Relevant bibliographies by topics / Plasticity transmission

Contents

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

Academic literature on the topic 'Plasticity transmission'

Author: Grafiati
Published: 4 June 2021
Last updated: 4 February 2022

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Journal articles on the topic "Plasticity transmission"

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Burnstock, G. "Plasticity of autonomic transmission." Journal of the Autonomic Nervous System 33, no. 2 (May 1991): 137–38. http://dx.doi.org/10.1016/0165-1838(91)90164-x.

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Harris, Kathryn P., and J. Troy Littleton. "Transmission, Development, and Plasticity of Synapses." Genetics 201, no. 2 (October 2015): 345–75. http://dx.doi.org/10.1534/genetics.115.176529.

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Kalia, Lorraine V., Jeffrey R. Gingrich, and Michael W. Salter. "Src in synaptic transmission and plasticity." Oncogene 23, no. 48 (October 2004): 8007–16. http://dx.doi.org/10.1038/sj.onc.1208158.

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ALKADHI, K., K. ALZOUBI, and A. ALEISA. "Plasticity of synaptic transmission in autonomic ganglia." Progress in Neurobiology 75, no. 2 (February 2005): 83–108. http://dx.doi.org/10.1016/j.pneurobio.2005.02.002.

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Rotman, Z., P. Y. Deng, and V. A. Klyachko. "Short-Term Plasticity Optimizes Synaptic Information Transmission." Journal of Neuroscience 31, no. 41 (October 12, 2011): 14800–14809. http://dx.doi.org/10.1523/jneurosci.3231-11.2011.

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Lomax, Alan E., Sabindra Pradhananga, and Paul P. Bertrand. "Plasticity of neuroeffector transmission during bowel inflammation1." American Journal of Physiology-Gastrointestinal and Liver Physiology 312, no. 3 (March 1, 2017): G165—G170. http://dx.doi.org/10.1152/ajpgi.00365.2016.

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Altered gastrointestinal (GI) function contributes to the debilitating symptoms of inflammatory bowel diseases (IBD). Nerve circuits contained within the gut wall and outside of the gut play important roles in modulating motility, mucosal fluid transport, and blood flow. The structure and function of these neuronal populations change during IBD. Superimposed on this plasticity is a diminished responsiveness of effector cells — smooth muscle cells, enterocytes, and vascular endothelial cells — to neurotransmitters. The net result is a breakdown in the precisely orchestrated coordination of motility, fluid secretion, and GI blood flow required for health. In this review, we consider how inflammation-induced changes to the effector innervation of these tissues, and changes to the tissues themselves, contribute to defective GI function in models of IBD. We also explore the evidence that reversing neuronal plasticity is sufficient to normalize function during IBD.
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Venkitaramani, D. V., J. Chin, W. J. Netzer, G. K. Gouras, S. Lesne, R. Malinow, and P. J. Lombroso. "-Amyloid Modulation of Synaptic Transmission and Plasticity." Journal of Neuroscience 27, no. 44 (October 31, 2007): 11832–37. http://dx.doi.org/10.1523/jneurosci.3478-07.2007.

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Lu, Bai, and Ana Chow. "Neurotrophins and hippocampal synaptic transmission and plasticity." Journal of Neuroscience Research 58, no. 1 (September 17, 1999): 76–87. http://dx.doi.org/10.1002/(sici)1097-4547(19991001)58:1<76::aid-jnr8>3.0.co;2-0.

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Mannan, Zubaer Ibna, Shyam Prasad Adhikari, Changju Yang, Ram Kaji Budhathoki, Hyongsuk Kim, and Leon Chua. "Memristive Imitation of Synaptic Transmission and Plasticity." IEEE Transactions on Neural Networks and Learning Systems 30, no. 11 (November 2019): 3458–70. http://dx.doi.org/10.1109/tnnls.2019.2892385.

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Maren, Stephen. "Synaptic transmission and plasticity in the amygdala." Molecular Neurobiology 13, no. 1 (August 1996): 1–22. http://dx.doi.org/10.1007/bf02740749.

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Dissertations / Theses on the topic "Plasticity transmission"

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Trommershäuser, Julia. "A semi-microscopic model of synaptic transmission and plasticity." [S.l.] : [s.n.], 2000. http://deposit.ddb.de/cgi-bin/dokserv?idn=963474626.

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Roberts, Lindsay A. "Plasticity related gene expression in the hippocampus." Thesis, University of Glasgow, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.360278.

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Gleizes, Marie. "Ectonucléotidases, adénosine et transmission synaptique." Thesis, Toulouse 3, 2017. http://www.theses.fr/2017TOU30306/document.

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Dans le cerveau, les fonctions de la phosphatase alcaline non spécifique des tissus (TNAP) ne sont pas clairement identifiées. La localisation et l'expression de cette enzyme au niveau neuronal suggère cependant, qu'elle joue un rôle important dans le développement et le fonctionnement du cerveau. Cela est supporté par la présence de graves crises d'épilepsie chez les humains porteurs d'une mutation de la TNAP. Ces crises d'épilepsie sont létales chez les souris KO pour la TNAP. Des études chez la souris montrent que la TNAP pourrait réguler l'inhibition postsynaptique médiée par le GABA et elle pourrait être impliquée dans l'inhibition présynaptique médiée par l'adénosine. L'adénosine est, en partie, synthétisée via la déphosphorylation successive de l'ATP en ADP puis en AMP par des ectonucléotidases. Parmi elles, la TNAP et l'ecto- 5'-nucléotidase (NT5E) catalysent l'hydrolyse de l'AMP en adénosine dans le cortex cérébral. L'adénosine agit principalement au niveau présynaptique par l'intermédiaire des récepteurs A1. Ainsi l'adénosine a une influence sur la transmission synaptique et sur la plasticité synaptique. Ceci pourrait expliquer, en partie, les crises d'épilepsie observées chez les souris KO pour la TNAP. Les deux objectifs principaux de ma thèse ont été : (1) évaluer la contribution de la TNAP dans la production d'adénosine dans le cerveau ; (2) étudier l'influence de l'adénosine sur la plasticité synaptique. Premièrement, l'étude de la contribution de la TNAP dans la production d'adénosine dans le cerveau a été réalisée au moyen de deux approches complémentaires. Une approche métabolomique (spectroscopie RMN du proton) sur des cerveaux entiers de souris KO pour la TNAP a permis de montrer que la TNAP participe, entre autre, à la synthèse d'adénosine dans le cerveau. Une deuxième approche, électrophysiologique sur tranches de cerveaux de souris in vitro, nous permet d'examiner les conséquences de l'inhibition des ectonucléotidases intervenant dans la synthèse de l'adénosine. Elle a révélé que l'inhibition des ectonucléotidases (TNAP et NT5E) ne supprime pas l'effet inhibiteur de l'AMP médiée par les récepteurs A1. Deuxièmement, nous avons étudié l'influence de l'adénosine sur la plasticité synaptique à courte terme. Nous avons enregistré des potentiels de champs dans la couche Ia du cortex piriforme en réponse à des stimulations électriques (3,125 à 100 Hz) présentée avec des fréquences recouvrant la gamme d'oscillations physiologiques. Nos résultats montrent qu'avec de fortes concentrations d'adénosine, la facilitation est accentuée par rapport à celle observée en situation contrôle. Cet effet est observé pour des fréquences supérieures ou égales à 25 Hz. De plus, cette accentuation est d'autant plus grande que la fréquence est élevée (maximum atteint à 100 Hz pour 100 µM). En bloquant l'action de l'adénosine endogène, l'effet contraire est observé : une facilitation déficitaire par rapport au contrôle et dont le défaut est croissant avec la fréquence de stimulation. Tous ces résultats convergent vers l'hypothèse qu'une déficience en TNAP, traduite par une absence d'adénosine, pourrait contribuer au maintien des processus épileptiques générés par un déséquilibre de l'inhibition et de l'excitation dû à une diminution de GABA. L'effet inhibiteur de l'AMP médié par les récepteurs A1 ne serait pas suffisant pour contrecarrer les crises d'épilepsie observées chez les sujets hypophosphatasiques et les souris KO pour la TNAP
The functions of Tissue Nonspecific Alkaline Phosphatase (TNAP) in the brain are not clearly identified. The localization and expression of TNAP at the neuronal level, however, suggests that it plays a prominent role in the development and the function in the brain. This is supported by the presence of severe epileptic seizures in humans carrying TNAP mutation. These epileptic seizures are lethal in TNAP KO mice. Studies in mice show that TNAP could regulate GABA-mediated postsynaptic inhibition and may be involved in presynaptic inhibition mediated by adenosine. Adenosine is, partly, synthesized via the successive dephosphorylation of ATP to ADP and then to AMP by ectonucleotidases. Among them TNAP and ecto-5'-nucleotidase (NT5E) are able to hydrolyze AMP into adenosine. Adenosine acts mainly at the presynaptic level via A1 receptors activation. Adenosine has an influence on synaptic transmission and thus on synaptic plasticity. This could partly explain the epileptic seizures observed in TNAP knock-out mice. The two main purposes of my thesis were: (1) to evaluate the contribution of TNAP in adenosine production in the brain; (2) to study the influence of adenosine on synaptic plasticity. Firstly, the study of the contribution of TNAP in adenosine production in the brain was carried out using two complementary approaches. A metabolomic approach (proton NMR spectroscopy) on whole brains of TNAP KO mice showed that TNAP in involved in adenosine synthesis in the brain. In a second approach, in vitro electrophysiological recordings on mouse brain slices allowed us to examine the consequences of the inhibition of the ectonucleotidases involved in adenosine synthesis. This revealed that inhibition of ectonucleotidases (TNAP and NT5E) did not suppress the inhibitory effect of AMP mediated by A1 receptors. Secondly, we studied the influence of adenosine on short-term synaptic plasticity. Field potentials were recorded in response to electrical stimulations (3.125 to 100 Hz) applied with frequencies encompassing the range of physiological oscillation. Our results show that, with high adenosine concentrations, the facilitation is emphasized compared to that observed in the control situation. This effect is observed for frequencies greater than or equal to 25 Hz. In addition, the higher the frequency, the greater the facilitation. Finally, by blocking the action of endogenous adenosine, the opposite effect was observed: a deficient facilitation with respect to the control, whose defect was increasing with stimulation frequency. All these results converge towards the hypothesis that TNAP deficiency, expressed by absence of adenosine, could contribute to the maintenance of the epileptic processes generated by an imbalance of the neuronal inhibition and the excitation due to a decrease of GABA. AMP inhibitory effect mediated by A1 receptors, would not be sufficient to counteract epileptic seizures observed in hypophosphatasic patients and TNAP KO mice
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Vaccaro, V. "The role of presynaptic mitochondria in neuronal transmission and plasticity." Thesis, University College London (University of London), 2015. http://discovery.ucl.ac.uk/1468434/.

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Mitochondria are essential for cellular processes such as energy provision and Ca2 + buffering. Due to the highly polarized architecture of neurons, the positioning of mitochondria to areas of high activity is crucial for normal neuronal function. It has previously been shown that mitochondria are trafficked dependent upon neuronal activity. In this thesis, the role of mitochondria at the presynaptic terminal is investigated in order to determine whether the presence of mitochondria in turn influences neuronal transmission. Dual-colour live imaging reveals that terminals occupied by a mitochondrion show lower Ca2 + responses and that transmitter release is reduced. Furthermore, evidence for a role of activity-dependent positioning of mitochondria in homeostatic plasticity is shown, which is dependent upon the function of the Ca2 + -sensitive mitochondrial protein Miro1. Furthermore, the role of Miro1 in positioning mitochondria at presynaptic terminals is investigated in a knockout mouse system. This shows that calcium buffering seems to be changed in the Miro1 knockout neurons and that activity-dependent positioning of mitochondria to presynaptic terminals is affected. Taken together, this thesis examines the functions of mitochondria in the presynaptic terminal and sheds light on how their presence in the terminal may be regulated.
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Fan, Kai Yoon. "GABAergic synaptic transmission, plasticity and integration in the subthalamic nucleus." Thesis, University of Sheffield, 2012. http://etheses.whiterose.ac.uk/3167/.

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Ivanco, Tammy L. "Activity dependent plasticity in pathways between subcortical and cortical sites." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ30095.pdf.

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Mercier, Marion. "Role of metabotropic glutamate receptor 8 in hippocampal synaptic transmission and plasticity." Thesis, University of Bristol, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.665156.

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Group III metabotropic glutamate (mGlu) receptors (mGlu4/6/7/8) are presynaptic G-protein coupled receptors which act as auto- and hetero-receptors throughout the central nervous system. The development of mGlu8 receptor-selective agonist (S)-3,4-dicarboxyphenylglycine (DCPG), and antagonist (RS)-a-methyl-3,4- dicarboxyphenylglycine (MDCPG), in 2001 (Thomas et al., 2001), has led to a body of research investigating the possible function of this receptor subtype, and linking it to a number of pathological conditions including anxiety and epilepsy. The aim of the current work was to explore the role of mGlu8 within the hippocampal formation specifically, employing DCPG and MDCPG to assess its function in synaptic transmission and plasticity. The mGlu8-selectivity of these compounds was first assessed in the lateral perforant path (LPP) input to the dentate gyrus, a pathway known to express high levels of mGlu8 receptors. Field recordings in hippocampal slices from rat, and mGlu8 receptor knock-out (KO) mice revealed non-selective effects of DCPG at concentrations > 1 μM. Further experiments in slices from mGlu4, mGlu7 and mGlu2 KO mice, as well as a mGlu2-deficient substrain of Wistar rat, indicated that higher concentrations of the agonist activate the group II receptor subtype, mGlu2. Conversely, MDCPG appeared to be selective for mGlu8 at up to the highest concentration tested (30 μM). During this work in the LPP, DCPG was found to induce a novel form of mGlu8-mediated chemical long-term depression (LTD). This was induced by prolonged application of a high concentration (100 μM) of the agonist, and was more pronounced in older animals. Importantly, the LTD could be transiently reversed by application of MDCPG, up to two hours after washout of DCPG. Finally, patch-clamp recordings revealed inhibitory effects of DCPG on glutamatergic and GABAergic transmission onto subsets of CAl interneurons, but not pyramidal cells. This. is consistent with the known target-cell specific expression of mGlu8 within the hippocampus.
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Jiang, Jianxiong Wooten Marie W. "Essential role for P62 in AMPA receptor trafficking and synaptic plasticity." Auburn, Ala, 2008. http://repo.lib.auburn.edu/EtdRoot/2008/SPRING/Biological_Sciences/Dissertation/Jiang_Jianxiong_41.pdf.

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Sweeney, Yann Aodh. "Functional relevance of homeostatic intrinsic plasticity in neurons and networks." Thesis, University of Edinburgh, 2016. http://hdl.handle.net/1842/20982.

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Maintaining the intrinsic excitability of neurons is crucial for stable brain activity. This can be achieved by the homeostatic regulation of membrane ion channel conductances, although it is not well understood how these processes influence broader aspects of neuron and network function. One of the many mechanisms which contribute towards this task is the modulation of potassium channel conductances by activity-dependent nitric oxide signalling. Here, we first investigate this mechanism in a conductance-based neuron model. By fitting the model to experimental data we find that nitric oxide signalling improves synaptic transmission fidelity at high firing rates, but that there is an increase in the metabolic cost of action potentials associated with this improvement. Although the improvement in function had been observed previously in experiment, the metabolic constraint was unknown. This additional constraint provides a plausible explanation for the selective activation of nitric oxide signalling only at high firing rates. In addition to mediating homeostatic control of intrinsic excitability, nitric oxide can diffuse freely across cell membranes, providing a unique mechanism for neurons to communicate within a network, independent of synaptic connectivity. We next conduct a theoretical investigation of the distinguishing roles of diffusive homeostasis mediated by nitric oxide in comparison with canonical non-diffusive homeostasis in cortical networks. We find that both forms of homeostasis robustly maintain stable activity. However, the resulting networks differ, with diffusive homeostasis maintaining substantial heterogeneity in activity levels of individual neurons, a feature disrupted in networks with non-diffusive homeostasis. This results in networks capable of representing input heterogeneity, and linearly responding over a broader range of inputs than those undergoing non-diffusive homeostasis. We further show that diffusive homeostasis interferes less than non-diffusive homeostasis in the synaptic weight dynamics of networks undergoing Hebbian plasticity. Overall, these results suggest a novel homeostatic mechanism for maintaining stable network activity while simultaneously minimising metabolic cost and conserving network functionality.
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Liu, Zhi. "Unconventional forms of synaptic plasticity in the hippocampus and the striatum." Thesis, University of British Columbia, 2008. http://hdl.handle.net/2429/2616.

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Synaptic transmission occurs as a result of either a spontaneous release of presynaptic vesicles or a batch release of presynaptic vesicles driven by action potentials. The physiological consequence of synaptic transmission driven by different patterns and frequencies of presynaptic stimulation has been extensively investigated. However, the physiological nature, mechanism as well as relevance of prolonged presynaptic stimulation have been poorly characterized. In this dissertation, I present three projects in which prolonged stimulation of synaptic transmission in different forms and different brain regions was studied for its effect on synaptic transmission, mechanisms and physiological relevance. In the first project, prolonged electrical stimulation (100 sec) at high frequency induced a deep synaptic depression in acute hippocampal slices, followed by a recovery of synaptic transmission after ~15 min. The deep synaptic depression was attributed to a complete depletion of presynaptic vesicle pools. In the second project, attempts were made to characterize the mechanism of nuclear activation of gene transcription induced by prolonged electrical stimulation (100 sec). Our results demonstrated that reduced inactivation of non-L-type calcium channels failed to provide calcium required for gene transcription, leaving the activation of gene transcription a selective function for L-type calcium channels. In the third project, we sought to study the physiological relevance of enhanced miniature events of inhibitory synapses induced by prolonged chemical stimulation. We showed that prolonged application (2 min) of nicotine to the striatal slice enhanced the frequency of miniature inhibitory currents that was accompanied with a reduction in the amplitude of evoked response. This reduction in the amplitude of evoked responses was ascribed to a compromised action potential invasion of presynaptic terminals possibly due to inactivation of sodium channels resulting from nicotine-induced depolarization. To summarize, prolonged stimulation of presynaptic vesicle release imposes significant influence upon neuron-to-neuron communication, with distinct mechanisms in different brain regions.
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Books on the topic "Plasticity transmission"

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Georg, Hertting, Spatz Hanns-Christof, and North Atlantic Treaty Organization. Scientific Affairs Division., eds. Modulation of synaptic transmission and plasticity in nervous systems. Berlin: Springer-Verlag, 1988.

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Hertting, Georg, and Hanns-Christof Spatz, eds. Modulation of Synaptic Transmission and Plasticity in Nervous Systems. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73160-0.

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McMahon, Gale N., and Rich G. Buckner. Synaptic plasticity: Cell biology, regulation and role in disease. New York: Nova Biomedical, 2012.

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Synaptic plasticity: Dynamics, development and disease. Wien: Springer, 2012.

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Taupin, Philippe. The hippocampus: Neurotransmission and plasticity in the nervous system. New York: Nova Biomedical Books, 2007.

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The cerebellum: Brain for an implicit self. Upper Saddle River, N.J: FT Press, 2012.

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Nonsynaptic diffusion neurotransmission and late brain reorganization. New York: Demos, 1995.

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F, Kaiser Tim, and Peters Felix J, eds. Synaptic plasticity: New research. New York: Nova Science Publishers, 2008.

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Modulation Of Synaptic Transmission And Plasticity In Nervous Systems. Springer, 2012.

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Sala, Carlo, and Michael R. Kreutz. Synaptic Plasticity: Dynamics, Development and Disease. Springer, 2012.

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Book chapters on the topic "Plasticity transmission"

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Marvizon, Juan Carlos. "Opioidergic Transmission in the Dorsal Horn." In Synaptic Plasticity in Pain, 139–73. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-0226-9_7.

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Xu, Zao C. "Alterations of Synaptic Transmission Following Transient Cerebral Ischemia." In Neuronal and Vascular Plasticity, 117–34. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0282-1_5.

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Stelzer, A., and R. K. S. Wong. "GABA Transmission in the Hippocampus: Postsynaptic Regulation." In Synaptic Plasticity in the Hippocampus, 67–69. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73202-7_20.

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Zeilhofer, Hanns Ulrich, Robert Witschi, and Torbjörn Johansson. "Fast Inhibitory Transmission of Pain in the Spinal Cord." In Synaptic Plasticity in Pain, 49–66. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-0226-9_3.

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Ingram, Rachel A., Mark L. Baccei, and Maria Fitzgerald. "Synaptic Transmission of Pain in the Developing Spinal Cord." In Synaptic Plasticity in Pain, 67–85. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-0226-9_4.

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Brandon, Robert N. "Phenotypic Plasticity, Cultural Transmission, and Human Sociobiology." In Sociobiology and Epistemology, 57–73. Dordrecht: Springer Netherlands, 1985. http://dx.doi.org/10.1007/978-94-009-5370-3_3.

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Sipilä, Sampsa T., and Kai K. Kaila. "GABAergic Transmission and Neuronal Network Events During Hippocampal Development." In Developmental Plasticity of Inhibitory Circuitry, 115–36. Boston, MA: Springer US, 2009. http://dx.doi.org/10.1007/978-1-4419-1243-5_7.

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Mishuris, Gennady, Wiktoria Miszuris, Andreas Öchsner, and Andrea Piccolroaz. "Transmission Conditions for Thin Elasto-Plastic Pressure-Dependent Interphases." In Plasticity of Pressure-Sensitive Materials, 205–51. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-40945-5_4.

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Swann, John W., Karen L. Smith, and Robert J. Brady. "Neural Networks and Synaptic Transmission in Immature Hippocampus." In Excitatory Amino Acids and Neuronal Plasticity, 161–71. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5769-8_19.

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Heinemann, U., H. Clusmann, J. Dreier, and J. Stabel. "Changes in Synaptic Transmission in the Kindled Hippocampus." In Excitatory Amino Acids and Neuronal Plasticity, 445–50. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5769-8_49.

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Conference papers on the topic "Plasticity transmission"

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Chu, M. Q., I. P. Jones, J. C. F. Millett, N. K. Bourne, G. T. Gray, Mark Elert, Michael D. Furnish, William W. Anderson, William G. Proud, and William T. Butler. "THE ROLE OF TRANSMISSION ELECTRON MICROSCOPY IN ASSESSING SHOCK PLASTICITY." In SHOCK COMPRESSION OF CONDENSED MATTER 2009: Proceedings of the American Physical Society Topical Group on Shock Compression of Condensed Matter. AIP, 2009. http://dx.doi.org/10.1063/1.3294996.

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Yang, Shengyuan, Scott Siechen, Jie Sun, Akira Chiba, and Taher Saif. "Learning by Tension." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176719.

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Memory and learning in animals is mediated by neurotransmission at the synaptic junctions (end point of axons). Neurotransmitters are carried by synaptic vesicles which cluster at the junctions, ready to be dispatched for transmission. The more a synapse is used, higher is the clustering, and higher is the neurotransmission efficiency (plasticity), i.e., the junction “remembers” its use in the near past, and modifies accordingly. This usage dependent plasticity offers the basic mechanism of memory and learning. A central dogma in neuroscience is that, clustering is the result of a complex biochemical signaling process. We show, using MEMS sensors and fruit fly (Drosophila) embryo nervous system, that mechanical tension in axons is essential for clustering. Without tension, clustering disappears, but reappears with application of tension. Nature maintains a rest tension of 1nN in axons of Drosophila for learning and memory.
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Birenis, Domas, Yuhei Ogawa, Hisao Matsunaga, Osamu Takakuwa, Junichiro Yamabe, Øystein Prytz, and Annett Thøgersen. "Hydrogen-Assisted Fatigue Crack Propagation in a Commercially Pure BCC Iron." In ASME 2018 Pressure Vessels and Piping Conference. American Society of Mechanical Engineers, 2018. http://dx.doi.org/10.1115/pvp2018-84783.

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Hydrogen effect on fatigue performance of commercially pure BCC iron has been studied with a combination of various electron microscopy techniques. The fatigue crack growth (FCG) in gaseous hydrogen was found to consist of two regimes corresponding to a slightly accelerated regime at relatively low stress intensity factor range, ΔK, (Stage I) and the highly accelerated regime at relatively high ΔK (Stage II). These regimes were manifested by the intergranular and quasicleavage types of fractures respectively. Scanning electron microscopy (SEM) observations demonstrated an increase in plastic deformation around the crack wake in the Stage I, but considerably lower amount of plasticity around the crack path in the Stage II. Transmission electron microscopy (TEM) results identified dislocation cell structure immediately beneath the fracture surface of the Stage I sample, and dislocation tangles in the Stage II sample corresponding to fracture at high and low plastic strain amplitudes respectively.
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Vargas, Pedro, Ben Crowder, and David Roberts. "Zap-Lok® Connection Testing and Axial Strength Design." In ASME 2011 30th International Conference on Ocean, Offshore and Arctic Engineering. ASMEDC, 2011. http://dx.doi.org/10.1115/omae2011-50209.

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Zap-Lok® is a pipe joining technology which relies on radial-interference elastic strain and surface friction to join pipes. The connection consists of a “bell” (expanded end) into which a “pin” (the straight end of the adjoining pipe) is forcefully inserted to provide an interference fit (See Figure 1). Joining is accomplished via a specialized hydraulic joining press provided by Zap-Lok® which grips both pipe sections and forces them together. A thin layer of the patented epoxy is applied internally to the bell end, and externally to the pin end, to provide lubrication for the insertion. The joining operation takes approximately ten seconds. Both the bell and the pin are formed to specified tolerances per specification by Zap-Lok® technicians, and may be done in the field or shop. Typical applications include gathering and distribution systems, transmission lines and specialized pipe installations on land and offshore. Of particular interest is the ability to withstand corrosive products with the application of an internal coating that does not sustain damage during the joining operation. To qualify this technology for use extensive testing and analyses was performed. We found that: • In sour service applications the plastic deformation of the bell necessitated a heat treatment to insure that the connection remained NACE compliant. • The axial strength capacity was found to be somewhat less than that of a welded joint. • Burst capacity of the joint was robust. • The joint did not leak even after several cycles of significant plasticity. • Fatigue performance of the joint rivaled that of a lower-end girth weld (i.e. F2 S-N curve). A design method was developed to correctly account for the axial strength using basic ASME-type design concepts. In this presentation we summarize the connection mechanics, testing results, analytical models and design method for the Zap-Lok® connection.
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5

Igarashi, Takahiro, Yoshiteru Aoyagi, and Yoshiyuki Kaji. "Multiphysics Modeling and Simulation for Stress Corrosion Cracking Considering Oxygen Atom Diffusion Along Grain Boundary." In 18th International Conference on Nuclear Engineering. ASMEDC, 2010. http://dx.doi.org/10.1115/icone18-29337.

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Aged degradations of structural materials of boiling water reactors by stress corrosion cracking (SCC) have been frequently reported. SCC is the results of the synergistic interaction of mechanical stress and corrosive environment, and the investigation of this phenomenon has been an important issue. Although many kinds of studies for SCC have been carried out, we have not clarified the fundamental mechanisms of SCC initiation and propagation yet. In the recent experimental studies, nano-scale observation around crack tips using transmission electron microscopy have shown three characteristics of SCC of nuclear structural materials as follows; the size of crack tip is nanometer order, the opening crack is filled with the oxides, and oxygen atoms exist in the grain boundary beyond the crack tips. The second and third ones show that the corrosive environment is mainly influenced on the SCC propagation behavior. Furthermore, electron back scatter diffraction pattern analyses have shown that about 10–20% of plastic strain exists around the crack tips and crack sides. The existence of oxygen atoms along grain boundaries and plastic strains around grain boundaries could be related to the crack propagation mechanism of SCC. In this study, in order to observe the influence of oxygen atoms on the SCC propagation behavior, the two-dimensional SCC propagation model considering diffusion of oxygen atoms along grain boundaries is developed. In this model, the stress distribution of polycrystalline system is obtained by the crystal plasticity theory, and the concentration of oxygen atoms depending on stress localization around cracks is calculated using the diffusion equation of oxygen atoms considering the stress gradient. The density distribution of oxygen atoms is adopted for the threshold of the crack propagation. Relation between the threshold of crack propagation as a viewpoint of density of oxygen atoms along grain boundaries and the geometry of SCC is discussed in this paper.
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