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Journal articles on the topic 'Dendritic Spine Plasticity'

Author: Grafiati

Published: 11 March 2023

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1

Power, John M., and Pankaj Sah. "Dendritic spine heterogeneity and calcium dynamics in basolateral amygdala principal neurons." Journal of Neurophysiology 112, no. 7 (2014): 1616–27. http://dx.doi.org/10.1152/jn.00770.2013.

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Glutamatergic synapses on pyramidal neurons are formed on dendritic spines where glutamate activates ionotropic receptors, and calcium influx via N-methyl-d-aspartate receptors leads to a localized rise in spine calcium that is critical for the induction of synaptic plasticity. In the basolateral amygdala, activation of metabotropic receptors is also required for synaptic plasticity and amygdala-dependent learning. Here, using acute brain slices from rats, we show that, in basolateral amygdala principal neurons, high-frequency synaptic stimulation activates metabotropic glutamate receptors and

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2

Rosado, James, Viet Duc Bui, Carola A. Haas, Jürgen Beck, Gillian Queisser, and Andreas Vlachos. "Calcium modeling of spine apparatus-containing human dendritic spines demonstrates an “all-or-nothing” communication switch between the spine head and dendrite." PLOS Computational Biology 18, no. 4 (2022): e1010069. http://dx.doi.org/10.1371/journal.pcbi.1010069.

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Dendritic spines are highly dynamic neuronal compartments that control the synaptic transmission between neurons. Spines form ultrastructural units, coupling synaptic contact sites to the dendritic shaft and often harbor a spine apparatus organelle, composed of smooth endoplasmic reticulum, which is responsible for calcium sequestration and release into the spine head and neck. The spine apparatus has recently been linked to synaptic plasticity in adult human cortical neurons. While the morphological heterogeneity of spines and their intracellular organization has been extensively demonstrated

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Rosado, James, Viet Duc Bui, Carola A. Haas, Jürgen Beck, Gillian Queisser, and Andreas Vlachos. "Calcium modeling of spine apparatus-containing human dendritic spines demonstrates an “all-or-nothing” communication switch between the spine head and dendrite." PLOS Computational Biology 18, no. 4 (2022): e1010069. http://dx.doi.org/10.1371/journal.pcbi.1010069.

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Dendritic spines are highly dynamic neuronal compartments that control the synaptic transmission between neurons. Spines form ultrastructural units, coupling synaptic contact sites to the dendritic shaft and often harbor a spine apparatus organelle, composed of smooth endoplasmic reticulum, which is responsible for calcium sequestration and release into the spine head and neck. The spine apparatus has recently been linked to synaptic plasticity in adult human cortical neurons. While the morphological heterogeneity of spines and their intracellular organization has been extensively demonstrated

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4

Lee, Kevin F. H., Cary Soares, and Jean-Claude Béïque. "Examining Form and Function of Dendritic Spines." Neural Plasticity 2012 (2012): 1–9. http://dx.doi.org/10.1155/2012/704103.

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The majority of fast excitatory synaptic transmission in the central nervous system takes place at protrusions along dendrites called spines. Dendritic spines are highly heterogeneous, both morphologically and functionally. Not surprisingly, there has been much speculation and debate on the relationship between spine structure and function. The advent of multi-photon laser-scanning microscopy has greatly improved our ability to investigate the dynamic interplay between spine form and function. Regulated structural changes occur at spines undergoing plasticity, offering a mechanism to account f

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Bloodgood, Brenda L., and Bernardo L. Sabatini. "Neuronal Activity Regulates Diffusion Across the Neck of Dendritic Spines." Science 310, no. 5749 (2005): 866–69. http://dx.doi.org/10.1126/science.1114816.

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In mammalian excitatory neurons, dendritic spines are separated from dendrites by thin necks. Diffusion across the neck limits the chemical and electrical isolation of each spine. We found that spine/dendrite diffusional coupling is heterogeneous and uncovered a class of diffusionally isolated spines. The barrier to diffusion posed by the neck and the number of diffusionally isolated spines is bidirectionally regulated by neuronal activity. Furthermore, coincident synaptic activation and postsynaptic action potentials rapidly restrict diffusion across the neck. The regulation of diffusional co

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6

Calabrese, Barbara, Margaret S. Wilson, and Shelley Halpain. "Development and Regulation of Dendritic Spine Synapses." Physiology 21, no. 1 (2006): 38–47. http://dx.doi.org/10.1152/physiol.00042.2005.

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Dendritic spines are small protrusions from neuronal dendrites that form the postsynaptic component of most excitatory synapses in the brain. They play critical roles in synaptic transmission and plasticity. Recent advances in imaging and molecular technologies reveal that spines are complex, dynamic structures that contain a dense array of cytoskeletal, transmembrane, and scaffolding molecules. Several neurological and psychiatric disorders exhibit dendritic spine abnormalities.

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7

Yu, Wendou, and Bingwei Lu. "Synapses and Dendritic Spines as Pathogenic Targets in Alzheimer’s Disease." Neural Plasticity 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/247150.

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Synapses are sites of cell-cell contacts that transmit electrical or chemical signals in the brain. Dendritic spines are protrusions on dendritic shaft where excitatory synapses are located. Synapses and dendritic spines are dynamic structures whose plasticity is thought to underlie learning and memory. No wonder neurobiologists are intensively studying mechanisms governing the structural and functional plasticity of synapses and dendritic spines in an effort to understand and eventually treat neurological disorders manifesting learning and memory deficits. One of the best-studied brain disord

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8

Khanal, Pushpa, and Pirta Hotulainen. "Dendritic Spine Initiation in Brain Development, Learning and Diseases and Impact of BAR-Domain Proteins." Cells 10, no. 9 (2021): 2392. http://dx.doi.org/10.3390/cells10092392.

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Dendritic spines are small, bulbous protrusions along neuronal dendrites where most of the excitatory synapses are located. Dendritic spine density in normal human brain increases rapidly before and after birth achieving the highest density around 2–8 years. Density decreases during adolescence, reaching a stable level in adulthood. The changes in dendritic spines are considered structural correlates for synaptic plasticity as well as the basis of experience-dependent remodeling of neuronal circuits. Alterations in spine density correspond to aberrant brain function observed in various neurode

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9

Roszkowska, Matylda, Anna Skupien, Tomasz Wójtowicz, et al. "CD44: a novel synaptic cell adhesion molecule regulating structural and functional plasticity of dendritic spines." Molecular Biology of the Cell 27, no. 25 (2016): 4055–66. http://dx.doi.org/10.1091/mbc.e16-06-0423.

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Synaptic cell adhesion molecules regulate signal transduction, synaptic function, and plasticity. However, their role in neuronal interactions with the extracellular matrix (ECM) is not well understood. Here we report that the CD44, a transmembrane receptor for hyaluronan, modulates synaptic plasticity. High-resolution ultrastructural analysis showed that CD44 was localized at mature synapses in the adult brain. The reduced expression of CD44 affected the synaptic excitatory transmission of primary hippocampal neurons, simultaneously modifying dendritic spine shape. The frequency of miniature

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10

Dittmer, Philip J., Mark L. Dell’Acqua, and William A. Sather. "Synaptic crosstalk conferred by a zone of differentially regulated Ca2+ signaling in the dendritic shaft adjoining a potentiated spine." Proceedings of the National Academy of Sciences 116, no. 27 (2019): 13611–20. http://dx.doi.org/10.1073/pnas.1902461116.

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Patterns of postsynaptic activity that induce long-term potentiation of fast excitatory transmission at glutamatergic synapses between hippocampal neurons cause enlargement of the dendritic spine and promote growth in spine endoplasmic reticulum (ER) content. Such postsynaptic activity patterns also impact Ca2+ signaling in the adjoining dendritic shaft, in a zone centered on the spine–shaft junction and extending ∼10–20 µm in either direction along the shaft. Comparing this specialized zone in the shaft with the dendrite in general, plasticity-inducing stimulation of a single spine causes mor

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11

Rangamani, Padmini, Michael G. Levy, Shahid Khan, and George Oster. "Paradoxical signaling regulates structural plasticity in dendritic spines." Proceedings of the National Academy of Sciences 113, no. 36 (2016): E5298—E5307. http://dx.doi.org/10.1073/pnas.1610391113.

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Transient spine enlargement (3- to 5-min timescale) is an important event associated with the structural plasticity of dendritic spines. Many of the molecular mechanisms associated with transient spine enlargement have been identified experimentally. Here, we use a systems biology approach to construct a mathematical model of biochemical signaling and actin-mediated transient spine expansion in response to calcium influx caused by NMDA receptor activation. We have identified that a key feature of this signaling network is the paradoxical signaling loop. Paradoxical components act bifunctionall

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12

Lei, Wenliang, Kenneth R. Myers, Yanfang Rui, Siarhei Hladyshau, Denis Tsygankov, and James Q. Zheng. "Phosphoinositide-dependent enrichment of actin monomers in dendritic spines regulates synapse development and plasticity." Journal of Cell Biology 216, no. 8 (2017): 2551–64. http://dx.doi.org/10.1083/jcb.201612042.

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Dendritic spines are small postsynaptic compartments of excitatory synapses in the vertebrate brain that are modified during learning, aging, and neurological disorders. The formation and modification of dendritic spines depend on rapid assembly and dynamic remodeling of the actin cytoskeleton in this highly compartmentalized space, but the precise mechanisms remain to be fully elucidated. In this study, we report that spatiotemporal enrichment of actin monomers (G-actin) in dendritic spines regulates spine development and plasticity. We first show that dendritic spines contain a locally enric

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13

Sala, Carlo, and Menahem Segal. "Dendritic Spines: The Locus of Structural and Functional Plasticity." Physiological Reviews 94, no. 1 (2014): 141–88. http://dx.doi.org/10.1152/physrev.00012.2013.

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The introduction of high-resolution time lapse imaging and molecular biological tools has changed dramatically the rate of progress towards the understanding of the complex structure-function relations in synapses of central spiny neurons. Standing issues, including the sequence of molecular and structural processes leading to formation, morphological change, and longevity of dendritic spines, as well as the functions of dendritic spines in neurological/psychiatric diseases are being addressed in a growing number of recent studies. There are still unsettled issues with respect to spine formati

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14

González Burgos, Ignacio, Irina Nikonenko, and Volker Korz. "Dendritic Spine Plasticity and Cognition." Neural Plasticity 2012 (2012): 1–2. http://dx.doi.org/10.1155/2012/875156.

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15

Gazzaley, A., S. Kay, and D. L. Benson. "Dendritic spine plasticity in hippocampus." Neuroscience 111, no. 4 (2002): 853–62. http://dx.doi.org/10.1016/s0306-4522(02)00021-0.

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16

Horner, Catherine H. "Plasticity of the dendritic spine." Progress in Neurobiology 41, no. 3 (1993): 281–321. http://dx.doi.org/10.1016/0301-0082(93)90002-a.

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17

Lippman, Jocelyn, and Anna Dunaevsky. "Dendritic spine morphogenesis and plasticity." Journal of Neurobiology 64, no. 1 (2005): 47–57. http://dx.doi.org/10.1002/neu.20149.

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18

Hotulainen, Pirta, and Casper C. Hoogenraad. "Actin in dendritic spines: connecting dynamics to function." Journal of Cell Biology 189, no. 4 (2010): 619–29. http://dx.doi.org/10.1083/jcb.201003008.

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Dendritic spines are small actin-rich protrusions from neuronal dendrites that form the postsynaptic part of most excitatory synapses and are major sites of information processing and storage in the brain. Changes in the shape and size of dendritic spines are correlated with the strength of excitatory synaptic connections and heavily depend on remodeling of its underlying actin cytoskeleton. Emerging evidence suggests that most signaling pathways linking synaptic activity to spine morphology influence local actin dynamics. Therefore, specific mechanisms of actin regulation are integral to the

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19

Mulholland, Patrick J., and L. Judson Chandler. "The Thorny Side of Addiction: Adaptive Plasticity and Dendritic Spines." Scientific World JOURNAL 7 (2007): 9–21. http://dx.doi.org/10.1100/tsw.2007.247.

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Dendritic spines are morphologically specialized structures that receive the vast majority of central excitatory synaptic inputs. Studies have implicated changes in the size, shape, and number of dendritic spines in activity-dependent plasticity, and have further demonstrated that spine morphology is highly dependent on the dynamic organizational and scaffolding properties of its postsynaptic density (PSD).In vitroandin vivomodels of experience-dependent plasticity have linked changes in the localization of glutamate receptors at the PSD with a molecular reorganization of the PSD and alteratio

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20

Kao, Yu-Chia, I.-Fang Wang, and Kuen-Jer Tsai. "miRNA-34c Overexpression Causes Dendritic Loss and Memory Decline." International Journal of Molecular Sciences 19, no. 8 (2018): 2323. http://dx.doi.org/10.3390/ijms19082323.

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Microribonucleic acids (miRNAs) play a pivotal role in numerous aspects of the nervous system and are increasingly recognized as key regulators in neurodegenerative diseases. This study hypothesized that miR-34c, a miRNA expressed in mammalian hippocampi whose expression level can alter the hippocampal dendritic spine density, could induce memory impairment akin to that of patients with Alzheimer’s disease (AD) in mice. In this study, we showed that miR-34c overexpression in hippocampal neurons negatively regulated dendritic length and spine density. Hippocampal neurons transfected with miR-34

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21

Graham, Bruce P., Ausra Saudargiene, and Stuart Cobb. "Spine Head Calcium as a Measure of Summed Postsynaptic Activity for Driving Synaptic Plasticity." Neural Computation 26, no. 10 (2014): 2194–222. http://dx.doi.org/10.1162/neco_a_00640.

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We use a computational model of a hippocampal CA1 pyramidal cell to demonstrate that spine head calcium provides an instantaneous readout at each synapse of the postsynaptic weighted sum of all presynaptic activity impinging on the cell. The form of the readout is equivalent to the functions of weighted, summed inputs used in neural network learning rules. Within a dendritic layer, peak spine head calcium levels are either a linear or sigmoidal function of the number of coactive synapses, with nonlinearity depending on the ability of voltage spread in the dendrites to reach calcium spike thres

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22

Walker, Alison S., Guilherme Neves, Federico Grillo, et al. "Distance-dependent gradient in NMDAR-driven spine calcium signals along tapering dendrites." Proceedings of the National Academy of Sciences 114, no. 10 (2017): E1986—E1995. http://dx.doi.org/10.1073/pnas.1607462114.

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Neurons receive a multitude of synaptic inputs along their dendritic arbor, but how this highly heterogeneous population of synaptic compartments is spatially organized remains unclear. By measuringN-methyl-d-aspartic acid receptor (NMDAR)-driven calcium responses in single spines, we provide a spatial map of synaptic calcium signals along dendritic arbors of hippocampal neurons and relate this to measures of synapse structure. We find that quantal NMDAR calcium signals increase in amplitude as they approach a thinning dendritic tip end. Based on a compartmental model of spine calcium dynamics

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23

Bencsik, Norbert, Zsófia Szíber, Hanna Liliom, et al. "Protein kinase D promotes plasticity-induced F-actin stabilization in dendritic spines and regulates memory formation." Journal of Cell Biology 210, no. 5 (2015): 771–83. http://dx.doi.org/10.1083/jcb.201501114.

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Actin turnover in dendritic spines influences spine development, morphology, and plasticity, with functional consequences on learning and memory formation. In nonneuronal cells, protein kinase D (PKD) has an important role in stabilizing F-actin via multiple molecular pathways. Using in vitro models of neuronal plasticity, such as glycine-induced chemical long-term potentiation (LTP), known to evoke synaptic plasticity, or long-term depolarization block by KCl, leading to homeostatic morphological changes, we show that actin stabilization needed for the enlargement of dendritic spines is depen

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24

Segal, Menahem, Andreas Vlachos, and Eduard Korkotian. "The Spine Apparatus, Synaptopodin, and Dendritic Spine Plasticity." Neuroscientist 16, no. 2 (2010): 125–31. http://dx.doi.org/10.1177/1073858409355829.

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25

Kanjhan, Refik, Peter G. Noakes, and Mark C. Bellingham. "Emerging Roles of Filopodia and Dendritic Spines in Motoneuron Plasticity during Development and Disease." Neural Plasticity 2016 (2016): 1–31. http://dx.doi.org/10.1155/2016/3423267.

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Motoneurons develop extensive dendritic trees for receiving excitatory and inhibitory synaptic inputs to perform a variety of complex motor tasks. At birth, the somatodendritic domains of mouse hypoglossal and lumbar motoneurons have dense filopodia and spines. Consistent with Vaughn’s synaptotropic hypothesis, we propose a developmental unified-hybrid model implicating filopodia in motoneuron spinogenesis/synaptogenesis and dendritic growth and branching critical for circuit formation and synaptic plasticity at embryonic/prenatal/neonatal period. Filopodia density decreases and spine density

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Woolfrey, Kevin M., and Deepak P. Srivastava. "Control of Dendritic Spine Morphological and Functional Plasticity by Small GTPases." Neural Plasticity 2016 (2016): 1–12. http://dx.doi.org/10.1155/2016/3025948.

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Structural plasticity of excitatory synapses is a vital component of neuronal development, synaptic plasticity, and behaviour. Abnormal development or regulation of excitatory synapses has also been strongly implicated in many neurodevelopmental, psychiatric, and neurodegenerative disorders. In the mammalian forebrain, the majority of excitatory synapses are located on dendritic spines, specialized dendritic protrusions that are enriched in actin. Research over recent years has begun to unravel the complexities involved in the regulation of dendritic spine structure. The small GTPase family of

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27

Dailey, M. E., and S. J. Smith. "Dynamics of dendrite development visualized by time-lapse confocal imaging in brain slices." Proceedings, annual meeting, Electron Microscopy Society of America 53 (August 13, 1995): 806–7. http://dx.doi.org/10.1017/s0424820100140403.

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In the mammalian CNS, dendritic neuronal branches typically are studded with numerous short (<3μm), lateral protrusions called “spines”. Such spines are the primary sites of excitatory synaptic input, and changes in spine morphology are thought to play important roles in plasticity of synaptic function in both the developing and adult animal. However, dynamic changes in spine number and structure are not easily determined by electron microscopy, and the small size of spines has made them difficult to study by conventional light microscopy. Recent advances in vital fluorescent staining and h

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Mendoza, Mònica B., Sara Gutierrez, Raúl Ortiz, et al. "The elongation factor eEF1A2 controls translation and actin dynamics in dendritic spines." Science Signaling 14, no. 691 (2021): eabf5594. http://dx.doi.org/10.1126/scisignal.abf5594.

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Synaptic plasticity involves structural modifications in dendritic spines that are modulated by local protein synthesis and actin remodeling. Here, we investigated the molecular mechanisms that connect synaptic stimulation to these processes. We found that the phosphorylation of isoform-specific sites in eEF1A2—an essential translation elongation factor in neurons—is a key modulator of structural plasticity in dendritic spines. Expression of a nonphosphorylatable eEF1A2 mutant stimulated mRNA translation but reduced actin dynamics and spine density. By contrast, a phosphomimetic eEF1A2 mutant

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29

Sau Wan Lai, Cora. "Intravital imaging of dendritic spine plasticity." IntraVital 3, no. 3 (2014): e944439. http://dx.doi.org/10.4161/21659087.2014.984504.

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30

Kozorovitskiy, Yevgenia, Mingzheng Wu, Samuel Minkowicz, Vasin Dumrongprechachan, Pauline Hamilton, and Lei Xiao. "Dopaminergic modulation of dendritic spine plasticity." IBRO Reports 6 (September 2019): S46. http://dx.doi.org/10.1016/j.ibror.2019.07.140.

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31

Harms, Kimberly J., and Anna Dunaevsky. "Dendritic spine plasticity: Looking beyond development." Brain Research 1184 (December 2007): 65–71. http://dx.doi.org/10.1016/j.brainres.2006.02.094.

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32

Johnson, Hong W., and Michael J. Schell. "Neuronal IP3 3-Kinase is an F-actin–bundling Protein: Role in Dendritic Targeting and Regulation of Spine Morphology." Molecular Biology of the Cell 20, no. 24 (2009): 5166–80. http://dx.doi.org/10.1091/mbc.e09-01-0083.

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The actin microstructure in dendritic spines is involved in synaptic plasticity. Inositol trisphosphate 3-kinase A (ITPKA) terminates Ins(1,4,5)P3 signals emanating from spines and also binds filamentous actin (F-actin) through its amino terminal region (amino acids 1-66, N66). Here we investigated how ITPKA, independent of its kinase activity, regulates dendritic spine F-actin microstructure. We show that the N66 region of the protein mediates F-actin bundling. An N66 fusion protein bundled F-actin in vitro, and the bundling involved N66 dimerization. By mutagenesis we identified a point muta

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Mahalakshmi, Arehally M., Bipul Ray, Sunanda Tuladhar, et al. "Impact of Pharmacological and Non-Pharmacological Modulators on Dendritic Spines Structure and Functions in Brain." Cells 10, no. 12 (2021): 3405. http://dx.doi.org/10.3390/cells10123405.

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Dendritic spines are small, thin, hair-like protrusions found on the dendritic processes of neurons. They serve as independent compartments providing large amplitudes of Ca2+ signals to achieve synaptic plasticity, provide sites for newer synapses, facilitate learning and memory. One of the common and severe complication of neurodegenerative disease is cognitive impairment, which is said to be closely associated with spine pathologies viz., decreased in spine density, spine length, spine volume, spine size etc. Many treatments targeting neurological diseases have shown to improve the spine str

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Chaichim, Chanchanok, Tamara Tomanic, Holly Stefen, et al. "Overexpression of Tropomyosin Isoform Tpm3.1 Does Not Alter Synaptic Function in Hippocampal Neurons." International Journal of Molecular Sciences 22, no. 17 (2021): 9303. http://dx.doi.org/10.3390/ijms22179303.

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Tropomyosin (Tpm) has been regarded as the master regulator of actin dynamics. Tpms regulate the binding of the various proteins involved in restructuring actin. The actin cytoskeleton is the predominant cytoskeletal structure in dendritic spines. Its regulation is critical for spine formation and long-term activity-dependent changes in synaptic strength. The Tpm isoform Tpm3.1 is enriched in dendritic spines, but its role in regulating the synapse structure and function is not known. To determine the role of Tpm3.1, we studied the synapse structure and function of cultured hippocampal neurons

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Wang, Xingxing, Qinfang Shi, Arpit Kumar Pradhan, Laura Ziegon, Martin Schlegel, and Gerhard Rammes. "Beta-Site Amyloid Precursor Protein-Cleaving Enzyme Inhibition Partly Restores Sevoflurane-Induced Deficits on Synaptic Plasticity and Spine Loss." International Journal of Molecular Sciences 23, no. 12 (2022): 6637. http://dx.doi.org/10.3390/ijms23126637.

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Evidence indicates that inhalative anesthetics enhance the β-site amyloid precursor protein (APP)-cleaving enzyme (BACE) activity, increase amyloid beta 1-42 (Aβ1–42) aggregation, and modulate dendritic spine dynamics. However, the mechanisms of inhalative anesthetics on hippocampal dendritic spine plasticity and BACE-dependent APP processing remain unclear. In this study, hippocampal slices were incubated with equipotent isoflurane (iso), sevoflurane (sevo), or xenon (Xe) with/without pretreatment of the BACE inhibitor LY2886721 (LY). Thereafter, CA1 dendritic spine density, APP processing-re

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Pozzo-Miller, Lucas D., Takafumi Inoue, and Diane Dieuliis Murphy. "Estradiol Increases Spine Density and NMDA-Dependent Ca2+ Transients in Spines of CA1 Pyramidal Neurons From Hippocampal Slices." Journal of Neurophysiology 81, no. 3 (1999): 1404–11. http://dx.doi.org/10.1152/jn.1999.81.3.1404.

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Estradiol increases spine density and NMDA-dependent Ca2+transients in spines of CA1 pyramidal neurons from hippocampal slices. To investigate the physiological consequences of the increase in spine density induced by estradiol in pyramidal neurons of the hippocampus, we performed simultaneous whole cell recordings and Ca2+ imaging in CA1 neuron spines and dendrites in hippocampal slices. Four- to eight-days in vitro slice cultures were exposed to 17β-estradiol (EST) for an additional 4- to 8-day period, and spine density was assessed by confocal microscopy of DiI-labeled CA1 pyramidal neurons

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Zagrebelsky, Marta, Charlotte Tacke, and Martin Korte. "BDNF signaling during the lifetime of dendritic spines." Cell and Tissue Research 382, no. 1 (2020): 185–99. http://dx.doi.org/10.1007/s00441-020-03226-5.

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Abstract Dendritic spines are tiny membrane specialization forming the postsynaptic part of most excitatory synapses. They have been suggested to play a crucial role in regulating synaptic transmission during development and in adult learning processes. Changes in their number, size, and shape are correlated with processes of structural synaptic plasticity and learning and memory and also with neurodegenerative diseases, when spines are lost. Thus, their alterations can correlate with neuronal homeostasis, but also with dysfunction in several neurological disorders characterized by cognitive i

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38

Yusifov, Rashad, Anja Tippmann, Jochen F. Staiger, Oliver M. Schlüter, and Siegrid Löwel. "Spine dynamics of PSD-95-deficient neurons in the visual cortex link silent synapses to structural cortical plasticity." Proceedings of the National Academy of Sciences 118, no. 10 (2021): e2022701118. http://dx.doi.org/10.1073/pnas.2022701118.

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Critical periods (CPs) are time windows of heightened brain plasticity during which experience refines synaptic connections to achieve mature functionality. At glutamatergic synapses on dendritic spines of principal cortical neurons, the maturation is largely governed by postsynaptic density protein-95 (PSD-95)-dependent synaptic incorporation of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors into nascent AMPA-receptor silent synapses. Consequently, in mouse primary visual cortex (V1), impaired silent synapse maturation in PSD-95-deficient neurons prevents the closure of

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Lin, Jun-Bin, Chan-Juan Zheng, Xuan Zhang, Juan Chen, Wei-Jing Liao, and Qi Wan. "Effects of Tetramethylpyrazine on Functional Recovery and Neuronal Dendritic Plasticity after Experimental Stroke." Evidence-Based Complementary and Alternative Medicine 2015 (2015): 1–10. http://dx.doi.org/10.1155/2015/394926.

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The 2,3,5,6-tetramethylpyrazine (TMP) has been widely used in the treatment of ischemic stroke by Chinese doctors. Here, we report the effects of TMP on functional recovery and dendritic plasticity after ischemic stroke. A classical model of middle cerebral artery occlusion (MCAO) was established in this study. The rats were assigned into 3 groups: sham group (sham operated rats treated with saline), model group (MCAO rats treated with saline) and TMP group (MCAO rats treated with 20 mg/kg/d TMP). The neurological function test of animals was evaluated using the modified neurological severity

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40

Huang, Lianyan, and Guang Yang. "Repeated Exposure to Ketamine–Xylazine during Early Development Impairs Motor Learning–dependent Dendritic Spine Plasticity in Adulthood." Anesthesiology 122, no. 4 (2015): 821–31. http://dx.doi.org/10.1097/aln.0000000000000579.

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Abstract Background: Recent studies in rodents suggest that repeated and prolonged anesthetic exposure at early stages of development leads to cognitive and behavioral impairments later in life. However, the underlying mechanism remains unknown. In this study, we tested whether exposure to general anesthesia during early development will disrupt the maturation of synaptic circuits and compromise learning-related synaptic plasticity later in life. Methods: Mice received ketamine–xylazine (20/3 mg/kg) anesthesia for one or three times, starting at either early (postnatal day 14 [P14]) or late (P

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Mendez, Pablo, Mathias De Roo, Lorenzo Poglia, Paul Klauser, and Dominique Muller. "N-cadherin mediates plasticity-induced long-term spine stabilization." Journal of Cell Biology 189, no. 3 (2010): 589–600. http://dx.doi.org/10.1083/jcb.201003007.

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Excitatory synapses on dendritic spines are dynamic structures whose stability can vary from hours to years. However, the molecular mechanisms regulating spine persistence remain essentially unknown. In this study, we combined repetitive imaging and a gain and loss of function approach to test the role of N-cadherin (NCad) on spine stability. Expression of mutant but not wild-type NCad promotes spine turnover and formation of immature spines and interferes with the stabilization of new spines. Similarly, the long-term stability of preexisting spines is reduced when mutant NCad is expressed but

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Gu, Jiaping, and James Q. Zheng. "Microtubules in Dendritic Spine Development and Plasticity." Open Neuroscience Journal 7, no. 1 (2014): 128–33. http://dx.doi.org/10.2174/1874082000903010128.

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Gu, Jiaping, and James Q. Zheng. "Microtubules in Dendritic Spine Development and Plasticity." Open Neuroscience Journal 3, no. 2 (2009): 128–33. http://dx.doi.org/10.2174/1874082000903020128.

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Schutter, Erik De, and James M. Bower. "Sensitivity of Synaptic Plasticity to the Ca2+ Permeability of NMDA Channels: A Model of Long-Term Potentiation in Hippocampal Neurons." Neural Computation 5, no. 5 (1993): 681–94. http://dx.doi.org/10.1162/neco.1993.5.5.681.

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We have examined a model by Holmes and Levy (1990) of the induction of associative long-term potentiation (LTP) by a rise in the free Ca2+ concentration ([Ca2+]) after synaptic activation of dendritic spines. The previously reported amplification of the change in [Ca2+] caused by coactivation of several synapses was found to be quite sensitive to changes in the permeability of the N-methyl-D-aspartate (NMDA) receptor channels to Ca2+. Varying this parameter indicated that maximum amplification is obtained at values that are close to Ca2+ permeabilities reported in the literature. However, ampl

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Pignataro, Annabella, Antonella Borreca, Martine Ammassari-Teule, and Silvia Middei. "CREB Regulates Experience-Dependent Spine Formation and Enlargement in Mouse Barrel Cortex." Neural Plasticity 2015 (2015): 1–11. http://dx.doi.org/10.1155/2015/651469.

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Experience modifies synaptic connectivity through processes that involve dendritic spine rearrangements in neuronal circuits. Although cAMP response element binding protein (CREB) has a key function in spines changes, its role in activity-dependent rearrangements in brain regions of rodents interacting with the surrounding environment has received little attention so far. Here we studied the effects of vibrissae trimming, a widely used model of sensory deprivation-induced cortical plasticity, on processes associated with dendritic spine rearrangements in the barrel cortex of a transgenic mouse

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Desai, Niraj S., Tanya M. Casimiro, Stephen M. Gruber, and Peter W. Vanderklish. "Early Postnatal Plasticity in Neocortex of Fmr1 Knockout Mice." Journal of Neurophysiology 96, no. 4 (2006): 1734–45. http://dx.doi.org/10.1152/jn.00221.2006.

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Fragile X syndrome is produced by a defect in a single X-linked gene, called Fmr1, and is characterized by abnormal dendritic spine morphologies with spines that are longer and thinner in neocortex than those from age-matched controls. Studies using Fmr1 knockout mice indicate that spine abnormalities are especially pronounced in the first month of life, suggesting that altered developmental plasticity underlies some of the behavioral phenotypes associated with the syndrome. To address this issue, we used intracellular recordings in neocortical slices from early postnatal mice to examine the e

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Bertan, Fabio, Lena Wischhof, Liudmila Sosulina, et al. "Loss of Ryanodine Receptor 2 impairs neuronal activity-dependent remodeling of dendritic spines and triggers compensatory neuronal hyperexcitability." Cell Death & Differentiation 27, no. 12 (2020): 3354–73. http://dx.doi.org/10.1038/s41418-020-0584-2.

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AbstractDendritic spines are postsynaptic domains that shape structural and functional properties of neurons. Upon neuronal activity, Ca2+ transients trigger signaling cascades that determine the plastic remodeling of dendritic spines, which modulate learning and memory. Here, we study in mice the role of the intracellular Ca2+ channel Ryanodine Receptor 2 (RyR2) in synaptic plasticity and memory formation. We demonstrate that loss of RyR2 in pyramidal neurons of the hippocampus impairs maintenance and activity-evoked structural plasticity of dendritic spines during memory acquisition. Further

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Porceddu, Riccardo, Cinzia Podda, Giovanna Mulas, et al. "Changes in Dendritic Spine Morphology and Density of Granule Cells in the Olfactory Bulb of Anguilla anguilla (L., 1758): A Possible Way to Understand Orientation and Migratory Behavior." Biology 11, no. 8 (2022): 1244. http://dx.doi.org/10.3390/biology11081244.

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Olfaction could represent a pivotal process involved in fish orientation and migration. The olfactory bulb can manage olfactive signals at the granular cell (GC) and dendritic spine levels for their synaptic plasticity properties and changing their morphology and structural stability after environmental odour cues. The GCs’ dendritic spine density and morphology were analysed across the life stages of the catadromous Anguilla anguilla. According to the head and neck morphology, spines were classified as mushroom (M), long thin (LT), stubby (S), and filopodia (F). Total spines’ density decrease

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Mikhaylova, Marina, and Michael R. Kreutz. "Clustered plasticity in Long-Term Potentiation: How strong synapses persist to maintain long-term memory." Neuroforum 24, no. 3 (2018): A127—A132. http://dx.doi.org/10.1515/nf-2018-a006.

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Abstract The storage of memory requires at least in part maintenance of long-term potentiation (LTP) in dendritic spine synapses. Neighboring synapses are frequently arranged into functional clusters. At present, it is still unclear how these clusters evolve, why they are stable for longer time periods and how spines interact within a cluster. In this review, we will provide an overview of current concepts of clustered plasticity and we will discuss cellular as well as molecular mechanisms that might be relevant for spine stability and associated functions in the context of LTP. We will propos

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Shu, Yu, and Tonghui Xu. "Chronic Social Defeat Stress Modulates Dendritic Spines Structural Plasticity in Adult Mouse Frontal Association Cortex." Neural Plasticity 2017 (2017): 1–13. http://dx.doi.org/10.1155/2017/6207873.

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Chronic stress is associated with occurrence of many mental disorders. Previous studies have shown that dendrites and spines of pyramidal neurons of the prefrontal cortex undergo drastic reorganization following chronic stress experience. So the prefrontal cortex is believed to play a key role in response of neural system to chronic stress. However, how stress induces dynamic structural changes in neural circuit of prefrontal cortex remains unknown. In the present study, we examined the effects of chronic social defeat stress on dendritic spine structural plasticity in the mouse frontal associ

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