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Literatura académica sobre el tema "Inhibitory synapse"

Autor: Grafiati

Publicado: 14 de diciembre de 2024

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Artículos de revistas sobre el tema "Inhibitory synapse"

Pettem, Katherine L., Daisaku Yokomaku, Hideto Takahashi, Yuan Ge y Ann Marie Craig. "Interaction between autism-linked MDGAs and neuroligins suppresses inhibitory synapse development". Journal of Cell Biology 200, n.º 3 (28 de enero de 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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Dejanovic, Borislav, Tiffany Wu, Ming-Chi Tsai, David Graykowski, Vineela D. Gandham, Christopher M. Rose, Corey E. Bakalarski et al. "Complement C1q-dependent excitatory and inhibitory synapse elimination by astrocytes and microglia in Alzheimer’s disease mouse models". Nature Aging 2, n.º 9 (20 de septiembre de 2022): 837–50. http://dx.doi.org/10.1038/s43587-022-00281-1.

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AbstractMicroglia and complement can mediate neurodegeneration in Alzheimer’s disease (AD). By integrative multi-omics analysis, here we show that astrocytic and microglial proteins are increased in TauP301S synapse fractions with age and in a C1q-dependent manner. In addition to microglia, we identified that astrocytes contribute substantially to synapse elimination in TauP301S hippocampi. Notably, we found relatively more excitatory synapse marker proteins in astrocytic lysosomes, whereas microglial lysosomes contained more inhibitory synapse material. C1q deletion reduced astrocyte–synapse association and decreased astrocytic and microglial synapses engulfment in TauP301S mice and rescued synapse density. Finally, in an AD mouse model that combines β-amyloid and Tau pathologies, deletion of the AD risk gene Trem2 impaired microglial phagocytosis of synapses, whereas astrocytes engulfed more inhibitory synapses around plaques. Together, our data reveal that astrocytes contact and eliminate synapses in a C1q-dependent manner and thereby contribute to pathological synapse loss and that astrocytic phagocytosis can compensate for microglial dysfunction.

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Hu, Xiaoge, Jian-hong Luo y 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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Suckow, Arthur T., Davide Comoletti, Megan A. Waldrop, Merrie Mosedale, Sonya Egodage, Palmer Taylor y Steven D. Chessler. "Expression of Neurexin, Neuroligin, and Their Cytoplasmic Binding Partners in the Pancreatic β-Cells and the Involvement of Neuroligin in Insulin Secretion". Endocrinology 149, n.º 12 (28 de agosto de 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. The inhibitory synapse-like character of the β-cells led us to hypothesize that members of these families of synapse-inducing adhesion molecules would be expressed in β-cells and that the pattern of expression would resemble that associated with neuronal inhibitory synaptogenesis. Here, we describe β-cell expression of the neuroligins, neurexins, and SynCAM, and show that neuroligin expression affects insulin secretion in INS-1 β-cells and rat islet cells. Our findings demonstrate that neuroligins and neurexins are expressed outside the central nervous system and help confer an inhibitory synaptic-like phenotype onto the β-cell surface. Analogous to their role in synaptic neurotransmission, neurexin-neuroligin interactions may play a role in the formation of the submembrane insulin secretory apparatus.

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Overstreet, Linda S. y Gary L. Westbrook. "Synapse Density Regulates Independence at Unitary Inhibitory Synapses". Journal of Neuroscience 23, n.º 7 (1 de abril de 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, n.º 6425 (24 de enero de 2019): 360.6–361. http://dx.doi.org/10.1126/science.363.6425.360-f.

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Jasinska, Malgorzata, Ewa Siucinska, Ewa Jasek, Jan A. Litwin, Elzbieta Pyza y 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 endoplasmic reticulum (sER), and spines containing spine apparatus. Using stereological analysis of serial sections examined by transmission electron microscopy, we found that the density of double-synapse spines containing spine apparatus was significantly increased in the conditioned mice. Learning also induced enhancement of the postsynaptic density area of inhibitory synapses as well as increase in the number of polyribosomes in such spines. In single-synapse spines, the effects of conditioning were less pronounced and included increase in the number of polyribosomes in sER-free spines. The results suggest that fear learning differentially affects single- and double-synapse spines in the barrel cortex: it promotes maturation and stabilization of double-synapse spines, which might possibly contribute to permanent memory formation, and upregulates protein synthesis in single-synapse spines.

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Jasinska, Malgorzata, Ewa Siucinska, Stansislaw Glazewski, Elzbieta Pyza y And Kossut. "Characterization and plasticity of the double synapse spines in the barrel cortex of the mouse". Acta Neurobiologiae Experimentalis 66, n.º 2 (30 de junio de 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 morphology of double synapse spines induced by classical conditioning in which stimulation of vibrissae was paired with a tail shock. The analysis was carried out by means of serial EM micrograph reconstruction. We showed that double spines account for about 10% of all analyzed spines. The morphology of a typical double synapse spine is similar to the morphology of single synapse spine and both consist of two parts  a large head and a narrow, long neck. Excitatory synapses are preferentially located on the head of double synapse spines and inhibitory synapses are usually located on the neck of these spines. The length of the double synapse spine neck decreases and the cross-section area of the spine neck increases significantly as a result of sensory conditioning. The correspondence should be addressed to E. Pyza, Email: pyza@zuk.iz.uj.edu.pl

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Wilson, Emily S. y Karen Newell-Litwa. "Stem cell models of human synapse development and degeneration". Molecular Biology of the Cell 29, n.º 24 (26 de noviembre de 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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Barreira da Silva, Rosa, Claudine Graf y Christian Münz. "Cytoskeletal stabilization of inhibitory interactions in immunologic synapses of mature human dendritic cells with natural killer cells". Blood 118, n.º 25 (15 de diciembre de 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 inhibitory molecules were enriched at the interface between DCs and NK cells earlier. Functional assays revealed that inhibition of f-actin polymerization in mature synapses led to an increase of IFN-γ secretion and cytotoxicity by NK cells. This elevated NK-cell reactivity resulted from decreased inhibitory signaling in the absence of MHC class I polarization at the interface, which was observed on inhibition of f-actin polymerization in DCs. Thus, inhibitory signaling is stabilized by f-actin at the synapse between mature DCs and resting NK cells.

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Tesis sobre el tema "Inhibitory synapse"

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.
Cataloged from PDF version of thesis. Page 75 blank.
Includes bibliographical references (pages 66-74).
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 inhibitory and excitatory synapse dynamics are not well understood. To address this issue, we utilized triple-color two photon microscopy to examine inhibitory and excitatory synapses across time with daily imaging. We found that the majority of dynamic spines at these intervals lacked a mature excitatory synapse as indicated by the absence of PSD-95. Inhibitory synapses were also highly dynamic during daily imaging, much more so than expected from previous results imaging at longer intervals, especially those located on spines which also contain an excitatory synapse. Surprisingly, we found that many inhibitory synapses, on the dendritic shaft and on spines, were also repeatedly removed and then reformed again at the same locations on the dendritic arbor. These recurrent inhibitory dynamic events at persistent locations represent a novel role for synapse dynamics, modulating local excitatory activity via their addition or removal. The rate of inhibitory synapse turnover was also modified by experience, as shown through their responses following monocular deprivation. We further sought to investigate these events on even shorter time scales by developing a dual color labeling strategy in combination with a newly developed line scanning temporal focusing two photon microscope, enabling imaging of the entire dendritic arbor and its inhibitory synapses in just a few minutes. This system allows for examination of synapse dynamics on the hourly time scale in vivo and can be expanded to study other molecular events that occur too fast for conventional two photon imaging.
by Kalen P. Berry.
Ph. D.

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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 and bind to partners positioned on the presynaptic side, physically fusing the two synapses in close apposition. Further to this function, the various NL isoforms (NL1-4) are essential regulators of the composition of the postsynaptic density. NL2 is primarily localised to inhibitory synapses, where it influences synaptic activity through interactions with, among others, gephyrin and collybistin. In contrast to neurotransmitter receptors, the membrane dynamics of the NL proteins are poorly understood. Thus, the aim of this thesis is to uncover the mechanisms underlying NL2 mobility on the membrane surface. Novel features of NL2 expression in non-neuronal cells were harnessed to create innovative systems in which the role of specific synaptic mechanisms was studied in isolation. Single particle tracking of NL2 with quantum dots in hippocampal neurons confirmed that endogenous NL2 exhibits transient confinement at inhibitory synapses, in line with previous findings on receptors. To uncover the underlying mechanisms, a number of important NL2 mutants were designed. Collectively, these experiments suggested that NL2 transient confinement primarily depends on intracellular interactions, specifically via phosphorylation and the PDZ and gephyrin binding domains, rather than trans-synaptic signalling mechanisms. Thus, the work described in this thesis contributes to the concept of the dynamic synapse and attributes a non-static membrane profile to NL2, which may ultimately influence synaptic remodelling and plasticity events.

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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 molecules (CAMs). Among the CAMs, neurexins and neuroligins are important synaptogenic proteins that act trans-synaptically to organize synapses: binding of axonal beta-neurexins by neuroligins is sufficient to cause development of a presynaptic specialization at that site, while binding of dendritic neuroligin-1 or neuroligin-2 by beta-neurexins is sufficient to cause development of postsynaptic excitatory or inhibitory specializations, respectively. In Chapter 2, we explore the role of alpha-neurexins in synapse organization. We find alpha-neurexins are able to specifically induce the formation of inhibitory synapses, presumably through clustering of postsynaptic neuroligin-2. Moreover, we find that the expression of various splice variants of alpha- and beta-neurexins is regulated both during development and by activity, suggesting a physiological role for alternative splicing in the modulation of synapse assembly. At the cellular level, it is now clear from live imaging studies that synapses and their formation are highly dynamic processes. A number of studies have established the temporal recruitment of pre- and postsynaptic components to nascent synapses and how synapse formation can influence neuron growth. However, these studies have focused on excitatory synapses. In Chapter 3, we explore the cellular mechanisms of inhibitory synapse formation and modulation. We find that entire synapses are highly mobile and can undergo dynamic structural modulation. New synapses are formed by gradual accumulation of components from diffuse cytoplasmic pools, with a significant contribution of presynaptic vesicles from previously recycling sites. These results provide new insights into the mechanisms of inhibitory synapse formation and how it is both similar and different from excitatory synapse formation.

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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 sur le nombre de GABAARs présents à la membrane postsynaptique, localisée face aux sites présynaptiques de libération de GABA. Le nombre de ces récepteurs aux synapses est rapidement régulé par un mécanisme de "diffusion-capture", dans lequel les GABAARs alternent entre une diffusion rapide à la membrane plasmique extrasynaptique et un ralentissement suivi d'un confinement aux synapses. De fait, ce confinement et cette agrégation synaptique sont médiés par l'interaction entre les GABAARs et leur principale protéine d'échafaudage synaptique, la géphyrine. La régulation de la diffusion latérale des récepteurs est considérée comme le principal mécanisme d'ajustement du nombre de récepteurs aux synapses en réponse à la demande synaptique. De plus, l'activité neuronale régule cette diffusion latérale des GABAARs, notamment en contrôlant la liaison des récepteurs à la géphyrine par la modulation de la phosphorylation des récepteurs et/ou de la géphyrine en aval des cascades de kinases, influençant ainsi la conformation de ces protéines. Au cours de ma thèse, j'ai étudié la régulation dynamique des synapses GABAergiques dans l'hippocampe à travers la phosphorylation de la géphyrine et la conformation des récepteurs, en utilisant notamment des techniques de microscopie optique de pointe, telles que le suivi de particules individuelles (SPT), la microscopie de reconstruction optique stochastique (STORM) et la microscopie de localisation photo-activée (PALM), en recourant à des stratégies pharmacologiques et de mutagenèse dirigée in vitro et in vivo. Plus précisément, mes recherches suggèrent que l'organisation synaptique des GABAARs et de la géphyrine dans l'hippocampe est régulée dynamiquement et est médiée, entre autres, par la phosphorylation de la géphyrine via la voie de signalisation sensible au chlorure WNK/SPAK/OSR1, une cascade de kinases précédemment liée à l'homéostasie des ions chlorures et à la transmission inhibitrice. D'autre part, mes résultats indiquent que l'état de conformation des GABAARs impacte leur régulation dynamique et leur organisation au niveau de la synapse. En somme, mes travaux doctoraux apportent de nouvelles perspectives sur la régulation dynamique de l'organisation et de la fonction des synapses GABAergiques dans l'hippocampe mature des modèles murins
The chloride ion permeant ionotropic γ-aminobutyric acid receptor (GABAAR) is the principal neurotransmitter receptor mediating inhibition in the mammalian brain. The GABAergic GABAergic transmission is subjected to a complex and multifactorial regulation. Shaped by the gating cycle of GABAAR, which dictates the switch between their resting, open, and desensitized conformation and by chloride homeostasis which dictates the polarity and efficacy of the GABAergic transmission, the GABAergic transmission also relies heavily on the number of GABAARs present in the postsynaptic membrane opposite to presynaptic GABA-releasing sites. The number of GABAARs at synapses is rapidly regulated by a “diffusion-capture” mechanism wherein receptors alternate between rapid diffusion into the extrasynaptic plasma membrane and slowing down and confinement to the synapses. This confinement and synaptic aggregation are mediated by the interaction between GABAARs and their primary scaffolding protein at the synapse, gephyrin. Regulation of receptor lateral diffusion is considered the first mechanism for adjusting the number of receptors at synapses in response to synaptic demand. Neuronal activity regulates the lateral diffusion of GABAARs, particularly by controlling receptor binding to gephyrin through the modulation of receptor and/or gephyrin phosphorylation downstream of kinase cascades, which subsequently influences the conformation of these proteins. During my PhD, I have investigated the dynamic regulation of GABAergic synapses in the hippocampus through the lens of gephyrin phosphorylation and receptor conformation, using state of the art optical microscopy techniques, such as Single Particle Tracking (SPT), STochastic Optical Reconstruction Microscopy (STORM) or Photo-Activated Localization Microscopy (PALM), and relying on pharmacological and directed mutagenesis strategies in vitro and in vivo. More specifically, my research suggests that GABAergic synapses in the hippocampus are dynamically regulated, with modulation of GABAAR and gephyrin synaptic organization mediated by gephyrin phosphorylation through the chloride-sensitive WNK/SPAK/OSR1 signaling pathway, a kinase cascade previously linked to chloride homeostasis and inhibitory transmission. Additionally, my findings indicate that the conformation state of GABAARs impacts their dynamic regulation and organization at the synapse. Overall, my doctoral work provides new insights into the dynamic regulation of GABAergic synapses organization and function in the mature hippocampus of murine models

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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 le fonctionnement des synapses. IL1RAPL1 est une protéine trans-membranaire qui est localisée dans les synapses excitatrices où elle interagit avec les protéines post-synaptiques PSD-95, RhoGAP2 et Mcf2l. De plus, IL1RAPL1 interagit en trans- avec une protéine phosphatase présynaptique, PTPd, via son domaine extracellulaire. Nous avons étudié les conséquences fonctionnelles de deux nouvelles mutations qui affectent le domaine extracellulaire d’IL1RAPL1 chez des patients présentant une DI. Ces mutations conduisent soit à une diminution de l’expression de la protéine, soit à une réduction de l’interaction avec PTPd affectant ainsi la capacité d’IL1RAPL1 à induire la formation de synapses excitatrices. En absence d’IL1RAPL1, le nombre ou la fonction des synapses excitatrices est diminué, ce qui mène à un déséquilibre entre les transmissions synaptiques excitatrice et inhibitrice dans des régions spécifiques du cerveau. Dans le cas particulier de l’amygdale latérale, nous avons montré que ce déséquilibre conduit à des défauts de mémoire associative chez la souris déficiente en Il1rapl1. L’ensemble des résultats qui font partie de ce travail montre que l’interaction IL1RAPL1/PTPd est essentielle pour la formation des synapses et suggère que les déficits cognitifs des patients avec une mutation dans il1rapl1 proviennent du déséquilibre de la balance excitation/ inhibition. Ces observations ouvrent des perspectives thérapeutiques visant à rétablir cette balance dans les réseaux neuronaux affectés
Preserving the integrity of neuronal synapses is important for the development and maintenance of cognitive capacities. Mutations on a growing number of genes coding for synaptic proteins are associated with intellectual disability (ID), a neurodevelopmental disease characterized by deficits in adaptive and intellectual functions. The present work is dedicated to the study of one of those genes, IL1RAPL1, and the role of its encoding protein in synapse formation and function. IL1RAPL1 is a trans-membrane protein that is localized at excitatory synapses, where it interacts with the postsynaptic proteins PSD-95, RhoGAP2 and Mcf2l. Moreover, the extracellular domain of IL1RAPL1 interacts trans-synaptically with the presynaptic phosphatase PTPd. We studied the functional consequences of two novel mutations identified in ID patients affecting this IL1RAPL1 domain. Those mutations lead either to a decrease of the protein expression or of its interaction with PTPd, affecting in both cases the IL1RAPL1-mediated excitatory synapse formation. In the absence of IL1RAPL1, the number or function of excitatory synapses is perturbed, leading to an imbalance of excitatory and inhibitory synaptic transmissions in specific brain circuits. In particular, we showed that this imbalance in the lateral amygdala results in associative memory deficits in mice lacking Il1rapl1. Altogether, the results included in this work show that IL1RAPL1/PTPd interaction is essential for synapse formation and suggest that the cognitive deficits in ID patients with mutations on IL1RAPL1 result from the imbalance of the excitatory and inhibitory transmission. These observations open therapeutic perspectives aiming to reestablish this balance in the affected neuronal circuits

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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 collaboration avec des chimistes et des physiciens afin de comprendre les paramètres impliqués dans le processus de diffusion-capture. Nous nous sommes intéressés au cas de la capture du récepteur de la glycine (RGly) par les agrégats de PEs des synapses inhibitrices, les géphyrines. Nous avons étudié l’impact de la liaison RGly-géphyrine sur le processus de diffusion-capture sous deux aspects. Le premier est lié à la nature bimodale de liaison du RGly. Le second aborde l’impact des phosphorylations de la boucle M3-M4 de la sous-unité β du RGly sur la liaison avec la géphyrine.Mon travail de thèse montre qu’il est maintenant possible, en utilisant des approches de microscopie super-résolutive, de quantifier les aspects thermodynamiques des interactions moléculaires dans les cellules vivantes
The synapse is a macromolecular structure whose components are constantly renewed while the assembly remains quasi-stable. At the mesoscopic level, neurotransmitter receptors (RNs) accumulate in the post-synaptic compartment (PSD). This accumulation is the result of the lateral diffusion of RNs in the neuronal membrane and transient immobilization within the PSD. This mechanism, called diffusion-trapping has been highlighted by single-molecule-tracking techniques. Scaffold proteins (PE) are localized under the post-synaptic membrane. These proteins form trapping-sites by interacting with RNs. Through an interdisciplinary approach in collaboration with chemists and physicists, the aim of my doctoral research was to understand the parameters that are involved in diffusion-trapping mechanisms. We especially focused on glycine receptor (RGly) trapping by PE clusters at inhibitory synapses, namely the scaffold protein gephyrin. The gephyrin- interaction motif of the GlyR is located within the cytoplasmic domain of the β-subunit of the receptor, the so-called β-loop. Two aspects of the impact of RGly-gephyrin binding on diffusion-trapping were studied. The first was to identify the source of the RGly-gephyrin bimodal binding. The second one addressed the regulation of gephyrin binding by phosphorylation of the GlyR βLoop.My research thus shows that it is now possible to quantify thermodynamic aspects of molecular interactions in living cells using high-density single-molecule-tracking

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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 pendant le développement ne sont pas intégralement élucidés. Afin de mieux comprendre le rôle de la microglie dans le développement cortical, nous avons utilisé le système des champs de tonneaux du cortex somatosensoriel de la souris, et combiné des manipulations in vivo avec des approches électrophysiologiques, optogénétique, pharmacologique et histologique sur tranches de cerveaux de souris génétiquement modifiées. Dans une première étude, nous nous sommes intéressés aux conséquences de l'arrivée de la microglie à proximité des zones de terminaison des fibres thalamiques (les centres des tonneaux) dans le cortex somatosensoriel au cours de la première semaine postnatale sur les propriétés fonctionnelles des synapses thalamocorticales et de l'inhibition disynaptique associée (inhibition antérograde ou feedforward). Nos résultats montrent qu'une déplétion de la microglie pendant la première semaine postnatale entraîne un retard de maturation fonctionnelle de la connexion thalamocorticale excitatrice monosynaptique et de l'inhibition feedforward disynaptique au niveau des cellules principales excitatrices de la couche 4 (CP) entre les 10ème et 12ème jours postnataux (P10-12). Nous avons ensuite testé si le facteur neurotrophique BDNF (brain-derived neurotrophic factor) pouvait être la molécule microgliale impliquée dans la maturation de ces synapses corticales en utilisant une approche transgénique (lignée CX3CR1+/CreERT2;BDNFlox/lox). Nos enregistrements indiquent que l'absence de BDNF microglial entraîne aussi un déficit de maturation fonctionnelle des connexions excitatrices monosynaptiques et inhibitrices disynaptiques thalamocorticales entre P10-12. Nous avons donc identifié un facteur microglial clé dans la maturation des synapses corticales, et nos enregistrements chez le jeune adulte suggèrent que la suppression de BDNF microglial pendant la première semaine postnatale altère la synapse thalamocorticale excitatrice sur le long terme. Dans une deuxième étude, nous avons examiné les conséquences de perturbations de la microglie au cours du développement embryonnaire sur la mise en place des réseaux corticaux. L'induction d'une activation immunitaire maternelle (MIA) par injection de lipopolysaccharide (LPS) bactérien ou la déplétion de la microglie aux stades embryonnaires modifie la répartition laminaire des interneurones inhibiteurs exprimant la parvalbumine (PV+) _cellules responsables de l'inhibition feedforward_ dans le cortex jusqu'à P20. Nos données fonctionnelles ont révélé que ces protocoles de MIA et de déplétion induisent une augmentation de l'inhibition périsomatique des CP à P20, ainsi qu'une exubérance horizontale de l'inhibition soutenue par les interneurones PV+. Cette inhibition exacerbée ne perdure pas et nos enregistrements chez l'adulte indiquent au contraire un affaiblissement des synapses inhibitrices entre les interneurones PV+ et les CP. Nous postulons donc que les cellules microgliales sont le chaînon manquant entre des stimulations immunitaires, telles qu'elles peuvent se produire durant une inflammation pendant la grossesse, et l'augmentation du risque de développer des pathologies neurodéveloppementales. Ainsi, nos résultats mettent en exergue le rôle crucial de la microglie dans le développement des réseaux neuronaux corticaux pendant la période périnatale
Microglial cells are a population of specialized macrophages residing in the CNS only. They have long been studied solely under pathological contexts and were thought to be active only upon homeostatic disturbance following a brain lesion. However, over the last decade, they have been increasingly recognized to be essential players in the physiological functioning of the CNS. Specifically, during the CNS formation, microglia has been shown to regulate apoptosis and neuronal survival. They are also able to directly interact with synapses, by eliminating supernumerary and inappropriate connections, by promoting synapse formation or by regulating their activity. However, mechanisms by which microglia influence wiring and functional maturation of cortical are not fully understood. To better assess the role of microglia in cortical development, we used the barrel field as a model of neuronal development and we combined in vivo manipulations together with electrophysiology, optogenetics, pharmacologic and histologic approaches on brain slices of genetically-engineered mice. We first explored the consequences of microglia entry near the terminals of thalamic afferents (center of the barrels) in the primary somatosensory cortex during the first postnatal week on functional properties of thalamocortical synapses and associated disynaptic feedforward inhibition. By selectively depleting microglia at early postnatal days by intracerebral injections of clodronate-encapsulated liposomes, we show that microglia absence during the first postnatal week delays the functional maturation of both monosynaptic thalamocortical synapse and feedforward inhibition of layer 4 principal cells of the barrel cortex (PC) up to the 10th and 12th postnatal days (P10-12). To identify the mechanism underlying this process, we used the CX3CR1+/CreERT2; BDNFlox/lox mouse line allowing the conditional deletion of microglial BDNF during the first postnatal week. Our recordings indicate that the absence of microglial BDNF, as well as early microglia depletion, leads to a deficit in the functional maturation of both monosynaptic excitatory and disynaptic inhibitory thalamocortical connexions between P10-12. We therefore identified a microglial key factor in the maturation of cortical synapses. Our recordings in the young adult suggest that early microglial BDNF deletion has a long-term effect on thalamocortical excitatory synapses. In a second study, we investigated the consequences of microglia dysfunction during embryonic development on cortical networks wiring. Maternal immune activation (MIA) triggered by bacterial lipopolysaccharide (LPS) injection modifies the laminar repartition of parvalbumin-expressing inhibitory interneurons (PV+), key actors in neuropsychiatric disease, in the cortex until P20. Our functional data revealed that these MIA and depletion protocols lead to an increase of layer 4 PC perisomatic inhibition at P20, as well as a horizontal exuberance of cortical inhibition supported by PV+ interneurons. This increased inhibition does not last within development as suggested by our recordings in the adult. On the opposite, it seems that MIA and early microglia depletion result in weaker inhibitory synapses at P60. To conclude, we postulate that microglial cells are the missing link between maternal immune challenge and à higher risk of having neurodevelopmental pathologies like autism or schizophrenia. Our results highlight the crucial role of microglial cells in neuronal network development during perinatal period

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Libros sobre el tema "Inhibitory synapse"

1966-, Hensch Takao K. y Fagiolini Michela, eds. Excitatory-inhibitory balance: Synapses, circuits, systems. New York: 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. y Arianna Maffei. Inhibitory Synaptic Plasticity. Springer, 2014.

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Woodin, Melanie A. y 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 y Michela Fagiolini (Editor), eds. Excitatory-Inhibitory Balance: Synapses, Circuits, Systems. Springer, 2003.

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

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(Compiler), Michael y 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 chapter reviews clinical features of botulism and tetanus and discusses their pathophysiological basis.

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Noebels, Jeffrey L., Massimo Avoli, Michael A. Rogawski, Annamaria Vezzani y Antonio V. Delgado-Escueta, eds. Jasper's Basic Mechanisms of the Epilepsies. 5^a 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 the EPM1 disease relatively well. Myoclonic seizures, preceded by microglial activation, develop at one month of age and are followed by progressive gray and white matter degeneration and motor problems. CSTB is an inhibitor of cysteine proteases of the cathepsin family showing both nuclear and cytoplasmic localization with partial co-localization with lysosomal markers. CSTB function has been linked to protecting neurons from oxidative damage through an oxidative stress-responsive cystatin B-cathepsin B signaling pathway. In the nucleus CSTB has been shown to participate in regulation of cell cycle, and histone H3 tail proteolytic cleavage. Downstream effects of CSTB dysfunction have also been implicated in apopotosis, microglial dysfunction, inflammation, neurogenesis and synapse physiology. Despite the progress made, the exact disease mechanisms in EPM1 remain elusive. This chapter discusses the clinical features of EPM1 and recent advances in understanding its pathophysiology.

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Capítulos de libros sobre el tema "Inhibitory synapse"

Le Saux, Guillaume, Esti Toledo-Ashkenazi y Mark Schvartzman. "Fabrication of Nanoscale Arrays to Study the Effect of Ligand Arrangement on Inhibitory Signaling in NK Cells". En The Immune Synapse, 313–25. New York, NY: 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 y Vibhakar C. Kotak. "Regulation of Inhibitory Synapse Function in the Developing Auditory CNS". En Developmental Plasticity of Inhibitory Circuitry, 43–69. Boston, MA: 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 y Chongbin Guo. "Robustness of Gamma-Oscillation in Networks of Excitatory and Inhibitory Neurons with Conductance-Based Synapse". En Advances in Neural Networks – ISNN 2011, 10–16. Berlin, Heidelberg: 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 y Jacek M. Zurada. "Differences in Input Space Stability Between Using the Inverted Output of Amplifier and Negative Conductance for Inhibitory Synapse". En Advances in Neural Networks – ISNN 2007, 1015–24. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-72383-7_119.

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Komatsu, Yukio y Yumiko Yoshimura. "Long-term Modification at Visual Cortical Inhibitory Synapses". En Excitatory-Inhibitory Balance, 75–87. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0039-1_5.

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Chiu, Chiayu Q. y Pablo E. Castillo. "Endocannabinoid Mediated Long-Term Depression at Inhibitory Synapses". En Inhibitory Synaptic Plasticity, 149–66. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-6978-1_11.

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Komatsu, Yukio y Yumiko Yoshimura. "Long-Term Modification at Inhibitory Synapses in Developing Visual Cortex". En Inhibitory Synaptic Plasticity, 17–27. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-6978-1_2.

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Kawaguchi, Shin-ya y Tomoo Hirano. "Molecular Mechanism of Long-Term Plasticity at Cerebellar Inhibitory Synapses". En Inhibitory Synaptic Plasticity, 29–38. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-6978-1_3.

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Eissmann, Philipp y Daniel M. Davis. "Inhibitory and Regulatory Immune Synapses". En Current Topics in Microbiology and Immunology, 63–79. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-03858-7_4.

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Gonzalez-Islas, Carlos E. y Peter Wenner. "Role of Spontaneous Activity in the Maturation of GABAergic Synapses in Embryonic Spinal Circuits". En Developmental Plasticity of Inhibitory Circuitry, 27–39. Boston, MA: Springer US, 2009. http://dx.doi.org/10.1007/978-1-4419-1243-5_3.

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Actas de conferencias sobre el tema "Inhibitory synapse"

Talanov, Max, Evgeniy Zykov, Victor Erokhin, Evgeni Magid, Salvatore Distefano, Yuriy Gerasimov y Jordi Vallverdú. "Modeling Inhibitory and Excitatory Synapse Learning in the Memristive Neuron Model". En 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 y Tuo-Hung Hou. "Neuromorphic pattern learning using HBM electronic synapse with excitatory and inhibitory plasticity". En 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. y S. S. Rathod. "Analysis of CMOS inhibitory synapse with varying neurotransmitter concentration, reuptake time and spread delay". En 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 y C. Steve Suh. "A Proposition for Describing Real-World Network Dynamics". En 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 dynamics can be quantified using information entropy which is a function of constituent energy. In real-world networks, differences between individual constituents exist due to differing mechanical properties and dynamics. Consequently, network dynamics are of different layers and hierarchies. Construct of network governing equations formulated under the general framework of complex networks are demonstrated using two real-world networks — a brain network and a lymph node network. Brain network is constructed by the neurons that each connected by the synapse. Brain network dynamics is composed by the law of coupling defined by the synaptic dynamics through the transmitting of neurotransmitters that couples the individual neuron dynamics. Since different classifications exist among neurotransmitters and neurons, the post synaptic neuron can present either inhibitory or excitatory action. The inhibitory and excitatory behavior of the neurons changes the mechanical properties of each neuron and further alters the brain network dynamics. Consequently, the brain network emerges dynamics with different layers. Lymph node network drains fluid from blood vessels, filter the lymph (the interstitial fluid lymphatic system collects from the blood circulation) through lymph nodes, and transport the lymph back to the blood circulation. Lymph node dynamics is composed by the dynamics of lymph transportation along the lymph node network and the individual lymph node dynamics that involves lymphocytes-pathogens interactions (adaptive immune response). In each lymph node, lymphocytes fight off the pathogens which also emerges a network dynamics such as the interaction between T cells and HIV viruses. Finally, the lymph is collected from each lymph nodes and drained back to the blood circulation. As a result, the lymph node network has the dynamics of different hierarchies where the lymphocytes-pathogens dynamics exists within each lymph node at the lower hierarchy is further under the influence of the lymph transportation dynamics among the whole lymph node network on the higher hierarchy. Since the constituent dynamics of the brain network and lymph node network can be defined by energy that follows normal distribution and both are bounded by physical constraints, the network dynamics of both cases can be quantified through information entropy. Features pertaining to the global as well as individual constituent dynamics of the networks are identified that are insightful to the control of such complex networks.

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Lecerf, Gwendal, Jean Tomas y Sylvain Saighi. "Excitatory and Inhibitory Memristive Synapses for Spiking Neural Networks". En 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 y Hiroyuki Kitajima. "Bifurcation in mutually coupled three neurons with inhibitory synapses". En 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 y Bo Xu. "Brain-inspired Balanced Tuning for Spiking Neural Networks". En Twenty-Seventh International Joint Conference on Artificial Intelligence {IJCAI-18}. California: 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); Secondly, specific proportions of excitatory and inhibitory neurons usually contribute to stable representations; Thirdly, the short-term plasticity (STP) is a general principle to keep the input and output of synapses balanced towards a better learning convergence. With these inspirations, we train SNNs with three steps: Firstly, the SNN model is trained with three brain-inspired principles; then weakly supervised learning is used to tune the membrane potential in the final layer for network classification; finally the learned information is consolidated from membrane potential into the weights of synapses by Spike-Timing Dependent Plasticity (STDP). The proposed approach is verified on the MNIST hand-written digit recognition dataset and the performance (the accuracy of 98.64%) indicates that the ideas of balancing state could indeed improve the learning ability of SNNs, which shows the power of proposed brain-inspired approach on the tuning of biological plausible SNNs.

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Schiller, Peter H. "ON and OFF channels of the visual system". En OSA Annual Meeting. Washington, D.C.: Optica Publishing Group, 1990. http://dx.doi.org/10.1364/oam.1990.thf2.

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The receptors of the mammalian retina, which all hyperpolarize to light, make signconserving synapses with OFF bipolars and sign-inverting synapses with ON bipolars. Several hypotheses have been generated to explain this arrangement. To test them we applied the neurotransmitter agonist 2-amino-4-phosphonobutyrate (APB) to the retina, which selectively blocks the ON bipolars. Two kinds of experiments were carried out: In one, we examined the visual responses of single cells while reversibly inactivating the ON channel with APB. In the other, we assessed the visual capacities of monkeys before and after the ON channel was blocked. Our single-cell recordings show that the ON and OFF channels remain segregated in the geniculo-striate system until the striate cortex, where they converge. The center/surround organization of the retinal ganglion cells and the orientation and direction-selectivity of cortical cells are not produced by interaction of the ON and OFF channels but by the lateral inhibitory networks. The behavioral experiments identify two reasons for the emergence of the ON and OFF channels: (1) to make possible the central transmission of both light-incremental and light-decremental information with excitatory processes and (2) to enhance contrast sensitivity.

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Baker, J. B., M. P. McGrogan, C. Simonsen, R. L. Gronke y B. W. Festoff. "STRUCTURE AND PROPERTIES OF PROTEASE NEXIN I". En XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644765.

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Human foreskin fibroblasts secrete several different serine protease inhibitors which differ in size and protease specificities. These proteins, called protease nexins (PNs) all form SDS-resistant complexes with their protease targets. Fibroblast surface receptors recognize the protease-PN complexes and mediate their delivery to lysosomes. PNI is a 45 kilodalton glycoprotein that rapidly inhibits several arg or lys-specific proteases including trypsin, thrombin, and urokinase (k assoc.∼ 4×l06,∼ 6×105 and ∼ 2×105, m−1s−1 respectively). Like antithrombin III, PNI binds heparin and inhibits thrombin at a vastly accelerated rate in the presence of this glycoaminoglycan. Immunofluorescence studies show that in addition to secreting PNI foreskin fibroblasts carry this inhibitor on their surfaces. PNI cDNA has been cloned and sequenced. A mixed oligonucleotide probe derived from PNI N-terminal sequence was used to probe a foreskin fibroblast cDNA library constructed with λGT10. Identification of PNI cDNAs has been verified by sequencing and by expressing active PNI protein in mammalian cells. The full amino acid sequence of PNI, deduced from cDNA sequencing, is 392 residues long and has 30% homology to antithrombin III. An arg-ser pair 32 residues from the C-terminus of the inhibitor is proposed as the reactive center P1-P1 residues. In the hinge region a lys residue is present in a position occupied by a ginor glu residue in other serpins. PNI mRNA exists in 2 slightly different forms:One (αPNI) yields a thr-arg-ser sequence wherethe other βPNI) yields a thr-thr-gly-ser sequence. The presence of the appropriate splice acceptor sites in the genome indicates that these forms are generated from a single gene by alternative splicing. Expressed aPNI and 0PNI proteins both bind thrombin and urokinase. In foreskin fibroblaststhe α form of PNI mRNA predominates over the β form by about 2:1. In foreskin fibroblast cultures secreted PNI inhibits the mitogenic response to thrombin and regulate secreted urokinase. Purified PNI added to human fibrosarcoma (HT1080) cells inhibitsthe tumor cell-mediated destruction of extracellular matrix and transiently, but dramatically, inhibits tumor cell growth. PNI or PNI-like inhibitors may function at multiple physiological sites. The β form of PNI is virtually identical to a glia-derived neurite promoting factor, the cDNA for which has been recently cloned and sequenced by Gloor et al (1). The neurite outgrowth activity of PNI may result from inhibition of a thrombin-like protease that is associated with neurons, since a number of thrombin inhibitors stimulate neurite extension. Recent immunofluoresence experiments, carried out with D. Hantai (Inserm; Paris) demonstrate that anti-PNI antibody intensely stains neuromuscular synapses. In addition, a PNI-like inhibitor is associated with platelets. At low (0.5 nM <) 125I-thrombin concentrations formation of 125I-thrombin-platelet PNI complexes accounts for most of the specific binding of 125I-thrombin to platelets (2). Although the platelet-associated form of PNI is electrophoretically and immunologically indistinguishable from fibroblast PNI, it does not bind urokinase, suggesting that it may be distinct.(1) Gloor, S., K. Odink, J. Guenther, H. Nick, and D. Monard. (1986) Cell 47:687-693.(2) Gronke, R.S., B.L. Bergman, and J.B. Baker. (1987) J. Biol. Chem. (in press)

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Yokota, R., H. Takahashi, A. Funamizu, M. Uchihara, J. Suzurikawa y R. Kanzaki. "Auditory Cortical Plasticity Induced by Intracortical Microstimulation under Pharmacological Blockage of Inhibitory Synapses". En 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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