Journal articles on the topic 'Dendritic Spine Plasticity'
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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 (October 1, 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 raises spine calcium by releasing calcium from inositol trisphosphate-sensitive calcium stores. This spine calcium release is unevenly distributed, being present in proximal spines, but largely absent in more distal spines. Activation of metabotropic receptors also generated calcium waves that differentially invaded spines as they propagated toward the soma. Dendritic wave invasion was dependent on diffusional coupling between the spine and parent dendrite which was determined by spine neck length, with waves preferentially invading spines with short necks. Spine calcium is a critical trigger for the induction of synaptic plasticity, and our findings suggest that calcium release from inositol trisphosphate-sensitive calcium stores may modulate homosynaptic plasticity through store-release in the spine head, and heterosynaptic plasticity of unstimulated inputs via dendritic calcium wave invasion of the spine head.
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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 (April 25, 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 in animal models, the influence of spine apparatus organelles on critical signaling pathways, such as calcium-mediated dynamics, is less well known in human dendritic spines. In this study we used serial transmission electron microscopy to anatomically reconstruct nine human cortical spines in detail as a basis for modeling and simulation of the calcium dynamics between spine and dendrite. The anatomical study of reconstructed human dendritic spines revealed that the size of the postsynaptic density correlates with spine head volume and that the spine apparatus volume is proportional to the spine volume. Using a newly developed simulation pipeline, we have linked these findings to spine-to-dendrite calcium communication. While the absence of a spine apparatus, or the presence of a purely passive spine apparatus did not enable any of the reconstructed spines to relay a calcium signal to the dendritic shaft, the calcium-induced calcium release from this intracellular organelle allowed for finely tuned “all-or-nothing” spine-to-dendrite calcium coupling; controlled by spine morphology, neck plasticity, and ryanodine receptors. Our results suggest that spine apparatus organelles are strategically positioned in the neck of human dendritic spines and demonstrate their potential relevance to the maintenance and regulation of spine-to-dendrite calcium communication.
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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 (April 25, 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 in animal models, the influence of spine apparatus organelles on critical signaling pathways, such as calcium-mediated dynamics, is less well known in human dendritic spines. In this study we used serial transmission electron microscopy to anatomically reconstruct nine human cortical spines in detail as a basis for modeling and simulation of the calcium dynamics between spine and dendrite. The anatomical study of reconstructed human dendritic spines revealed that the size of the postsynaptic density correlates with spine head volume and that the spine apparatus volume is proportional to the spine volume. Using a newly developed simulation pipeline, we have linked these findings to spine-to-dendrite calcium communication. While the absence of a spine apparatus, or the presence of a purely passive spine apparatus did not enable any of the reconstructed spines to relay a calcium signal to the dendritic shaft, the calcium-induced calcium release from this intracellular organelle allowed for finely tuned “all-or-nothing” spine-to-dendrite calcium coupling; controlled by spine morphology, neck plasticity, and ryanodine receptors. Our results suggest that spine apparatus organelles are strategically positioned in the neck of human dendritic spines and demonstrate their potential relevance to the maintenance and regulation of spine-to-dendrite calcium communication.
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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 for the well-described correlation between spine size and synapse strength. In turn, spine structure can influence the degree of biochemical and perhaps electrical compartmentalization at individual synapses. Here, we review the relationship between dendritic spine morphology, features of spine compartmentalization and synaptic plasticity. We highlight emerging molecular mechanisms that link structural and functional changes in spines during plasticity, and also consider circumstances that underscore some divergence from a tight structure-function coupling. Because of the intricate influence of spine structure on biochemical and electrical signalling, activity-dependent changes in spine morphology alone may thus contribute to the metaplastic potential of synapses. This possibility asserts a role for structural dynamics in neuronal information storage and aligns well with current computational models.
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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 (November 3, 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 coupling provides a possible mechanism for determining the amplitude of postsynaptic potentials and the accumulation of plasticity-inducing molecules within the spine head.
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Calabrese, Barbara, Margaret S. Wilson, and Shelley Halpain. "Development and Regulation of Dendritic Spine Synapses." Physiology 21, no. 1 (February 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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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 disorders that prominently feature synaptic and dendritic spine pathology is Alzheimer’s disease (AD). Recent studies have revealed molecular mechanisms underlying the synapse and spine pathology in AD, including a role for mislocalized tau in the postsynaptic compartment. Synaptic and dendritic spine pathology is also observed in other neurodegenerative disease. It is possible that some common pathogenic mechanisms may underlie the synaptic and dendritic spine pathology in neurodegenerative diseases.
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Khanal, Pushpa, and Pirta Hotulainen. "Dendritic Spine Initiation in Brain Development, Learning and Diseases and Impact of BAR-Domain Proteins." Cells 10, no. 9 (September 12, 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 neurodevelopmental and neuropsychiatric disorders. Dendritic spine initiation affects spine density. In this review, we discuss the importance of spine initiation in brain development, learning, and potential complications resulting from altered spine initiation in neurological diseases. Current literature shows that two Bin Amphiphysin Rvs (BAR) domain-containing proteins, MIM/Mtss1 and SrGAP3, are involved in spine initiation. We review existing literature and open databases to discuss whether other BAR-domain proteins could also take part in spine initiation. Finally, we discuss the potential molecular mechanisms on how BAR-domain proteins could regulate spine initiation.
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Roszkowska, Matylda, Anna Skupien, Tomasz Wójtowicz, Anna Konopka, Adam Gorlewicz, Magdalena Kisiel, Marek Bekisz, 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 (December 15, 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 excitatory postsynaptic currents decreased, accompanied by dendritic spine elongation and thinning. These structural and functional alterations went along with a decrease in the number of presynaptic Bassoon puncta, together with a reduction of PSD-95 levels at dendritic spines, suggesting a reduced number of functional synapses. Lack of CD44 also abrogated spine head enlargement upon neuronal stimulation. Moreover, our results indicate that CD44 contributes to proper dendritic spine shape and function by modulating the activity of actin cytoskeleton regulators, that is, Rho GTPases (RhoA, Rac1, and Cdc42). Thus CD44 appears to be a novel molecular player regulating functional and structural plasticity of dendritic spines.
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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 (June 17, 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 more profound depletion of Ca2+ stores in the ER, a greater degree of interaction between stromal interaction molecule 1 (STIM1) and L-type Ca2+ channels, and thus stronger STIM1 inhibition of these channels. Here we show that the length of this zone along the dendritic axis can be approximately doubled through the neuromodulatory action of β-adrenergic receptors (βARs). The mechanism of βAR enlargement of the zone arises from protein kinase A-mediated enhancement of L-type Ca2+ current, which in turn lowers [Ca2+]ER through ryanodine receptor-dependent Ca2+-induced Ca2+ release and activates STIM1 feedback inhibition of L-type Ca2+ channels. An important function of this dendritic zone is to support crosstalk between spines along its length such that spines neighboring a strongly stimulated spine are enabled to undergo structural plasticity in response to stimulation that would otherwise be subthreshold for spine structural plasticity. This form of crosstalk requires L-type Ca2+ channel current to activate STIM1, and βAR activity extends the range along the shaft over which such spine-to-spine communication can occur.
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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 (August 22, 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 bifunctionally in signaling networks, and their role is to control both the activation and the inhibition of a desired response function (protein activity or spine volume). Using ordinary differential equation (ODE)-based modeling, we show that the dynamics of different regulators of transient spine expansion, including calmodulin-dependent protein kinase II (CaMKII), RhoA, and Cdc42, and the spine volume can be described using paradoxical signaling loops. Our model is able to capture the experimentally observed dynamics of transient spine volume. Furthermore, we show that actin remodeling events provide a robustness to spine volume dynamics. We also generate experimentally testable predictions about the role of different components and parameters of the network on spine dynamics.
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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 (June 28, 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 enriched pool of G-actin that can be regulated by synaptic activity. We further find that this G-actin pool functions in spine development and its modification during synaptic plasticity. Mechanistically, the relatively immobile G-actin pool in spines depends on the phosphoinositide PI(3,4,5)P3 and involves the actin monomer–binding protein profilin. Together, our results have revealed a novel mechanism by which dynamic enrichment of G-actin in spines regulates the actin remodeling underlying synapse development and plasticity.
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Sala, Carlo, and Menahem Segal. "Dendritic Spines: The Locus of Structural and Functional Plasticity." Physiological Reviews 94, no. 1 (January 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 formation and plasticity: Are spines formed first, followed by synapse formation, or are synapses formed first, followed by emergence of a spine? What are the immediate and long-lasting changes in spine properties following exposure to plasticity-producing stimulation? Is spine volume/shape indicative of its function? These and other issues are addressed in this review, which highlights the complexity of molecular pathways involved in regulation of spine structure and function, and which contributes to the understanding of central synaptic interactions in health and disease.
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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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Gazzaley, A., S. Kay, and D. L. Benson. "Dendritic spine plasticity in hippocampus." Neuroscience 111, no. 4 (June 2002): 853–62. http://dx.doi.org/10.1016/s0306-4522(02)00021-0.
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Horner, Catherine H. "Plasticity of the dendritic spine." Progress in Neurobiology 41, no. 3 (September 1993): 281–321. http://dx.doi.org/10.1016/0301-0082(93)90002-a.
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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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Hotulainen, Pirta, and Casper C. Hoogenraad. "Actin in dendritic spines: connecting dynamics to function." Journal of Cell Biology 189, no. 4 (May 10, 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 formation, maturation, and plasticity of dendritic spines and to learning and memory.
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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 alterations in spine morphology. Chronic ethanol consumption results in adaptive changes in neuronal function that manifest as tolerance, physical dependence, and addiction. A potential mechanism supporting these adaptive changes that we recently identified is the homeostatic targeting of NR2B-containing NMDA receptors to the synapse. This increase is associated with and dependent on a corresponding increase in the localization of the scaffolding protein PSD-95 at the PSD, and with an actin-dependent increase in the size of dendritic spines. These observations led us to propose a molecular model for ethanol-induced plasticity at excitatory synapses in which increases in NR2B-containing NMDA receptors and PSD-95 at the PSD provide an expanded scaffolding platform for the recruitment and activation of signaling molecules that regulate spine actin dynamics, protein translation, and synaptic plasticity. This model is consistent with accumulating evidence that glutamatergic modulation of spine actin by the PSD plays a role in the aberrant plasticity of addiction.
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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 (August 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-34c had shorter dendrites on average and fewer filopodia and spines than those not transfected with miR-34c (control mice). Because dendrites and synapses are key sites for signal transduction and fundamental structures for memory formation and storage, disrupted dendrites can contribute to AD. Therefore, we supposed that miR-34c, through its effects on dendritic spine density, influences synaptic plasticity and plays a key role in AD pathogenesis.
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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 (October 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 threshold. This is strongly controlled by the potassium A-type current, with calcium spikes and the consequent sigmoidal increase in peak spine head calcium present only when the A-channel density is low. Other membrane characteristics influence the gain of the relationship between peak calcium and the number of active synapses. In particular, increasing spine neck resistance increases the gain due to increased voltage responses to synaptic input in spine heads. Colocation of stimulated synapses on a single dendritic branch also increases the gain of the response. Input pathways cooperate: CA3 inputs to the proximal apical dendrites can strongly amplify peak calcium levels due to weak EC input to the distal dendrites, but not so strongly vice versa. CA3 inputs to the basal dendrites can boost calcium levels in the proximal apical dendrites, but the relative electrical compactness of the basal dendrites results in the reverse effect being less significant. These results give pointers as to how to better describe the contributions of pre- and postsynaptic activity in the learning “rules” that apply in these cells. The calcium signal is closer in form to the activity measures used in traditional neural network learning rules than to the spike times used in spike-timing-dependent plasticity.
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Walker, Alison S., Guilherme Neves, Federico Grillo, Rachel E. Jackson, Mark Rigby, Cian O’Donnell, Andrew S. Lowe, Gema Vizcay-Barrena, Roland A. Fleck, and Juan Burrone. "Distance-dependent gradient in NMDAR-driven spine calcium signals along tapering dendrites." Proceedings of the National Academy of Sciences 114, no. 10 (February 16, 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, we propose that this biased distribution in calcium signals is governed by a gradual, distance-dependent decline in spine size, which we visualized using serial block-face scanning electron microscopy. Our data describe a cell-autonomous feature of principal neurons, where tapering dendrites show an inverse distribution of spine size and NMDAR-driven calcium signals along dendritic trees, with important implications for synaptic plasticity rules and spine function.
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Bencsik, Norbert, Zsófia Szíber, Hanna Liliom, Krisztián Tárnok, Sándor Borbély, Márton Gulyás, Anikó Rátkai, 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 (August 24, 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 dependent on PKD activity. Consequently, impaired PKD functions attenuate activity-dependent changes in hippocampal dendritic spines, including LTP formation, cause morphological alterations in vivo, and have deleterious consequences on spatial memory formation. We thus provide compelling evidence that PKD controls synaptic plasticity and learning by regulating actin stability in dendritic spines.
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Segal, Menahem, Andreas Vlachos, and Eduard Korkotian. "The Spine Apparatus, Synaptopodin, and Dendritic Spine Plasticity." Neuroscientist 16, no. 2 (April 2010): 125–31. http://dx.doi.org/10.1177/1073858409355829.
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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 initially increases until postnatal day 15 (P15) and then decreases by P30. Spine distribution shifts towards the distal dendrites, and spines become shorter (stubby), coinciding with decreases in frequency and increases in amplitude of excitatory postsynaptic currents with maturation. In transgenic mice, either overexpressing the mutated human Cu/Zn-superoxide dismutase (hSOD1G93A) gene or deficient in GABAergic/glycinergic synaptic transmission (gephyrin, GAD-67, or VGAT gene knockout), hypoglossal motoneurons develop excitatory glutamatergic synaptic hyperactivity. Functional synaptic hyperactivity is associated with increased dendritic growth, branching, and increased spine and filopodia density, involving actin-based cytoskeletal and structural remodelling. Energy-dependent ionic pumps that maintain intracellular sodium/calcium homeostasis are chronically challenged by activity and selectively overwhelmed by hyperactivity which eventually causes sustained membrane depolarization leading to excitotoxicity, activating microglia to phagocytose degenerating neurons under neuropathological conditions.
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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 proteins have emerged as key regulators of structural plasticity, linking extracellular signals with the modulation of dendritic spines, which potentially underlies their ability to influence cognition. Here we review a number of studies that examine how small GTPases are activated and regulated in neurons and furthermore how they can impact actin dynamics, and thus dendritic spine morphology. Elucidating this signalling process is critical for furthering our understanding of the basic mechanisms by which information is encoded in neural circuits but may also provide insight into novel targets for the development of effective therapies to treat cognitive dysfunction seen in a range of neurological disorders.
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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 high resolution confocal imaging in tissue slices now afford the possibility of assessing changes in morphology of individual spines on single dendrite branches over time.To investigate the dynamics and plasticity of dendritic structure during development, vital fluorescent staining and time-lapse confocal imaging methods were applied to preparations of live brain slices from developing rat. Tissue slices were prepared from hippocampus of neonatal rat (postnatal day 2-7) and cultured for variable periods of time (hours to weeks).
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Mendoza, Mònica B., Sara Gutierrez, Raúl Ortiz, David F. Moreno, Maria Dermit, Martin Dodel, Elena Rebollo, Miquel Bosch, Faraz K. Mardakheh, and Carme Gallego. "The elongation factor eEF1A2 controls translation and actin dynamics in dendritic spines." Science Signaling 14, no. 691 (July 13, 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 exhibited decreased association with F-actin and was inactive as a translation elongation factor. Activation of metabotropic glutamate receptor signaling triggered transient dissociation of eEF1A2 from its regulatory guanine exchange factor (GEF) protein in dendritic spines in a phosphorylation-dependent manner. We propose that eEF1A2 establishes a cross-talk mechanism that coordinates translation and actin dynamics during spine remodeling.
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Sau Wan Lai, Cora. "Intravital imaging of dendritic spine plasticity." IntraVital 3, no. 3 (September 2, 2014): e944439. http://dx.doi.org/10.4161/21659087.2014.984504.
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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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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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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 (December 15, 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 mutation in a predicted helical region that eliminated both F-actin binding and bundling, rendering the enzyme cytosolic. A fusion protein containing a minimal helical region (amino acids 9-52, N9-52) bound F-actin in vitro and in cells, but had lower affinity. In hippocampal neurons, GFP-tagged N66 expression was highly polarized, with targeting of the enzyme predominantly to spines. By contrast, N9-52-GFP expression occurred in actin-rich structures in dendrites and growth cones. Expression of N66-GFP tripled the length of dendritic protrusions, induced longer dendritic spine necks, and induced polarized actin motility in time-lapse assays. These results suggest that, in addition to its ability to regulate intracellular Ca2+ via Ins(1,4,5)P3 metabolism, ITPKA regulates structural plasticity.
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Mahalakshmi, Arehally M., Bipul Ray, Sunanda Tuladhar, Tousif Ahmed Hediyal, Praveen Raj, Annan Gopinath Rathipriya, M. Walid Qoronfleh, Musthafa Mohamed Essa, and Saravana Babu Chidambaram. "Impact of Pharmacological and Non-Pharmacological Modulators on Dendritic Spines Structure and Functions in Brain." Cells 10, no. 12 (December 2, 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 structure and distribution. However, concise data on the various modulators of dendritic spines are imperative and a need of the hour. Hence, in this review we made an attempt to consolidate the effects of various pharmacological (cholinergic, glutamatergic, GABAergic, serotonergic, adrenergic, and dopaminergic agents) and non-pharmacological modulators (dietary interventions, enriched environment, yoga and meditation) on dendritic spines structure and functions. These data suggest that both the pharmacological and non-pharmacological modulators produced significant improvement in dendritic spine structure and functions and in turn reversing the pathologies underlying neurodegeneration. Intriguingly, the non-pharmacological approaches have shown to improve intellectual performances both in preclinical and clinical platforms, but still more technology-based evidence needs to be studied. Thus, we conclude that a combination of pharmacological and non-pharmacological intervention may restore cognitive performance synergistically via improving dendritic spine number and functions in various neurological disorders.
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Chaichim, Chanchanok, Tamara Tomanic, Holly Stefen, Esmeralda Paric, Lucy Gamaroff, Alexandra K. Suchowerska, Peter W. Gunning, Yazi D. Ke, Thomas Fath, and John Power. "Overexpression of Tropomyosin Isoform Tpm3.1 Does Not Alter Synaptic Function in Hippocampal Neurons." International Journal of Molecular Sciences 22, no. 17 (August 27, 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 from transgenic mice overexpressing Tpm3.1. We recorded hippocampal field excitatory postsynaptic potentials (fEPSPs) from brain slices to examine if Tpm3.1 overexpression alters long-term synaptic plasticity. Tpm3.1-overexpressing cultured neurons did not show a significantly altered dendritic spine morphology or synaptic activity. Similarly, we did not observe altered synaptic transmission or plasticity in brain slices. Furthermore, expression of Tpm3.1 at the postsynaptic compartment does not increase the local F-actin levels. The results suggest that although Tpm3.1 localises to dendritic spines in cultured hippocampal neurons, it does not have any apparent impact on dendritic spine morphology or function. This is contrary to the functional role of Tpm3.1 previously observed at the tip of growing neurites, where it increases the F-actin levels and impacts growth cone dynamics.
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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 (June 14, 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-related molecule expressions, nectin-3 levels, and long-term potentiation (LTP) were tested. The nectin-3 downregulation on LTP and dendritic spines were evaluated. Sevo treatment increased hippocampal mouse Aβ1–42 (mAβ1–42), abolished CA1-LTP, and decreased spine density and nectin-3 expressions in the CA1 region. Furthermore, CA1-nectin-3 knockdown blocked LTP and reduced spine density. Iso treatment decreased spine density and attenuated LTP. Although Xe blocked LTP, it did not affect spine density, mAβ1–42, or nectin-3. Finally, antagonizing BACE activity partly restored sevo-induced deficits. Taken together, our study suggests that sevo partly elevates BACE activity and interferes with synaptic remodeling, whereas iso mildly modulates synaptic changes in the CA1 region of the hippocampus. On the other hand, Xe does not alternate dendritic spine remodeling.
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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 (March 1, 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. Spine density was doubled in both apical and basal dendrites of the CA1 region in EST-treated slices; consistently, a reduction in cell input resistance was observed in EST-treated CA1 neurons. Double immunofluorescence staining of presynaptic (synaptophysin) and postsynaptic (α-subunit of CaMKII) proteins showed an increase in synaptic density after EST treatment. The slopes of the input/output curves of both α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and N-methyl-d-aspartate (NMDA) postsynaptic currents were steeper in EST-treated CA1 neurons, consistent with the observed increase in synapse density. To characterize NMDA-dependent synaptic currents and dendritic Ca2+ transients during Schaffer collaterals stimulation, neurons were maintained at +40 mV in the presence of nimodipine, picrotoxin, and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). No differences in resting spine or dendritic Ca2+ levels were observed between control and EST-treated CA1 neurons. Intracellular Ca2+transients during afferent stimulation exhibited a faster slope and reached higher levels in spines than in adjacent dendrites. Peak Ca2+ levels were larger in both spines and dendrites of EST-treated CA1 neurons. Ca2+ gradients between spine heads and dendrites during afferent stimulation were also larger in EST-treated neurons. Both spine and dendritic Ca2+transients during afferent stimulation were reversibly blocked byd,l-2-amino-5-phosphonovaleric acid (d,l-APV). The increase in spine density and the enhanced NMDA-dependent Ca2+ signals in spines and dendrites induced by EST may underlie a threshold reduction for induction of NMDA-dependent synaptic plasticity in the hippocampus.
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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 (June 14, 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 impairment. Therefore, it is important to understand how different stages in the life of a dendritic spine, including formation, maturation, and plasticity, are strictly regulated. In this context, brain-derived neurotrophic factor (BDNF), belonging to the NGF-neurotrophin family, is among the most intensively investigated molecule. This review would like to report the current knowledge regarding the role of BDNF in regulating dendritic spine number, structure, and plasticity concentrating especially on its signaling via its two often functionally antagonistic receptors, TrkB and p75NTR. In addition, we point out a series of open points in which, while the role of BDNF signaling is extremely likely conclusive, evidence is still missing.
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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 (March 1, 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 the CP for juvenile ocular dominance plasticity (jODP). A structural hallmark of jODP is increased spine elimination, induced by brief monocular deprivation (MD). However, it is unknown whether impaired silent synapse maturation facilitates spine elimination and also preserves juvenile structural plasticity. Using two-photon microscopy, we assessed spine dynamics in apical dendrites of layer 2/3 pyramidal neurons (PNs) in binocular V1 during ODP in awake adult mice. Under basal conditions, spine formation and elimination ratios were similar between PSD-95 knockout (KO) and wild-type (WT) mice. However, a brief MD affected spine dynamics only in KO mice, where MD doubled spine elimination, primarily affecting newly formed spines, and caused a net reduction in spine density similar to what has been observed during jODP in WT mice. A similar increase in spine elimination after MD occurred if PSD-95 was knocked down in single PNs of layer 2/3. Thus, structural plasticity is dictated cell autonomously by PSD-95 in vivo in awake mice. Loss of PSD-95 preserves hallmark features of spine dynamics in jODP into adulthood, revealing a functional link of PSD-95 for experience-dependent synapse maturation and stabilization during CPs.
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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 score (mNSS) at 3 d, 7 d, and 14 d after MCAO. Animals were euthanized for immunohistochemical labeling to measure MAP-2 levels in the peri-infarct area. Golgi-Cox staining was performed to test effect of TMP on dendritic plasticity at 14 d after MCAO. TMP significantly improved neurological function at 7 d and 14 d after ischemia, increased MAP-2 level at 14 d after ischemia, and enhanced spine density of basilar dendrites. TMP failed to affect the spine density of apical dendrites and the total dendritic length. Data analyses indicate that there was significant negative correlation between mNSS and plasticity measured at 14 d after MCAO. Thus, enhanced dendritic plasticity contributes to TMP-elicited functional recovery after ischemic stroke.
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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 (April 1, 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 (P21) stages of development (n = 105). Control mice received saline injections (n = 34). At P30, mice were subjected to rotarod motor training and fear conditioning. Motor learning–induced synaptic remodeling was examined in vivo by repeatedly imaging fluorescently labeled postsynaptic dendritic spines in the primary motor cortex before and after training using two-photon microscopy. Results: Three exposures to ketamine–xylazine anesthesia between P14 and P18 impair the animals’ motor learning and learning-dependent dendritic spine plasticity (new spine formation, 8.4 ± 1.3% [mean ± SD] vs. 13.4 ± 1.8%, P = 0.002) without affecting fear memory and cell apoptosis. One exposure at P14 or three exposures between P21 and P25 has no effects on the animals’ motor learning or spine plasticity. Finally, enriched motor experience ameliorates anesthesia-induced motor learning impairment and synaptic deficits. Conclusions: Our study demonstrates that repeated exposures to ketamine–xylazine during early development impair motor learning and learning-dependent dendritic spine plasticity later in life. The reduction in synaptic structural plasticity may underlie anesthesia-induced behavioral impairment.
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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 (May 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 enhanced in spines expressing NCad-EGFP clusters. Activity and long-term potentiation (LTP) induction selectively promote formation of NCad clusters in stimulated spines. Although activity-mediated expression of NCad-EGFP switches synapses to a highly stable state, expression of mutant NCad or short hairpin RNA–mediated knockdown of NCad prevents LTP-induced long-term stabilization of synapses. These results identify NCad as a key molecular component regulating long-term synapse persistence.
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Gu, Jiaping, and James Q. Zheng. "Microtubules in Dendritic Spine Development and Plasticity." Open Neuroscience Journal 7, no. 1 (June 13, 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 (December 1, 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 (September 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, amplification failed if permeability is reduced by more than 50%. We also found that the maximum free [Ca2+] reached in an individual spine during synaptic coactivation of several spines depended on the location of that spine on the dendritic tree. Distal spines attained a higher [Ca2+] than proximal ones, with differences of up to 80%. The implications of this result for the uniformity of induction of associative LTP in spines in different regions of the dendrite are discussed.
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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 model of CREB downregulation (mCREB mice). We found that sensory deprivation through prolonged whisker trimming leads to an increased number of thin spines in the layer V of related barrel cortex (Contra) in wild type but not mCREB mice. In the barrel field controlling spared whiskers (Ipsi), the same trimming protocol results in a CREB-dependent enlargement of dendritic spines. Last, we demonstrated that CREB regulates structural rearrangements of synapses that associate with dynamic changes of dendritic spines. Our findings suggest that CREB plays a key role in dendritic spine dynamics and synaptic circuits rearrangements that account for new brain connectivity in response to changes in the environment.
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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 (October 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 effects of Fmr1 disruption on two forms of plasticity active during development. One of these, long-term potentiation of intrinsic excitability, is intrinsic in expression and requires mGluR5 activation. The other, spike timing-dependent plasticity, is synaptic in expression and requires N-methyl-d-aspartate receptor activation. While intrinsic plasticity was normal in the knockout mice, synaptic plasticity was altered in an unusual and striking way: long-term depression was robust but long-term potentiation was entirely absent. These findings underscore the ideas that Fmr1 has highly selective effects on plasticity and that abnormal postnatal development is an important component of the disorder.
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Bertan, Fabio, Lena Wischhof, Liudmila Sosulina, Manuel Mittag, Dennis Dalügge, Alessandra Fornarelli, Fabrizio Gardoni, 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 (July 8, 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. Furthermore, post-developmental deletion of RyR2 causes loss of excitatory synapses, dendritic sparsification, overcompensatory excitability, network hyperactivity and disruption of spatially tuned place cells. Altogether, our data underpin RyR2 as a link between spine remodeling, circuitry dysfunction and memory acquisition, which closely resemble pathological mechanisms observed in neurodegenerative disorders.
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Porceddu, Riccardo, Cinzia Podda, Giovanna Mulas, Francesco Palmas, Luca Picci, Claudia Scano, Saturnino Spiga, and Andrea Sabatini. "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 (August 21, 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 decreased from juvenile migrants to no-migrant stages, to increase again in the adult migrant stage. Mean spines’ density was comparable between glass and silver eels as an adaptation to migration. At non-migrating phases, spines’ density decreased for M and LT, while M, LT, and S density increased in silver eels. A great dendritic spine development was found in the two migratory phases, regressing in trophic phases, but that could be recreated in adults, tracing the migratory memory of the routes travelled in juvenile phases. For its phylogenetic Elopomorph attribution and its complex life cycle, A. anguilla could be recommended as a model species to study the development of dendritic spines in GCs of the olfactory bulb as an index of synaptic plasticity involved in the modulation of olfactory stimuli. If olfaction is involved in the orientation and migration of A. anguilla and if eels possess a memory, these processes could be influenced by the modification of environmental stimuli (ocean alterations and rapid climate change) contributing to threatening this critically endangered species.
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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 (August 28, 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 propose that dynamics of initially formed clusters depend on compartmentalization of dendrites and that activity-dependent gene expression kicks in to preserve differences in synaptic weight. We will discuss how mechanisms of synaptic tagging, the presence of secretory organelles in dendrites and the incorporation of synaptic scaling factors that are encoded by immediate early genes interact to preserve clustered plasticity.
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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 association (FrA) cortexin vivousing two-photon microscopy. We found that chronic stress altered spine dynamics in FrA and increased the connectivity in FrA neural circuits. We also found that the changes in spine dynamics in FrA are correlated with the deficit of sucrose preference in defeated mice. Our findings suggest that chronic stress experience leads to adaptive change in neural circuits that may be important for encoding stress experience related memory and anhedonia.