Relevant bibliographies by topics / Synaptic turnover

Academic literature on the topic 'Synaptic turnover'

Author: Grafiati
Published: 10 March 2023

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Journal articles on the topic "Synaptic turnover"

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Zimmermann, H., W. Volknandt, B. Wittich, and A. Hausinger. "Synaptic vesicle life cycle and synaptic turnover." Journal of Physiology-Paris 87, no. 3 (January 1993): 159–70. http://dx.doi.org/10.1016/0928-4257(93)90027-q.

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Jones, Rachel. "Kinetics of Synaptic Protein Turnover Regulate Synaptic Size." PLoS Biology 4, no. 11 (November 7, 2006): e404. http://dx.doi.org/10.1371/journal.pbio.0040404.

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Nabavi, Melinda, and P. Robin Hiesinger. "Turnover of synaptic adhesion molecules." Molecular and Cellular Neuroscience 124 (March 2023): 103816. http://dx.doi.org/10.1016/j.mcn.2023.103816.

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Alvarez-Castelao, Beatriz, and Erin M. Schuman. "The Regulation of Synaptic Protein Turnover." Journal of Biological Chemistry 290, no. 48 (October 9, 2015): 28623–30. http://dx.doi.org/10.1074/jbc.r115.657130.

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Murphy, T. H., D. D. Wright, and J. M. Baraban. "Phosphoinositide Turnover Associated with Synaptic Transmission." Journal of Neurochemistry 59, no. 6 (October 5, 2006): 2336–39. http://dx.doi.org/10.1111/j.1471-4159.1992.tb10130.x.

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Schaefers, Andrea T. U., Keren Grafen, Gertraud Teuchert-Noodt, and York Winter. "Synaptic Remodeling in the Dentate Gyrus, CA3, CA1, Subiculum, and Entorhinal Cortex of Mice: Effects of Deprived Rearing and Voluntary Running." Neural Plasticity 2010 (2010): 1–11. http://dx.doi.org/10.1155/2010/870573.

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Hippocampal cell proliferation is strongly increased and synaptic turnover decreased after rearing under social and physical deprivation in gerbils (Meriones unguiculatus). We examined if a similar epigenetic effect of rearing environment on adult neuroplastic responses can be found in mice (Mus musculus). We examined synaptic turnover rates in the dentate gyrus, CA3, CA1, subiculum, and entorhinal cortex. No direct effects of deprived rearing on rates of synaptic turnover were found in any of the studied regions. However, adult wheel running had the effect of leveling layer-specific differences in synaptic remodeling in the dentate gyrus, CA3, and CA1, but not in the entorhinal cortex and subiculum of animals of both rearing treatments. Epigenetic effects during juvenile development affected adult neural plasticity in mice, but seemed to be less pronounced than in gerbils.
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Tao-Cheng, J. H., A. Dosemeci, P. E. Gallant, S. Miller, J. A. Galbraith, C. A. Winters, R. Azzam, and T. S. Reese. "Rapid turnover of spinules at synaptic terminals." Neuroscience 160, no. 1 (April 2009): 42–50. http://dx.doi.org/10.1016/j.neuroscience.2009.02.031.

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Nath, Arup R., Ileea Larente, Taufik Valiante, and Elise F. Stanley. "Synaptic Vesicle Turnover in Human Brain Synaptosomes." Biophysical Journal 108, no. 2 (January 2015): 100a. http://dx.doi.org/10.1016/j.bpj.2014.11.575.

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Cohen, Laurie D., Rina Zuchman, Oksana Sorokina, Anke Müller, Daniela C. Dieterich, J. Douglas Armstrong, Tamar Ziv, and Noam E. Ziv. "Metabolic Turnover of Synaptic Proteins: Kinetics, Interdependencies and Implications for Synaptic Maintenance." PLoS ONE 8, no. 5 (May 2, 2013): e63191. http://dx.doi.org/10.1371/journal.pone.0063191.

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Lin, Amy W., and Heng-Ye Man. "Ubiquitination of Neurotransmitter Receptors and Postsynaptic Scaffolding Proteins." Neural Plasticity 2013 (2013): 1–10. http://dx.doi.org/10.1155/2013/432057.

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The human brain is made up of an extensive network of neurons that communicate by forming specialized connections called synapses. The amount, location, and dynamic turnover of synaptic proteins, including neurotransmitter receptors and synaptic scaffolding molecules, are under complex regulation and play a crucial role in synaptic connectivity and plasticity, as well as in higher brain functions. An increasing number of studies have established ubiquitination and proteasome-mediated degradation as universal mechanisms in the control of synaptic protein homeostasis. In this paper, we focus on the role of the ubiquitin-proteasome system (UPS) in the turnover of major neurotransmitter receptors, including glutamatergic and nonglutamatergic receptors, as well as postsynaptic receptor-interacting proteins.
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Dissertations / Theses on the topic "Synaptic turnover"

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Wall, M. J., D. R. Collins, S. L. Chery, Z. D. Allen, E. D. Pastuzyn, A. J. George, V. D. Nikolova, et al. "The temporal dynamics of Arc expression regulate cognitive flexibility." 2018. http://hdl.handle.net/10454/16201.

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Yes
Neuronal activity regulates the transcription and translation of the immediate-early gene Arc/Arg3.1, a key mediator of synaptic plasticity. Proteasomedependent degradation of Arc tightly limits its temporal expression, yet the significance of this regulation remains unknown. We disrupted the temporal control of Arc degradation by creating an Arc knockin mouse (ArcKR) where the predominant Arc ubiquitination sites were mutated. ArcKR mice had intact spatial learning but showed specific deficits in selecting an optimal strategy during reversal learning. This cognitive inflexibility was coupled to changes in Arc mRNA and protein expression resulting in a reduced threshold to induce mGluR-LTD and enhanced mGluR-LTD amplitude. These findings show that the abnormal persistence of Arc protein limits the dynamic range of Arc signaling pathways specifically during reversal learning. Our work illuminates how the precise temporal control of activity-dependent molecules, such as Arc, regulates synaptic plasticity and is crucial for cognition.
Open access funded by Biotechnology and Biological Sciences Research Council
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Conti, Emilia. "In vivo optical imaging of cortical plasticity induced by rehabilitation after stroke." Doctoral thesis, 2019. http://hdl.handle.net/2158/1152568.

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In my PhD thesis I have studied the changes in functional and structural plasticity induced by a photothrombotic stroke in mouse primary motor cortex. In order to dissect the multiple aspects consequent to the damage we exploit fluorescent imaging techniques that allow to investigate the functional and structural rearrangement of the cortex at different scale, from the entire hemisphere, with wide-field calcium imaging, up to the single synapse with two-photon microscopy. To promote a functional recovery of the mouse forelimb we applied different rehabilitative strategies in order to both foster the stabilization of regions of the cortex linked to the stroke core, and stimulate the remodelling of peri-infarct areas. We took advantage of a robotic platform (M-Platform), developed by our collaborator in Pisa, to perform the rehabilitation of mouse forelimb through a repetitive motor training. Together with this approach we applied different strategies to mould cortical activity. We temporary inhibited the healthy primary motor cortex, with an intracortical injection of Botulin Neuro Toxin E, in order to counterbalance the iper-excitability of the healthy hemisphere and to promote the structural and functional remodelling of the peri-infarct cortex. This combined rehabilitative protocol promotes the recovery of cortical maps of activation during motor training and the rewiring of interhemispheric connectivity, both from functional and structural level. Then we applied an optogenetic approach as a pro-plasticizing treatment by stimulating with light the region of the cortex surrounding the damage. By coupling this treatment with an intense motor training on the M-Platform we observed a generalized recovery of forelimb functionality in terms of manual dexterity and cortical profiles of activation. In this study, we have shown that different rehabilitative protocols that combines repetitive motor training and neuronal modulation of specific cortical regions induce a synergic effect on neuronal plasticity that promotes the recovery of structural features of healthy neuronal networks.
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Book chapters on the topic "Synaptic turnover"

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Lynch, M. A., M. P. Clements, M. L. Errington, and T. V. P. Bliss. "On the Mechanism of Increased Transmitter Release in LTP: Measurements of Calcium Concentration and Phosphatidylinositol Turnover in CA3 Synaptosomes." In Synaptic Plasticity in the Hippocampus, 110–13. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73202-7_32.

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Benarroch, Eduardo E. "Axonal Transport." In Neuroscience for Clinicians, edited by Eduardo E. Benarroch, 144–55. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780190948894.003.0009.

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Axonal transport is fundamental for neuronal survival and maintenance of neuronal connectivity and synaptic function. Anterograde transport delivers membrane-bound organelles synthesized and packaged in the cell body to the axon and synaptic compartments, and also allows traffic and turnover of cytoskeletal and metabolic components to dendrites and axons. Retrograde transport is necessary for removal and degradation of materials via the endosome-lysosome and autophagy-lysosome systems and for delivery of target-derived neurotrophic signals or injury signals back to the cell body. Bidirectional transport of mitochondria is important for energy delivery and mitochondria quality control. Axonal transport requires intact microtubules, motor proteins such as kinesin for anterograde and the dynein-dynactin complex for retrograde transport, correct attachment of cargo to motors, and sufficient ATP supplied by mitochondria. Impaired axonal transport is a prominent feature of many neurodevelopmental or adult-onset neurodegenerative disorders.
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Kaur, Ramneek, Harleen Kaur, Rashi Rajput, Sachin Kumar, Rachana R., and Manisha Singh. "Neurodegenerative Disorders Progression." In Advances in Medical Diagnosis, Treatment, and Care, 129–52. IGI Global, 2019. http://dx.doi.org/10.4018/978-1-5225-5282-6.ch006.

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Neurodegenerative disorders (NDs) are a diverse group of disorders characterized by selective and progressive loss of neural systems that cause dysfunction of the central nervous system (CNS). The examples of NDs include Alzheimer's disease (AD), amyotrophic lateral sclerosis (ALS), Parkinson's disease (PD), and Huntington's disease (HD). The aggregated proteins block or disrupt the normal proteosomal turnover, autophagy, and become abnormally modified with time, generating toxicity via pathways thereby resulting in neurodegeneration and neuron death. The chapter highlights the understanding in the areas of AD, PD, HD as illustrative of major research so as to define the key factors and events in the improvement of NDs. It defines the physiological functioning of neural transmission (presynaptic, postsynaptic activity) at neural signaling pathway, then the dynamics of neuronal dysfunctioning and its molecular mechanism. Further, it also discusses the progression from synaptic dysfunction to transmission failure followed by NDs.
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