Academic literature on the topic 'Dendritic Spine Plasticity'
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Journal articles on the topic "Dendritic Spine Plasticity"
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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.
Dissertations / Theses on the topic "Dendritic Spine Plasticity"
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Critchlow, Hannah Marion. "The role of dendritic spine plasticity in schizophrenia." Thesis, University of Cambridge, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.612238.
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Pfeiffer, Thomas. "Super-resolution STED and two-photon microscopy of dendritic spine and microglial dynamics." Thesis, Bordeaux, 2017. http://www.theses.fr/2017BORD0743/document.
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Les changements des connections neuronales interviendraient dans la formation de la mémoire. J’ai développé de nouvelles approches basées sur l’imagerie photonique pour étudier (i) les interactions entre les microglies et les épines dendritiques, et (ii) le renouvellement des épines dans l’hippocampe in vivo. Ces deux phénomènes contribueraient au remodelage des circuits synaptiques intervenant dans la mémoire. (i) Les microglies sont impliquées dans de nouvelles fonctions en condition saine. J’ai examiné l’effet de la plasticité synaptique sur la dynamique morphologique des microglies, et sur leur interaction avec les épines. En combinant l’électrophysiologie et l’imagerie bi-photonique dans des tranches aigües de souris transgéniques, je démontre que la microglie intensifie son interaction physique avec les épines. Ainsi pour continuer l’étude de ces interactions et leur impact fonctionnel plus précisément, j’ai optimisé l’imagerie STED dans des tranches aigües. (ii) La plasticité structurale des épines est cruciale pour la mémoire, mais les connaissances à ce sujet dans l’hippocampe in vivo restent limitées. J’ai donc établi une technique d’imagerie chronique STED in vivo pour visualiser les épines dans l’hippocampe. Cette approche a révélé une densité double de celle reportée précédemment à l’aide de la microscopie bi-photonique. De plus j’ai observé un renouvellement des épines de 40% en 5 jours, représentant un taux important de remodelage synaptique dans l’hippocampe. Les approches d’imagerie super-résolutive permettent l’étude des interactions microglie-épine, et du renouvellement des épines hippocampiques avec une résolution inédite chez la souris vivanteActivity-dependent changes in neuronal connectivity are thought to underlie learning and memory. I developed and applied novel high-resolution imaging-based approaches to study (i) microglia-spine interactions and (ii) the turnover of dendritic spines in the mouse hippocampus, which are both thought to contribute to the remodeling of synaptic circuits underlying memory formation. (i) Microglia have been implicated in a variety of novel tasks beyond their classic immune defensive roles. I examined the effect of synaptic plasticity on microglial morphological dynamics and interactions with spines, using a combination of electrophysiology and two-photon microscopy in acute brain slices. I demonstrated that microglia intensify their physical interactions with spines after the induction of hippocampal synaptic plasticity. To study these interactions and their functional impact in greater detail, I optimized and applied time-lapse STED imaging in acute brain slices. (ii) Spine structural plasticity is thought to underpin memory formation. Yet, we know very little about it in the hippocampus in vivo, which is the archetypical memory center of the mammalian brain. I established chronic in vivo STED imaging of hippocampal spines in the living mouse using a modified cranial window technique. The super-resolution approach revealed a spine density that was two times higher than reported in the two-photon literature, and a spine turnover of 40% over 5 days, indicating a high level of structural remodeling of hippocampal synaptic circuits. The developed super-resolution imaging approaches enable the examination of microglia-synapse interactions and dendritic spines with unprecedented resolution in the living brain (tissue)
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Chiang, Chih-Yuan. "Cortical development & plasticity in the FMRP KO mouse." Thesis, University of Edinburgh, 2016. http://hdl.handle.net/1842/22055.
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Autism is one of the leading causes of human intellectual disability (ID). More than 1% of the human population has autism spectrum disorders (ASDs), and it has been estimated that over 50% of those with ASDs also have ID. Fragile X syndrome (FXS) is the most common inherited form of mental retardation and is the leading known genetic cause of autism, affecting approximately 1 in 4000 males and 1 in 8000 females. Approximately 30% of boys with FXS will be diagnosed with autism in their later lives. The cause of FXS is through an over-expansion of the CGG trinucleotide repeat located at the 5’ untranslated region of the FMR1 gene, leading to hypermethylation of the surrounding sequence and eventually partially or fully silencing of the gene. Therefore, the protein product of the gene, fragile X mental retardation protein (FMRP), is reduced or missing. As a single-gene disorder, FXS offers a scientifically tractable way to examine the underlying mechanism of the disease and also shed some light on understanding ASD and ID. The mouse model of FXS (Fmr1−/y mice) is widely accepted and used as a good model, offering good structural and face validity. Since a primary deficit of FXS is believed to be altered neuronal communication, in this thesis I examined white matter tract and dendritic spine abnormalities in the mouse model of FXS. Loss of FMRP does not alter the gross morphology of the white matter. However, recent brain imaging studies indicated that loss of FMRP could lead to some minute abnormalities in different major white matter tracts in the human brain. The gross white matter morphology and myelination was unaltered in the Fmr1−/y mice, however, a small but significant increase of axon diameter in the corpus callosum (CC) was found compared to wild-type (WT) controls. Our computation model suggested that the increase of axon diameter in the Fmr1−/y mice could lead to an increase of conduction velocity in these animals. One of the key phenotypes reported previously in the loss of FMRP is the increase of “immature” dendritic spines. The increase of long and thin spines was reported in several brain regions including the somatosensory cortex and visual cortex in both FXS patients and the mouse model of FXS. Although recent studies which employed state-of-the-art microscopy techniques suggested that only minute differences were noticed between the WT and Fmr1−/y mice. In agreement with previous findings, I found an increase of dendritic spine density in the visual cortex in the Fmr1−/y mice, and spine morphology was also different between the two genotypes. We found that the spine head diameter is significantly increased in the CA1 area of the apical dendrites of the Fmr1−/y mice compared to WT controls. Dendritic spine length is also significantly increased in the same region of the Fmr1−/y mice. However, apical spine head size does not alter between the two genotypes in the V1 region of the visual cortex, and spine length is significantly decreased in the Fmr1−/y mice compared to WT animals in this region. Lovastatin, a drug known as one of the 3-hydroxy-3-methyl-glutaryl-CoA (HMG-CoA) reductase inhibitors, functions as a modulator of the mitogen-activated protein kinases (MAPK) pathway through inhibiting Ras farnesylation, was used in an attempt to rescue the dendritic spine abnormalities in the Fmr1−/y mice. Mice lacking FMRP are susceptible to audiogenic seizure (AGS). Previous work has shown that 48 hr of lovastatin treatment reduced the incidence of AGS in the Fmr1−/y mice. However, chronic lovastatin treatment failed to rescue the spine density and morphology abnormalities in the Fmr1−/y mice. Mouse models are invaluable tools for modelling human diseases. However inter-strain differences have often confounded results between laboratories. In my final Chapter of this thesis, I compared two commonly used C57BL/6 substrains of mice by recording their electrophysiological responses to visual stimuli in vivo. I found a significant increase of high-frequency gamma power in adult C57BL/6JOla mice, and this phenomenon was reduced during the critical period. My results suggested that the C57BL/6JOla substrain has a significant stronger overall inhibitory network activity in the visual cortex than the C57BL/6J substrain. This is in good agreement with previous findings showing a lack of open-eye potentiation to monocular deprivation in the C57BL/6JOla substrain, and highlights the need for appropriate choice of mouse strain when studying neurodevelopmental models. They also give valuable insights into the genetic mechanisms that permit experience-dependent developmental plasticity. In summary, these findings give us a better understanding of the fine structure abnormalities of the Fmr1−/y mice, which in turn can benefit future discoveries of the underlying mechanisms of neurodevelopmental disorders such as ID and ASDs.
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O'Donnell, Cian. "Implications of stochastic ion channel gating and dendritic spine plasticity for neural information processing and storage." Thesis, University of Edinburgh, 2012. http://hdl.handle.net/1842/5886.
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On short timescales, the brain represents, transmits, and processes information through the electrical activity of its neurons. On long timescales, the brain stores information in the strength of the synaptic connections between its neurons. This thesis examines the surprising implications of two separate, well documented microscopic processes — the stochastic gating of ion channels and the plasticity of dendritic spines — for neural information processing and storage. Electrical activity in neurons is mediated by many small membrane proteins called ion channels. Although single ion channels are known to open and close stochastically, the macroscopic behaviour of populations of ion channels are often approximated as deterministic. This is based on the assumption that the intrinsic noise introduced by stochastic ion channel gating is so weak as to be negligible. In this study we take advantage of newly developed efficient computer simulation methods to examine cases where this assumption breaks down. We find that ion channel noise can mediate spontaneous action potential firing in small nerve fibres, and explore its possible implications for neuropathic pain disorders of peripheral nerves. We then characterise the magnitude of ion channel noise for single neurons in the central nervous system, and demonstrate through simulation that channel noise is sufficient to corrupt synaptic integration, spike timing and spike reliability in dendritic neurons. The second topic concerns neural information storage. Learning and memory in the brain has long been believed to be mediated by changes in the strengths of synaptic connections between neurons — a phenomenon termed synaptic plasticity. Most excitatory synapses in the brain are hosted on small membrane structures called dendritic spines, and plasticity of these synapses is dependent on calcium concentration changes within the dendritic spine. In the last decade, it has become clear that spines are highly dynamic structures that appear and disappear, and can shrink and enlarge on rapid timescales. It is also clear that this spine structural plasticity is intimately linked to synaptic plasticity. Small spines host weak synapses, and large spines host strong synapses. Because spine size is one factor which determines synaptic calcium concentration, it is likely that spine structural plasticity influences the rules of synaptic plasticity. We theoretically study the consequences of this observation, and find that different spine-size to synaptic-strength relationships can lead to qualitative differences in long-term synaptic strength dynamics and information storage. This novel theory unifies much existing disparate data, including the unimodal distribution of synaptic strength, the saturation of synaptic plasticity, and the stability of strong synapses.
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Zhang, Shengxiang. "Imaging dendritic spine structural plasticity during development in vitro and after acute stroke in vivo." Thesis, University of British Columbia, 2006. http://hdl.handle.net/2429/31194.
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The plasticity of dendritic spine structure is important for neural development and synaptic function and is altered in many pathological conditions. In this study, we investigated the mechanisms underlying spine structural plasticity during development and the pathological changes in spine structure during ischemic stroke by using confocal and two-photon microscopy. We first investigated spine structural dynamics during development and the role of intracellular Ca²⁺ in determining basal spine motility in cultured hippocampal neurons. We found that young cultured neurons displayed significantly more spine motility than older neurons. In addition, we found that global buffering of intracellular Ca²⁺ failed to alter the basal motility of developing spines. Thus basal spine motility may represent an intrinsic feature of developing neurons and is not necessarily choreographed by ongoing changes in intracellular Ca²⁺ levels. We then examined spine structure changes during cerebral ischemia in vivo and investigated the relationships between cortical microcirculation and spine structure and function. We found moderate ischemia did not significantly affect spines within a 5-h time span; however, severe ischemia caused a rapid loss of spines and induced beading of dendrite structure within as little as 10 min following stroke. Surprisingly this damage was found to be reversible if reperfusion occurred within 20-60 min. By monitoring both cortical microcirculation and dendritic spine structure, we found that dendritic integrity deteriorated proportionally with the fraction of blocked vessels and the volume of affected brain during stroke. In ischemic border regions, we demonstrated that intact dendritic structure could be stably maintained for hours by blood flow from vessels that were on average 81 μm away. Functional imaging of intrinsic optical signals indicated that signal changes induced by limb movement were blocked in areas with blebbed dendrites, but were present at ~225 μm and beyond from the border of dendritic damage, suggesting peri-infarct tissues could function under acute ischemia in the core. In summary, our findings indicate that basal spine motility is maintained in a Ca²⁺ independent manner, and changes in spine structure during ischemia can now be directly linked to alterations in synaptic function and reductions in the cortical microcirculation.Medicine, Faculty of
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Robertson, Holly Rochelle. "Regulation of dendritic spine structure and function by A-kinase anchoring protein 79/150 /." Connect to full text via ProQuest. Limited to UCD Anschutz Medical Campus, 2008.
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Thesis (Ph.D. in Pharmacology) -- University of Colorado Denver, 2008.Typescript. Includes bibliographical references (leaves 135-162). Free to UCD affiliates. Online version available via ProQuest Digital Dissertations;
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Bauer, Rachel J. "THE EFFECTS OF LONG-TERM DEAFNESS ON DENSITY AND DIAMETER OF DENDRITIC SPINES ON PYRAMIDAL NEURONS IN THE DORSAL ZONE OF THE FELINE AUDITORY CORTEX." VCU Scholars Compass, 2019. https://scholarscompass.vcu.edu/etd/6028.
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Neuroplasticity has been researched in many different ways, from the growing neonatal brain to neural responses to trauma and injury. According to recent research, neuroplasticity is also prevalent in the ability of the brain to repurpose areas that are not of use, like in the case of a loss of a sense. Specifically, behavioral studies have shown that deaf humans (Bavalier and Neville, 2002) and cats have increased visual ability, and that different areas of the auditory cortex enhance specific kinds of sight. One such behavioral test demonstrated that the dorsal zone (DZ) of the auditory cortex enhances sensitivity to visual motion through cross-modal plasticity (Lomber et. al., 2010). Current research seeks to examine the anatomical structures responsible for these changes through analysis of excitatory neuron dendritic spine density and spine head diameter. This present study focuses on the examination of DZ neuron spine density, distribution, and size in deaf and hearing cats to corroborate the visual changes seen in behavioral studies. Using Golgi-stained tissue and light microscopy, our results showed a decrease in overall spine density but slight increase in spine head diameter in deaf cats compared to hearing cats. These results, along with several other studies, support multiple theories on how cross-modal reorganization of the auditory cortex occurs after deafening
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VETERE, GISELLA. "Neuronal plasticity of hippocampal and cortical circuitry modulates the formation and extinction of remote adversive memories." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2010. http://hdl.handle.net/2108/1179.
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Una delle funzioni principali della memoria risiede nella sua capacità di conservare le informazioni nel tempo. Il modello più accreditato si basa sulla premessa che le informazioni vengono temporaneamente immagazzinate nell’ippocampo dove rimangono vulnerabili alle interferenze provocate da contingenze esterne. Attraverso un processo molto lento, la traccia mnestica è trasferita in altre strutture del cervello dove la memoria è resa stabile e non più vulnerabile alle interferenze. Questo processo richiede tempo per essere portato a termine ed è chiamato consolidamento (Mueller and Pilzecher, 1900). Varie teorie ipotizzano che i meccanismi attraverso i quali le memorie possono essere acquisite e consolidate nel cervello dei mammiferi implichino modificazioni nella plasticità strutturale (Cajal, 1891).
Lo scopo principale di questo lavoro è quello di ricercare le modificazioni morfologiche necessarie alla formazione e all’estinzione della memoria.
Nel primo lavoro esposto mostriamo la presenza di cambiamenti plastici (sotto forma di aumento in densità di spine dendritiche) nell’ippocampo, immediatamente dopo un addestramento in un condizionamento avversivo al contesto. Questi cambiamenti sono temporanei poiché scompaiono 36 giorni dopo. Contemporaneamente in corteccia anteriore cingolata è visibile un aumento di spine dendritiche solo dopo aver testato gli animali per la loro memoria a lungo termine ma non dopo il test di memoria a breve termine, mostrando un pattern inverso rispetto a quello trovato in ippocampo.
Nel secondo lavoro esposto, blocchiamo la possibilità di aumentare il numero di spine in corteccia anteriore cingolata e troviamo una finestra temporale durante la quale i rimodellamenti sinaptici che avvengono in questa regione sono fondamentali per un corretto consolidamento delle memorie a lungo termine.
Nel terzo lavoro presentato mostriamo come l’estinzione di un comportamento indotto dal consolidamento di una memoria precedentemente acquisita modifichi nuovamente la rete sinaptica che si era lentamente formata nella corteccia anteriore cingolata. Contemporaneamente troviamo un aumento in connettività sinaptica nei neuroni della corteccia infralimbica indotto dal consolidamento che persiste dopo l’estinzione.
I nostri risultati puntano sulla versatilità e plasticità delle reti neuronali che sottostanno ai processi di memoria.It is generally believed that in order to enable long-term episodic memory, the information is temporarily stored in the hippocampus where it remains vulnerable to interference. Via a slow read-out process, the information is transferred into other brain structures where the memory is established and no longer vulnerable to interference. This slow read-out is termed consolidation (Mueller and Pilzecker, 1900). The mechanisms by which memories can be acquired and consolidated in the mammalian brain are assumed to involve modifications in structural plasticity (Cajal, 1891). The main goal of this work is to discover the morphological modification requested in memory formation and extinction. In study I we shown that plastic changes (i.e. dendritic spine density increase) immediately develop in CA1 field of the hippocampus after a training in the contextual fear conditioning. These modifications are only transient because they disappear 36 days later, while an inverse pattern of spine density in recent and remote memory recall were found in the anterior cingulate cortex. In study II we block the possibility to increase the number of spines in the aCC after training and we found an early temporal window in which synaptic remodelling occurring in this region is fundamental for the correct consolidation of memory. In study III we presented a new and conflicting memory (extinction) after the consolidation of an old one, founding a disruption of the synaptic network in the aCC field. At the same time, we found an increase of connectivity in the Infra limbic cortex induced by consolidation that persist after extinction. Our results point on a dynamic view of memory consolidation: a regulated balance of synaptic stability and synaptic plasticity is required for optimal memory retention to allow the incorporation of new memories in neuronal circuits.
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Hamel, Michelle Grace. "Modulation of neural plasticity by the ADAMTSs (a disintegrin and metalloproteinase with thrombospondin motifs)." [Tampa, Fla] : University of South Florida, 2006. http://purl.fcla.edu/usf/dc/et/SFE0001684.
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Chen, Jian Hua [Verfasser], Peter Jomo [Akademischer Betreuer] Walla, Reinhard [Akademischer Betreuer] Jahn, and Andreas [Akademischer Betreuer] Janshoff. "Spatial-temporal actin dynamics during synaptic plasticity of single dendritic spine investigated by two-photon fluorescence correlation spectroscopy / Jian Hua Chen. Gutachter: Reinhard Jahn ; Andreas Janshoff. Betreuer: Peter Jomo Walla." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2013. http://d-nb.info/1045776246/34.
Full textBooks on the topic "Dendritic Spine Plasticity"
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Rasia-Filho, Alberto A., Rochelle S. Cohen, and Oliver von Bohlen und Halbach, eds. Frontiers in Synaptic Plasticity: Dendritic Spines, Circuitries and Behavior. Frontiers Media SA, 2016. http://dx.doi.org/10.3389/978-2-88919-947-1.
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Koch, Christof. Biophysics of Computation. Oxford University Press, 1998. http://dx.doi.org/10.1093/oso/9780195104912.001.0001.
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Neural network research often builds on the fiction that neurons are simple linear threshold units, completely neglecting the highly dynamic and complex nature of synapses, dendrites, and voltage-dependent ionic currents. Biophysics of Computation: Information Processing in Single Neurons challenges this notion, using richly detailed experimental and theoretical findings from cellular biophysics to explain the repertoire of computational functions available to single neurons. The author shows how individual nerve cells can multiply, integrate, or delay synaptic inputs and how information can be encoded in the voltage across the membrane, in the intracellular calcium concentration, or in the timing of individual spikes. Key topics covered include the linear cable equation; cable theory as applied to passive dendritic trees and dendritic spines; chemical and electrical synapses and how to treat them from a computational point of view; nonlinear interactions of synaptic input in passive and active dendritic trees; the Hodgkin-Huxley model of action potential generation and propagation; phase space analysis; linking stochastic ionic channels to membrane-dependent currents; calcium and potassium currents and their role in information processing; the role of diffusion, buffering and binding of calcium, and other messenger systems in information processing and storage; short- and long-term models of synaptic plasticity; simplified models of single cells; stochastic aspects of neuronal firing; the nature of the neuronal code; and unconventional models of sub-cellular computation. Biophysics of Computation: Information Processing in Single Neurons serves as an ideal text for advanced undergraduate and graduate courses in cellular biophysics, computational neuroscience, and neural networks, and will appeal to students and professionals in neuroscience, electrical and computer engineering, and physics.
Book chapters on the topic "Dendritic Spine Plasticity"
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Rall, Wilfrid, and Idan Segev. "Dendritic Spine Synapses, Excitable Spine Clusters, and Plasticity." In Cellular Mechanisms of Conditioning and Behavioral Plasticity, 221–36. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4757-9610-0_22.
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Kreutz, M. R., I. König, M. Mikhaylova, C. Spilker, and W. Zuschratter. "Molecular Mechanisms of Dendritic Spine Plasticity in Development and Aging." In Handbook of Neurochemistry and Molecular Neurobiology, 245–59. Boston, MA: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-32671-9_10.
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Johansson, B. B., and P. V. Belichenko. "Environmental Influence on Neuronal and Dendritic Spine Plasticity After Permanent Focal Brain Ischemia." In Maturation Phenomenon in Cerebral Ischemia IV, 77–83. Berlin, Heidelberg: Springer Berlin Heidelberg, 2001. http://dx.doi.org/10.1007/978-3-642-59446-5_10.
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Penzes, Peter, and Igor Rafalovich. "Regulation of the Actin Cytoskeleton in Dendritic Spines." In Synaptic Plasticity, 81–95. Vienna: Springer Vienna, 2012. http://dx.doi.org/10.1007/978-3-7091-0932-8_4.
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De Roo, Mathias, and Adema Ribic. "Analyzing Structural Plasticity of Dendritic Spines in Organotypic Slice Culture." In Methods in Molecular Biology, 277–89. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-6688-2_19.
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Stein, Ivar S., Travis C. Hill, Won Chan Oh, Laxmi K. Parajuli, and Karen Zito. "Two-Photon Glutamate Uncaging to Study Structural and Functional Plasticity of Dendritic Spines." In Neuromethods, 65–85. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9702-2_4.
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Makino, Hiroshi, and Bo Li. "Monitoring Synaptic Plasticity by Imaging AMPA Receptor Content and Dynamics on Dendritic Spines." In Methods in Molecular Biology, 269–75. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-444-9_25.
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Koch, Christof. "Dendritic Spines." In Biophysics of Computation. Oxford University Press, 1998. http://dx.doi.org/10.1093/oso/9780195104912.003.0018.
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Dendritic spines, sometimes also called dendritic thorns, are tiny, specialized protoplasmic protuberances that cover the surface of many neurons. First described by Ramón y Cajal (1909; 1991) in light-microscopic studies of Golgi stained tissue, they are among the most striking subneuronal features of many neurons. Indeed, the presence of a high density of dendritic spines allows the unambiguous classification of neuronal types into spiny and aspiny, sparsely spiny, or smooth neurons. Over 90% of all excitatory synapses that occur in the cortex are located on dendritic spines. Spines can be found in all vertebrates as well as in invertebrates (e.g., the dendrites of Kenyon cells in the mushroom bodies in the olfactory system of the insect brain). The intimate association of spines with synaptic traffic suggests some crucial role in synaptic transmission and plasticity. Because of their submicrometer size (see below), physiological hypotheses as to the function of dendritic spines have only very recently become accessible to the experimentalist. For the previous two decades, spine properties have been investigated through analytical and computational studies based on morphological data, providing a very fertile ground for the crosspollination of theory and experiment. (For a very readable historical account of this see Segev et al., 1995.) The recent technical advances in the direct visualization of calcium dynamics in dendrites and spines are now permitting direct tests of some of these theoretical inferences (Guthrie, Segal, and Kater, 1991; Müller and Connor, 1991; Yuste and Denk, 1995; Denk, Sugimori, and Llinás, 1995; Svoboda, Tank, and Denk, 1996). As discussed in this chapter and, more extensively, in Chap. 19, the theoretical models that have endowed spines with active properties giving rise to all-or-none behavior (Perkel and Perkel, 1985; Shepherd et al., 1985; Segev and Rail, 1988; Baer and Rinzel, 1991) have, in general, been confirmed experimentally. Historically, the possibility of implementing synaptic memory by modulating the electroanatomy of spines was recognized early on (Chang, 1952) and was subsequently analyzed in depth by Rail (1970, 1974, 1978) and many others. Because small changes in the spine morphology can lead to large changes in the amplitude of the EPSP induced by the excitatory synapse on the spine, spines have been considered to contribute to the modulation of synaptic “weight” during long-term potentiation (see Chap. 13).
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Luine, Victoria N., and Maya Frankfurt. "Estrogenic Regulation of Recognition Memory and Spinogenesis." In Estrogens and Memory, 159–69. Oxford University Press, 2020. http://dx.doi.org/10.1093/oso/9780190645908.003.0011.
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This chapter reviews the relationship between estrogens, memory, and dendritic spine plasticity. Estrogens, given systemically or directly into the hippocampus, enhance memory consolidation in object recognition and object placement tasks within minutes of application. Dendritic spine density in the CA1 area of the hippocampus and medial prefrontal cortex increases under the same conditions, suggesting that changes in dendritic spine density are an important component of estrogen’s ability to impact memory processes. Possible receptors and signaling pathways mediating the molecular mechanisms in response to estrogen are discussed. Although the precise mechanisms remain to be elucidated, research to date suggests that modulation of dendritic spines by estradiol is a key component in promotion of memory consolidation.
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Ammassari-Teule, Martine, and Menahem Segal. "Dendritic Spine Plasticity and Memory Formation." In Learning and Memory: A Comprehensive Reference, 199–215. Elsevier, 2017. http://dx.doi.org/10.1016/b978-0-12-809324-5.21113-9.
Full textConference papers on the topic "Dendritic Spine Plasticity"
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Elibol, Rahmi. "A computational model of the growth of dendritic spines with synaptic plasticity." In 2022 30th Signal Processing and Communications Applications Conference (SIU). IEEE, 2022. http://dx.doi.org/10.1109/siu55565.2022.9864973.
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Basu, Subhadip, Punam K. Saha, Jakub Wlodarczyk, Marta Magnowska, Matylda Babraj, Nirmal Das, Ewa Baczynska, and Indranil Guha. "Segmentation and assessment of structural plasticity of hippocampal dendritic spines from 3D confocal light microscopy." In Biomedical Applications in Molecular, Structural, and Functional Imaging, edited by Barjor Gimi and Andrzej Krol. SPIE, 2018. http://dx.doi.org/10.1117/12.2292924.
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