed. Oxford University PressNew York, 2024. http://dx.doi.org/10.1093/med/9780197549469.001.0001.

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Abstract Unverricht-Lundborg disease (ULD; EPM1) is an inherited neurodegenerative disorder characterized by onset at 6–15 years, stimulus-sensitive, action-activated myoclonus, epilepsy, and progressive neurological deterioration. It is caused by biallelic pathogenic variants in the CSTB gene, encoding a cystatin B. The most common of these is an unstable expansion of a dodecamer repeat element in the promoter region of the gene, leading to marked downregulation of CSTB expression. Total loss of CSTB is associated with severe neonatal-onset encephalopathy. A cystatin B–deficient mouse models
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Części książek na temat "Inhibitory synapse"

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Le Saux, Guillaume, Esti Toledo-Ashkenazi, and Mark Schvartzman. "Fabrication of Nanoscale Arrays to Study the Effect of Ligand Arrangement on Inhibitory Signaling in NK Cells." In The Immune Synapse. Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-3135-5_20.

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Sanes, Dan H., Emma C. Sarro, Anne E. Takesian, Chiye Aoki, and Vibhakar C. Kotak. "Regulation of Inhibitory Synapse Function in the Developing Auditory CNS." In Developmental Plasticity of Inhibitory Circuitry. Springer US, 2009. http://dx.doi.org/10.1007/978-1-4419-1243-5_4.

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Shi, Haibo, Zhijie Wang, Jinli Xie, and Chongbin Guo. "Robustness of Gamma-Oscillation in Networks of Excitatory and Inhibitory Neurons with Conductance-Based Synapse." In Advances in Neural Networks – ISNN 2011. Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-21105-8_2.

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Kang, Min-Jae, Ho-Chan Kim, Wang-Cheol Song, Junghoon Lee, Hee-Sang Ko, and Jacek M. Zurada. "Differences in Input Space Stability Between Using the Inverted Output of Amplifier and Negative Conductance for Inhibitory Synapse." In Advances in Neural Networks – ISNN 2007. Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-72383-7_119.

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Komatsu, Yukio, and Yumiko Yoshimura. "Long-term Modification at Visual Cortical Inhibitory Synapses." In Excitatory-Inhibitory Balance. Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0039-1_5.

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Chiu, Chiayu Q., and Pablo E. Castillo. "Endocannabinoid Mediated Long-Term Depression at Inhibitory Synapses." In Inhibitory Synaptic Plasticity. Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-6978-1_11.

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Komatsu, Yukio, and Yumiko Yoshimura. "Long-Term Modification at Inhibitory Synapses in Developing Visual Cortex." In Inhibitory Synaptic Plasticity. Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-6978-1_2.

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Kawaguchi, Shin-ya, and Tomoo Hirano. "Molecular Mechanism of Long-Term Plasticity at Cerebellar Inhibitory Synapses." In Inhibitory Synaptic Plasticity. Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-6978-1_3.

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Eissmann, Philipp, and Daniel M. Davis. "Inhibitory and Regulatory Immune Synapses." In Current Topics in Microbiology and Immunology. Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-03858-7_4.

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Gonzalez-Islas, Carlos E., and Peter Wenner. "Role of Spontaneous Activity in the Maturation of GABAergic Synapses in Embryonic Spinal Circuits." In Developmental Plasticity of Inhibitory Circuitry. Springer US, 2009. http://dx.doi.org/10.1007/978-1-4419-1243-5_3.

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Streszczenia konferencji na temat "Inhibitory synapse"

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Talanov, Max, Evgeniy Zykov, Victor Erokhin, et al. "Modeling Inhibitory and Excitatory Synapse Learning in the Memristive Neuron Model." In 14th International Conference on Informatics in Control, Automation and Robotics. SCITEPRESS - Science and Technology Publications, 2017. http://dx.doi.org/10.5220/0006478805140521.

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Chou, Teyuh, Jen-Chieh Liu, Li-Wen Chiu, I.-Ting Wang, Chia-Ming Tsai, and Tuo-Hung Hou. "Neuromorphic pattern learning using HBM electronic synapse with excitatory and inhibitory plasticity." In 2015 International Symposium on VLSI Technology, Systems and Application (VLSI-TSA). IEEE, 2015. http://dx.doi.org/10.1109/vlsi-tsa.2015.7117582.

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Pradyumna, S. G., and S. S. Rathod. "Analysis of CMOS inhibitory synapse with varying neurotransmitter concentration, reuptake time and spread delay." In 2015 19th International Symposium on VLSI Design and Test (VDAT). IEEE, 2015. http://dx.doi.org/10.1109/isvdat.2015.7208112.

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Yang, Chun-Lin, Nandan Shettigar, and C. Steve Suh. "A Proposition for Describing Real-World Network Dynamics." In ASME 2021 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2021. http://dx.doi.org/10.1115/imece2021-73360.

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Abstract This study presents a proposition for describing the dynamics of real-world networks under the general framework of complex networks. Outward behaviors of complex networks are the manifestation of the coupled dynamics at the macroscopic level and the individual dynamics at the microscopic level. At the macroscopic level a law of coupling governs the interactions of network constituents. At the microscopic level, the dynamics of individual constituent is defined by energy that follows normal distribution. Constituent dynamics are bounded by physical constraints. Consequently, network d
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Lecerf, Gwendal, Jean Tomas, and Sylvain Saighi. "Excitatory and Inhibitory Memristive Synapses for Spiking Neural Networks." In 2013 IEEE International Symposium on Circuits and Systems (ISCAS). IEEE, 2013. http://dx.doi.org/10.1109/iscas.2013.6572171.

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Ioka, Eri, Yasuyuki Matusya, and Hiroyuki Kitajima. "Bifurcation in mutually coupled three neurons with inhibitory synapses." In 2011 European Conference on Circuit Theory and Design (ECCTD). IEEE, 2011. http://dx.doi.org/10.1109/ecctd.2011.6043617.

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Zhang, Tielin, Yi Zeng, Dongcheng Zhao, and Bo Xu. "Brain-inspired Balanced Tuning for Spiking Neural Networks." In Twenty-Seventh International Joint Conference on Artificial Intelligence {IJCAI-18}. International Joint Conferences on Artificial Intelligence Organization, 2018. http://dx.doi.org/10.24963/ijcai.2018/229.

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Due to the nature of Spiking Neural Networks (SNNs), it is challenging to be trained by biologically plausible learning principles. The multi-layered SNNs are with non-differential neurons, temporary-centric synapses, which make them nearly impossible to be directly tuned by back propagation. Here we propose an alternative biological inspired balanced tuning approach to train SNNs. The approach contains three main inspirations from the brain: Firstly, the biological network will usually be trained towards the state where the temporal update of variables are equilibrium (e.g. membrane potential
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Yokota, R., H. Takahashi, A. Funamizu, M. Uchihara, J. Suzurikawa, and R. Kanzaki. "Auditory Cortical Plasticity Induced by Intracortical Microstimulation under Pharmacological Blockage of Inhibitory Synapses." In Conference Proceedings. Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2006. http://dx.doi.org/10.1109/iembs.2006.260281.

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Yokota, R., H. Takahashi, A. Funamizu, M. Uchihara, J. Suzurikawa, and R. Kanzaki. "Auditory Cortical Plasticity Induced by Intracortical Microstimulation under Pharmacological Blockage of Inhibitory Synapses." In Conference Proceedings. Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2006. http://dx.doi.org/10.1109/iembs.2006.4398557.

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Breese, Amanda J., and John Macdonald. "Implementation of the Hopfield model with excitatory and inhibitory synapses and static thresholding." In SPIE Proceedings, edited by Steven K. Rogers, Eustace L. Dereniak, P. McGeehin, Donald B. Carlin, David B. Kay, and Robert E. Sampson. SPIE, 1990. http://dx.doi.org/10.1117/12.21191.

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