Journal articles: 'Plasticity transmission'

1

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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10

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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Araque, Alfonso, Ana Covelo, Michelle Corkrum, and Paulo Kofuji. "Astrocytic control of synaptic transmission and plasticity." IBRO Reports 6 (September 2019): S9. http://dx.doi.org/10.1016/j.ibror.2019.07.012.

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12

Gambrill, Abigail C., Granville P. Storey, and Andres Barria. "Dynamic Regulation of NMDA Receptor Transmission." Journal of Neurophysiology 105, no. 1 (January 2011): 162–71. http://dx.doi.org/10.1152/jn.00457.2010.

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N-methyl-d-aspartate receptors (NMDARs) are critical for establishing, maintaining, and modifying glutamatergic synapses in an activity-dependent manner. The subunit composition, synaptic expression, and some of the properties of NMDARs are regulated by synaptic activity, affecting processes like synaptic plasticity. NMDAR transmission is dynamic, and we were interested in studying the effect of acute low or null synaptic activity on NMDA receptors and its implications for synaptic plasticity. Periods of no stimulation or low-frequency stimulation increased NMDAR transmission. Changes became stable after periods of 20 min of low or no stimulation. These changes in transmission have a postsynaptic origin and are explained by incorporation of GluN2B-containing receptors to synapses. Importantly, periods of low or no stimulation facilitate long-term potentiation induction. Moreover, recovery after a weak preconditioning stimulus that normally blocks subsequent potentiation is facilitated by a nonstimulation period. Thus synaptic activity dynamically regulates the level of NMDAR transmission adapting constantly the threshold for plasticity.

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Nieto Mendoza, Elizabeth, and Elizabeth Hernández Echeagaray. "Dopaminergic Modulation of Striatal Inhibitory Transmission and Long-Term Plasticity." Neural Plasticity 2015 (2015): 1–15. http://dx.doi.org/10.1155/2015/789502.

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Dopamine (DA) modulates glutamatergic synaptic transmission and its plasticity in the striatum; however it is not well known how DA modulates long-term plasticity of striatal GABAergic inhibitory synapses. This work focused on the analysis of both dopaminergic modulation of inhibitory synapses and the synaptic plasticity established between GABAergic afferents to medium spiny neurons (MSNs). Our results showed that low and high DA concentrations mainly reduced the amplitude of inhibitory synaptic response; however detailed analysis of the D1 and D2 participation in this modulation displayed a wide variability in synaptic response. Analyzing DA participation in striatal GABAergic plasticity we observed that high frequency stimulation (HFS) of GABAergic interneurons in the presence of DA at a low concentration (200 nM) favored the expression of inhibitory striatal LTD, whereas higher concentration of DA (20 μM) primarily induced LTP. Interestingly, the plasticity induced in an animal model of striatal degeneration mimicked that induced in the presence of DA at a high concentration, which was not abolished with D2 antagonist but was prevented by PKA blocker.

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Nakanishi, Shigetada. "Metabotropic glutamate receptors: Synaptic transmission, modulation, and plasticity." Neuron 13, no. 5 (November 1994): 1031–37. http://dx.doi.org/10.1016/0896-6273(94)90043-4.

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15

Kornijcuk, Vladimir, Omid Kavehei, Hyungkwang Lim, Jun Yeong Seok, Seong Keun Kim, Inho Kim, Wook-Seong Lee, Byung Joon Choi, and Doo Seok Jeong. "Multiprotocol-induced plasticity in artificial synapses." Nanoscale 6, no. 24 (2014): 15151–60. http://dx.doi.org/10.1039/c4nr03405h.

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Bernardinelli, Yann, Dominique Muller, and Irina Nikonenko. "Astrocyte-Synapse Structural Plasticity." Neural Plasticity 2014 (2014): 1–13. http://dx.doi.org/10.1155/2014/232105.

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The function and efficacy of synaptic transmission are determined not only by the composition and activity of pre- and postsynaptic components but also by the environment in which a synapse is embedded. Glial cells constitute an important part of this environment and participate in several aspects of synaptic functions. Among the glial cell family, the roles played by astrocytes at the synaptic level are particularly important, ranging from the trophic support to the fine-tuning of transmission. Astrocytic structures are frequently observed in close association with glutamatergic synapses, providing a morphological entity for bidirectional interactions with synapses. Experimental evidence indicates that astrocytes sense neuronal activity by elevating their intracellular calcium in response to neurotransmitters and may communicate with neurons. The precise role of astrocytes in regulating synaptic properties, function, and plasticity remains however a subject of intense debate and many aspects of their interactions with neurons remain to be investigated. A particularly intriguing aspect is their ability to rapidly restructure their processes and modify their coverage of the synaptic elements. The present review summarizes some of these findings with a particular focus on the mechanisms driving this form of structural plasticity and its possible impact on synaptic structure and function.

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Duprat, Fabrice, Michael Daw, Wonil Lim, Graham Collingridge, and John Isaac. "GluR2 protein-protein interactions and the regulation of AMPA receptors during synaptic plasticity." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 358, no. 1432 (April 29, 2003): 715–20. http://dx.doi.org/10.1098/rstb.2002.1215.

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AMPA-type glutamate receptors mediate most fast excitatory synaptic transmissions in the mammalian brain. They are critically involved in the expression of long-term potentiation and long-term depression, forms of synaptic plasticity that are thought to underlie learning and memory. A number of synaptic proteins have been identified that interact with the intracellular C-termini of AMPA receptor subunits. Here, we review recent studies and present new experimental data on the roles of these interacting proteins in regulating the AMPA receptor function during basal synaptic transmission and plasticity.

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Croft, Wayne, Katharine L. Dobson, and Tomas C. Bellamy. "Plasticity of Neuron-Glial Transmission: Equipping Glia for Long-Term Integration of Network Activity." Neural Plasticity 2015 (2015): 1–11. http://dx.doi.org/10.1155/2015/765792.

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The capacity of synaptic networks to express activity-dependent changes in strength and connectivity is essential for learning and memory processes. In recent years, glial cells (most notably astrocytes) have been recognized as active participants in the modulation of synaptic transmission and synaptic plasticity, implicating these electrically nonexcitable cells in information processing in the brain. While the concept of bidirectional communication between neurons and glia and the mechanisms by which gliotransmission can modulate neuronal function are well established, less attention has been focussed on the computational potential of neuron-glial transmission itself. In particular, whether neuron-glial transmission is itself subject to activity-dependent plasticity and what the computational properties of such plasticity might be has not been explored in detail. In this review, we summarize current examples of plasticity in neuron-glial transmission, in many brain regions and neurotransmitter pathways. We argue that induction of glial plasticity typically requires repetitive neuronal firing over long time periods (minutes-hours) rather than the short-lived, stereotyped trigger typical of canonical long-term potentiation. We speculate that this equips glia with a mechanism for monitoring average firing rates in the synaptic network, which is suited to the longer term roles proposed for astrocytes in neurophysiology.

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Castañeda-Hernàndez, Gilberto C., and Paul Bach-y-Rita. "Volume Transmission and Pain Perception." Scientific World JOURNAL 3 (2003): 677–83. http://dx.doi.org/10.1100/tsw.2003.53.

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Volume transmission (VT) is the diffusion through the brain extracellular fluid of neurotransmitters released at points that may be remote from the target cells with the resulting activation of extrasynaptic receptors. VT appears to play multiple roles in the brain in normal and abnormal activity, brain plasticity and drug actions. The relevance of VT to pain perception has been explored in this review.

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20

Peng, Xiang-Long, Gan-Yun Huang, and Swantje Bargmann. "Gradient Crystal Plasticity: A Grain Boundary Model for Slip Transmission." Materials 12, no. 22 (November 15, 2019): 3761. http://dx.doi.org/10.3390/ma12223761.

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Interaction between dislocations and grain boundaries (GBs) in the forms of dislocation absorption, emission, and slip transmission at GBs significantly affects size-dependent plasticity in fine-grained polycrystals. Thus, it is vital to consider those GB mechanisms in continuum plasticity theories. In the present paper, a new GB model is proposed by considering slip transmission at GBs within the framework of gradient polycrystal plasticity. The GB model consists of the GB kinematic relations and governing equations for slip transmission, by which the influence of geometric factors including the misorientation between the incoming and outgoing slip systems and GB orientation, GB defects, and stress state at GBs are captured. The model is numerically implemented to study a benchmark problem of a bicrystal thin film under plane constrained shear. It is found that GB parameters, grain size, grain misorientation, and GB orientation significantly affect slip transmission and plastic behaviors in fine-grained polycrystals. Model prediction qualitatively agrees with experimental observations and results of discrete dislocation dynamics simulations.

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21

Giros, B. "Increased Dopamine Transmission Impairs Behavioral Flexibility and Synaptic Plasticity." European Psychiatry 24, S1 (January 2009): 1. http://dx.doi.org/10.1016/s0924-9338(09)70426-2.

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In addition to its key roles in motor and reward systems, brain dopamine (DA) has also been implicated in integrative functions contributing to adaptive behaviors such as attention, learning and memory, which processing involved the plastic changes of synaptic strength. Since the first formal evidence for Long Term Plasticity mechanism (LTP) in the Hippocampal Formation (HF), the phenomenon of synaptic plasticity has been described in various brain areas. It is appealing to consider that this is particularly true for brain regions that receive DA inputs, including the striatum and the frontal cortex being those most studied beside the hippocampus.We have observed, using mice lacking the dopamine transporter (DAT) which constitute a unique genetic model of persistent functional hyperdopaminergia, a strong deficit of LTD and an enhancement of LTP in the CA1 region of hippocampal slices. This finding suggests that the augmentation of endogenous dopamine by DAT knockout modulates the plastic property of bidirectional synaptic plasticity by inducing a metaplastic shift in the HF. This deficit of LTD can be reversed by the D2 antagonist haloperidol, whereas the LTP increase is not altered. In the same animals, we observed a major impairment of cued-learning in the Morris watermaze, as well as more subtle, but solid, deficits in the spatial learning. These deficits of behavioral flexibility are reversed using haloperidol. Finally, in control animals, the direct blockade of the DAT using GBR12935, can reproduce the LTD and the behavioral deficits, indicating that they are not a consequence of developmental changes.

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22

Calabresi, P. "Synaptic transmission in the striatum: from plasticity to neurodegeneration." Progress in Neurobiology 61, no. 3 (June 2000): 231–65. http://dx.doi.org/10.1016/s0301-0082(99)00030-1.

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23

Madrigal, María Pilar, Adrián Portalés, María Pérez SanJuan, and Sandra Jurado. "Postsynaptic SNARE Proteins: Role in Synaptic Transmission and Plasticity." Neuroscience 420 (November 2019): 12–21. http://dx.doi.org/10.1016/j.neuroscience.2018.11.012.

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24

Lüscher, Christian, and Matthew Frerking. "Restless AMPA receptors: implications for synaptic transmission and plasticity." Trends in Neurosciences 24, no. 11 (November 2001): 665–70. http://dx.doi.org/10.1016/s0166-2236(00)01959-7.

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25

Breustedt, J., A. Gundlfinger, F. Varoqueaux, K. Reim, N. Brose, and D. Schmitz. "Munc13-2 Differentially Affects Hippocampal Synaptic Transmission and Plasticity." Cerebral Cortex 20, no. 5 (August 21, 2009): 1109–20. http://dx.doi.org/10.1093/cercor/bhp170.

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26

Reig, Ramon, and Maria V. Sanchez-Vives. "Synaptic Transmission and Plasticity in an Active Cortical Network." PLoS ONE 2, no. 8 (August 1, 2007): e670. http://dx.doi.org/10.1371/journal.pone.0000670.

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27

Pimentel, Diogo O., and Troy W. Margrie. "Glutamatergic transmission and plasticity between olfactory bulb mitral cells." Journal of Physiology 586, no. 8 (April 14, 2008): 2107–19. http://dx.doi.org/10.1113/jphysiol.2007.149575.

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Verhage, Matthijs. "Presynaptic plasticity: modulation of secretion, co-transmission and neurodegeneration." Parkinsonism & Related Disorders 13 (2007): S250. http://dx.doi.org/10.1016/s1353-8020(08)70011-7.

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29

Rohrbough, Jeffrey, Michael S. Grotewiel, Ronald L. Davis, and Kendal Broadie. "Integrin-Mediated Regulation of Synaptic Morphology, Transmission, and Plasticity." Journal of Neuroscience 20, no. 18 (September 15, 2000): 6868–78. http://dx.doi.org/10.1523/jneurosci.20-18-06868.2000.

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30

Jang, Seil, Daeyoung Oh, Yeunkum Lee, Eric Hosy, Hyewon Shin, Christoph van Riesen, Daniel Whitcomb, et al. "Synaptic adhesion molecule IgSF11 regulates synaptic transmission and plasticity." Nature Neuroscience 19, no. 1 (November 23, 2015): 84–93. http://dx.doi.org/10.1038/nn.4176.

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31

Sarabdjitsingh, Ratna Angela, Julie Jezequel, Natasha Pasricha, Lenka Mikasova, Amber Kerkhofs, Henk Karst, Laurent Groc, and Marian Joëls. "Ultradian corticosterone pulses balance glutamatergic transmission and synaptic plasticity." Proceedings of the National Academy of Sciences 111, no. 39 (September 15, 2014): 14265–70. http://dx.doi.org/10.1073/pnas.1411216111.

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32

Scholz, Joachim, and Perrine Inquimbert. "The Painful Plasticity of Signal Transmission in theSpinal Cord." Clinical Journal of Pain 27, no. 3 (2011): 282–83. http://dx.doi.org/10.1097/ajp.0b013e3181f1586b.

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Pereda, Alberto E., Sebastian Curti, Gregory Hoge, Roger Cachope, Carmen E. Flores, and John E. Rash. "Gap junction-mediated electrical transmission: Regulatory mechanisms and plasticity." Biochimica et Biophysica Acta (BBA) - Biomembranes 1828, no. 1 (January 2013): 134–46. http://dx.doi.org/10.1016/j.bbamem.2012.05.026.

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34

Held, Katharina, Marie Mulier, Nele Van Ranst, Yang Ge, Thomas Voets, Yu Tian Wang, and Joris Vriens. "TRPM3 Inhibits Synaptic Transmission and Plasticity in the Hippocampus." Biophysical Journal 118, no. 3 (February 2020): 21a. http://dx.doi.org/10.1016/j.bpj.2019.11.297.

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35

Henneberger, Christian, and Dmitri A. Rusakov. "Synaptic plasticity and Ca2+ signalling in astrocytes." Neuron Glia Biology 6, no. 3 (August 2010): 141–46. http://dx.doi.org/10.1017/s1740925x10000153.

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There is a growing body of evidence suggesting a functional relationship between Ca2+ signals generated in astroglia and the functioning of nearby excitatory synapses. Interference with endogenous Ca2+ homeostasis inside individual astrocytes has been shown to affect synaptic transmission and its use-dependent changes. However, establishing the causal link between source-specific, physiologically relevant intracellular Ca2+ signals, the astrocytic release machinery and the consequent effects on synaptic transmission has proved difficult. Improved methods of Ca2+ monitoring in situ will be essential for resolving the ambiguity in understanding the underlying Ca2+ signalling cascades.

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Arendt, Kristin L., Zhenjie Zhang, Subhashree Ganesan, Maik Hintze, Maggie M. Shin, Yitai Tang, Ahryon Cho, Isabella A. Graef, and Lu Chen. "Calcineurin mediates homeostatic synaptic plasticity by regulating retinoic acid synthesis." Proceedings of the National Academy of Sciences 112, no. 42 (October 6, 2015): E5744—E5752. http://dx.doi.org/10.1073/pnas.1510239112.

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Homeostatic synaptic plasticity is a form of non-Hebbian plasticity that maintains stability of the network and fidelity for information processing in response to prolonged perturbation of network and synaptic activity. Prolonged blockade of synaptic activity decreases resting Ca2+ levels in neurons, thereby inducing retinoic acid (RA) synthesis and RA-dependent homeostatic synaptic plasticity; however, the signal transduction pathway that links reduced Ca2+-levels to RA synthesis remains unknown. Here we identify the Ca2+-dependent protein phosphatase calcineurin (CaN) as a key regulator for RA synthesis and homeostatic synaptic plasticity. Prolonged inhibition of CaN activity promotes RA synthesis in neurons, and leads to increased excitatory and decreased inhibitory synaptic transmission. These effects of CaN inhibitors on synaptic transmission are blocked by pharmacological inhibitors of RA synthesis or acute genetic deletion of the RA receptor RARα. Thus, CaN, acting upstream of RA, plays a critical role in gating RA signaling pathway in response to synaptic activity. Moreover, activity blockade-induced homeostatic synaptic plasticity is absent in CaN knockout neurons, demonstrating the essential role of CaN in RA-dependent homeostatic synaptic plasticity. Interestingly, in GluA1 S831A and S845A knockin mice, CaN inhibitor- and RA-induced regulation of synaptic transmission is intact, suggesting that phosphorylation of GluA1 C-terminal serine residues S831 and S845 is not required for CaN inhibitor- or RA-induced homeostatic synaptic plasticity. Thus, our study uncovers an unforeseen role of CaN in postsynaptic signaling, and defines CaN as the Ca2+-sensing signaling molecule that mediates RA-dependent homeostatic synaptic plasticity.

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Albiñana, Elisa, Javier Gutierrez-Luengo, Natalia Hernández-Juarez, Andrés M. Baraibar, Eulalia Montell, Josep Vergés, Antonio G. García, and Jesus M. Hernández-Guijo. "Chondroitin Sulfate Induces Depression of Synaptic Transmission and Modulation of Neuronal Plasticity in Rat Hippocampal Slices." Neural Plasticity 2015 (2015): 1–12. http://dx.doi.org/10.1155/2015/463854.

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It is currently known that in CNS the extracellular matrix is involved in synaptic stabilization and limitation of synaptic plasticity. However, it has been reported that the treatment with chondroitinase following injury allows the formation of new synapses and increased plasticity and functional recovery. So, we hypothesize that some components of extracellular matrix may modulate synaptic transmission. To test this hypothesis we evaluated the effects of chondroitin sulphate (CS) on excitatory synaptic transmission, cellular excitability, and neuronal plasticity using extracellular recordings in the CA1 area of rat hippocampal slices. CS caused a reversible depression of evoked field excitatory postsynaptic potentials in a concentration-dependent manner. CS also reduced the population spike amplitude evoked after orthodromic stimulation but not when the population spikes were antidromically evoked; in this last case a potentiation was observed. CS also enhanced paired-pulse facilitation and long-term potentiation. Our study provides evidence that CS, a major component of the brain perineuronal net and extracellular matrix, has a function beyond the structural one, namely, the modulation of synaptic transmission and neuronal plasticity in the hippocampus.

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Shefa, Ulfuara, Dokyoung Kim, Min-Sik Kim, Na Young Jeong, and Junyang Jung. "Roles of Gasotransmitters in Synaptic Plasticity and Neuropsychiatric Conditions." Neural Plasticity 2018 (2018): 1–15. http://dx.doi.org/10.1155/2018/1824713.

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Synaptic plasticity is important for maintaining normal neuronal activity and proper neuronal functioning in the nervous system. It is crucial for regulating synaptic transmission or electrical signal transduction to neuronal networks, for sharing essential information among neurons, and for maintaining homeostasis in the body. Moreover, changes in synaptic or neural plasticity are associated with many neuropsychiatric conditions, such as schizophrenia (SCZ), bipolar disorder (BP), major depressive disorder (MDD), and Alzheimer’s disease (AD). The improper maintenance of neural plasticity causes incorrect neurotransmitter transmission, which can also cause neuropsychiatric conditions. Gas neurotransmitters (gasotransmitters), such as hydrogen sulfide (H2S), nitric oxide (NO), and carbon monoxide (CO), play roles in maintaining synaptic plasticity and in helping to restore such plasticity in the neuronal architecture in the central nervous system (CNS). Indeed, the upregulation or downregulation of these gasotransmitters may cause neuropsychiatric conditions, and their amelioration may restore synaptic plasticity and proper neuronal functioning and thereby improve such conditions. Understanding the specific molecular mechanisms underpinning these effects can help identify ways to treat these neuropsychiatric conditions.

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Skrebitskii, V. G., and M. B. Shtark. "THE FUNDAMENTS OF NEURONAL PLASTICITY." Annals of the Russian academy of medical sciences 67, no. 9 (September 10, 2012): 39–44. http://dx.doi.org/10.15690/vramn.v67i9.405.

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Plasticity of the nervous system is determined by the modification of efficacy of synaptic transmission: long- term potentiation and long- term depression. Different modern technical approaches such as: registration of ionic currents in single neuron, molecular- genetic analysis, neurovisualization, and others reveal the molecular mechanisms of synaptic plasticity. The understanding of these mechanisms, in its turn, stimulates the development of methods of pharmacological correction of different forms of brain pathology such as Alzheimer disease, parkinsonism, alcoholism, aging and others.

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Félix-Oliveira, A., R. B. Dias, M. Colino-Oliveira, D. M. Rombo, and A. M. Sebastião. "Homeostatic plasticity induced by brief activity deprivation enhances long-term potentiation in the mature rat hippocampus." Journal of Neurophysiology 112, no. 11 (December 1, 2014): 3012–22. http://dx.doi.org/10.1152/jn.00058.2014.

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Different forms of plasticity occur concomitantly in the nervous system. Whereas homeostatic plasticity monitors and maintains neuronal activity within a functional range, Hebbian changes such as long-term potentiation (LTP) modify the relative strength of specific synapses after discrete changes in activity and are thought to provide the cellular basis for learning and memory. Here, we assessed whether homeostatic plasticity could influence subsequent LTP in acute hippocampal slices that had been briefly deprived of activity by blocking action potential generation and N-methyl-d-aspartate (NMDA) receptor activation for 3 h. Activity deprivation enhanced the frequency and the amplitude of spontaneous miniature excitatory postsynaptic currents and enhanced basal synaptic transmission in the absence of significant changes in intrinsic excitability. Changes in the threshold for Hebbian plasticity were evaluated by inducing LTP with stimulation protocols of increasing strength. We found that activity-deprived slices consistently showed higher LTP magnitude compared with control conditions even when using subthreshold theta-burst stimulation. Enhanced LTP in activity-deprived slices was also observed when picrotoxin was used to prevent the modulation of GABAergic transmission. Finally, we observed that consecutive LTP inductions attained a higher magnitude of facilitation in activity-deprived slices, suggesting that the homeostatic plasticity mechanisms triggered by a brief period of neuronal silencing can both lower the threshold and raise the ceiling for Hebbian modifications. We conclude that even brief periods of altered activity are able to shape subsequent synaptic transmission and Hebbian plasticity in fully developed hippocampal circuits.

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McLeod, David V., and Troy Day. "Pathogen evolution under host avoidance plasticity." Proceedings of the Royal Society B: Biological Sciences 282, no. 1814 (September 7, 2015): 20151656. http://dx.doi.org/10.1098/rspb.2015.1656.

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Host resistance consists of defences that limit pathogen burden, and can be classified as either adaptations targeting recovery from infection or those focused upon infection avoidance. Conventional theory treats avoidance as a fixed strategy which does not vary from one interaction to the next. However, there is increasing empirical evidence that many avoidance strategies are triggered by external stimuli, and thus should be treated as phenotypically plastic responses. Here, we consider the implications of avoidance plasticity for host–pathogen coevolution. We uncover a number of predictions challenging current theory. First, in the absence of pathogen trade-offs, plasticity can restrain pathogen evolution; moreover, the pathogen exploits conditions in which the host would otherwise invest less in resistance, causing resistance escalation. Second, when transmission trades off with pathogen-induced mortality, plasticity encourages avirulence, resulting in a superior fitness outcome for both host and pathogen. Third, plasticity ensures the sterilizing effect of pathogens has consequences for pathogen evolution. When pathogens castrate hosts, selection forces them to minimize mortality virulence; moreover, when transmission trades off with sterility alone, resistance plasticity is sufficient to prevent pathogens from evolving to fully castrate.

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42

Lalo, Ulyana, Alexander Bogdanov, Guy W. Moss, and Yuriy Pankratov. "Astroglia-Derived BDNF and MSK-1 Mediate Experience- and Diet-Dependent Synaptic Plasticity." Brain Sciences 10, no. 7 (July 18, 2020): 462. http://dx.doi.org/10.3390/brainsci10070462.

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Experience- and diet-dependent regulation of synaptic plasticity can underlie beneficial effects of active lifestyle on the aging brain. Our previous results demonstrate a key role for brain-derived neurotrophic factor (BDNF) and MSK1 kinase in experience-related homeostatic synaptic scaling. Astroglia has been recently shown to release BDNF via a calcium-dependent mechanism. To elucidate a role for astroglia-derived BDNF in homeostatic synaptic plasticity in the aging brain, we explored the experience- and diet-related alterations of synaptic transmission and plasticity in transgenic mice with impairment of the BDNF/MSK1 pathway (MSK1 kinase dead knock-in mice, MSK1 KD) and impairment of glial exocytosis (dnSNARE mice). We found that prolonged tonic activation of astrocytes caused BDNF-dependent increase in the efficacy of excitatory synapses accompanied by enlargement of synaptic boutons. We also observed that exposure to environmental enrichment (EE) and caloric restriction (CR) enhanced the Ca2+ signalling in cortical astrocytes and strongly up-regulated the excitatory and down-regulated inhibitory synaptic currents in old wild-type mice, thus counterbalancing the impact of ageing on astroglial and synaptic signalling. The EE- and CR-induced up-scaling of excitatory synaptic transmission in neocortex was accompanied by the enhancement of long-term synaptic potentiation. Importantly, effects of EE and CR on synaptic transmission and plasticity was significantly reduced in the MSK1 KD and dnSNARE mice. Combined, our results suggest that astroglial release of BDNF is important for the homeostatic regulation of cortical synapses and beneficial effects of EE and CR on synaptic transmission and plasticity in aging brain.

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Srivastava, Akriti, Brati Das, Annie Y. Yao, and Riqiang Yan. "Metabotropic Glutamate Receptors in Alzheimer’s Disease Synaptic Dysfunction: Therapeutic Opportunities and Hope for the Future." Journal of Alzheimer's Disease 78, no. 4 (December 8, 2020): 1345–61. http://dx.doi.org/10.3233/jad-201146.

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Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by the presence of neuritic plaques and neurofibrillary tangles. The impaired synaptic plasticity and dendritic loss at the synaptic level is an early event associated with the AD pathogenesis. The abnormal accumulation of soluble oligomeric amyloid-β (Aβ), the major toxic component in amyloid plaques, is viewed to trigger synaptic dysfunctions through binding to several presynaptic and postsynaptic partners and thus to disrupt synaptic transmission. Over time, the abnormalities in neural transmission will result in cognitive deficits, which are commonly manifested as memory loss in AD patients. Synaptic plasticity is regulated through glutamate transmission, which is mediated by various glutamate receptors. Here we review recent progresses in the study of metabotropic glutamate receptors (mGluRs) in AD cognition. We will discuss the role of mGluRs in synaptic plasticity and their modulation as a possible strategy for AD cognitive improvement.

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Cachope, Roger. "Functional diversity on synaptic plasticity mediated by endocannabinoids." Philosophical Transactions of the Royal Society B: Biological Sciences 367, no. 1607 (December 5, 2012): 3242–53. http://dx.doi.org/10.1098/rstb.2011.0386.

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Endocannabinoids (eCBs) act as modulators of synaptic transmission through activation of a number of receptors, including, but not limited to, cannabinoid receptor 1 (CB1). eCBs share CB1 receptors as a common target with Δ 9 -tetrahydrocannabinol (THC), the main psychoactive ingredient in marijuana. Although THC has been used for recreational and medicinal purposes for thousands of years, little was known about its effects at the cellular level or on neuronal circuits. Identification of CB1 receptors and the subsequent development of its specific ligands has therefore enhanced our ability to study and bring together a substantial amount of knowledge regarding how marijuana and eCBs modify interneuronal communication. To date, the eCB system, composed of cannabinoid receptors, ligands and the relevant enzymes, is recognized as the best-described retrograde signalling system in the brain. Its impact on synaptic transmission is widespread and more diverse than initially thought. The aim of this review is to succinctly present the most common forms of eCB-mediated modulation of synaptic transmission, while also illustrating the multiplicity of effects resulting from specializations of this signalling system at the circuital level.

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Leibold, Christian, and Michael H. K. Bendels. "Learning to Discriminate Through Long-Term Changes of Dynamical Synaptic Transmission." Neural Computation 21, no. 12 (December 2009): 3408–28. http://dx.doi.org/10.1162/neco.2009.12-08-929.

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Short-term synaptic plasticity is modulated by long-term synaptic changes. There is, however, no general agreement on the computational role of this interaction. Here, we derive a learning rule for the release probability and the maximal synaptic conductance in a circuit model with combined recurrent and feedforward connections that allows learning to discriminate among natural inputs. Short-term synaptic plasticity thereby provides a nonlinear expansion of the input space of a linear classifier, whereas the random recurrent network serves to decorrelate the expanded input space. Computer simulations reveal that the twofold increase in the number of input dimensions through short-term synaptic plasticity improves the performance of a standard perceptron up to 100%. The distributions of release probabilities and maximal synaptic conductances at the capacity limit strongly depend on the balance between excitation and inhibition. The model also suggests a new computational interpretation of spikes evoked by stimuli outside the classical receptive field. These neuronal activities may reflect decorrelation of the expanded stimulus space by intracortical synaptic connections.

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Stroeymeyt, Nathalie, Anna V. Grasse, Alessandro Crespi, Danielle P. Mersch, Sylvia Cremer, and Laurent Keller. "Social network plasticity decreases disease transmission in a eusocial insect." Science 362, no. 6417 (November 22, 2018): 941–45. http://dx.doi.org/10.1126/science.aat4793.

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Animal social networks are shaped by multiple selection pressures, including the need to ensure efficient communication and functioning while simultaneously limiting disease transmission. Social animals could potentially further reduce epidemic risk by altering their social networks in the presence of pathogens, yet there is currently no evidence for such pathogen-triggered responses. We tested this hypothesis experimentally in the antLasius nigerusing a combination of automated tracking, controlled pathogen exposure, transmission quantification, and temporally explicit simulations. Pathogen exposure induced behavioral changes in both exposed ants and their nestmates, which helped contain the disease by reinforcing key transmission-inhibitory properties of the colony’s contact network. This suggests that social network plasticity in response to pathogens is an effective strategy for mitigating the effects of disease in social groups.

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Huupponen, J., T. Atanasova, T. Taira, and S. E. Lauri. "GluA4 subunit of AMPA receptors mediates the early synaptic response to altered network activity in the developing hippocampus." Journal of Neurophysiology 115, no. 6 (June 1, 2016): 2989–96. http://dx.doi.org/10.1152/jn.00435.2015.

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Development of the neuronal circuitry involves both Hebbian and homeostatic plasticity mechanisms that orchestrate activity-dependent refinement of the synaptic connectivity. AMPA receptor subunit GluA4 is expressed in hippocampal pyramidal neurons during early postnatal period and is critical for neonatal long-term potentiation; however, its role in homeostatic plasticity is unknown. Here we show that GluA4-dependent plasticity mechanisms allow immature synapses to promptly respond to alterations in network activity. In the neonatal CA3, the threshold for homeostatic plasticity is low, and a 15-h activity blockage with tetrodotoxin triggers homeostatic upregulation of glutamatergic transmission. On the other hand, attenuation of the correlated high-frequency bursting in the CA3-CA1 circuitry leads to weakening of AMPA transmission in CA1, thus reflecting a critical role for Hebbian synapse induction in the developing CA3-CA1. Both of these developmentally restricted forms of plasticity were absent in GluA4 −/− mice. These data suggest that GluA4 enables efficient homeostatic upscaling and responsiveness to temporal activity patterns during the critical period of activity-dependent refinement of the circuitry.

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Costa, Rui Ponte, Zahid Padamsey, James A. D’Amour, Nigel J. Emptage, Robert C. Froemke, and Tim P. Vogels. "Synaptic Transmission Optimization Predicts Expression Loci of Long-Term Plasticity." Neuron 96, no. 1 (September 2017): 177–89. http://dx.doi.org/10.1016/j.neuron.2017.09.021.

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Stjärne, Lennart, Jian-xin Bao, Francois Gonon, Mussie Msghina, and Eivor Stiiime. "On the geometry, kinetics and plasticity of sympathetic neuromuscular transmission." Japanese Journal of Pharmacology 58 (1992): 158–65. http://dx.doi.org/10.1016/s0021-5198(19)59908-5.

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Lüscher, Christian, Houhui Xia, Eric C. Beattie, Reed C. Carroll, Mark von Zastrow, Robert C. Malenka, and Roger A. Nicoll. "Role of AMPA Receptor Cycling in Synaptic Transmission and Plasticity." Neuron 24, no. 3 (November 1999): 649–58. http://dx.doi.org/10.1016/s0896-6273(00)81119-8.

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Journal articles on the topic 'Plasticity transmission'

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