Academic literature on the topic 'Dendritic arborization'
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Journal articles on the topic "Dendritic arborization"
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Schaefer, Andreas T., Matthew E. Larkum, Bert Sakmann, and Arnd Roth. "Coincidence Detection in Pyramidal Neurons Is Tuned by Their Dendritic Branching Pattern." Journal of Neurophysiology 89, no. 6 (June 2003): 3143–54. http://dx.doi.org/10.1152/jn.00046.2003.
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Neurons display a variety of complex dendritic morphologies even within the same class. We examined the relationship between dendritic arborization and the coupling between somatic and dendritic action potential (AP) initiation sites in layer 5 (L5) neocortical pyramidal neurons. Coupling was defined as the relative reduction in threshold for initiation of a dendritic calcium AP due to a coincident back-propagating AP. Simulations based on reconstructions of biocytin-filled cells showed that addition of oblique branches of the main apical dendrite in close proximity to the soma ( d < 140 μm) increases the coupling between the apical and axosomatic AP initiation zones, whereas incorporation of distal branches decreases coupling. Experimental studies on L5 pyramids in acute brain slices revealed a highly significant ( n = 28, r = 0.63, P < 0.0005) correlation: increasing the fraction of proximal oblique dendrites ( d < 140 μm), e.g., from 30 to 60% resulted on average in an increase of the coupling from approximately 35% to almost 60%. We conclude that variation in dendritic arborization may be a key determinant of variability in coupling (49 ± 17%; range 19–83%; n = 37) and is likely to outweigh the contribution made by variations in active membrane properties. Thus coincidence detection of inputs arriving from different cortical layers is strongly regulated by differences in dendritic arborization.
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Chen, Chiung-Ya, Chia-Wen Lin, Chiung-Ying Chang, Si-Tse Jiang, and Yi-Ping Hsueh. "Sarm1, a negative regulator of innate immunity, interacts with syndecan-2 and regulates neuronal morphology." Journal of Cell Biology 193, no. 4 (May 9, 2011): 769–84. http://dx.doi.org/10.1083/jcb.201008050.
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Dendritic arborization is a critical neuronal differentiation process. Here, we demonstrate that syndecan-2 (Sdc2), a synaptic heparan sulfate proteoglycan that triggers dendritic filopodia and spine formation, regulates dendritic arborization in cultured hippocampal neurons. This process is controlled by sterile α and TIR motif–containing 1 protein (Sarm1), a negative regulator of Toll-like receptor 3 (TLR3) in innate immunity signaling. We show that Sarm1 interacts with and receives signal from Sdc2 and controls dendritic arborization through the MKK4–JNK pathway. In Sarm1 knockdown mice, dendritic arbors of neurons were less complex than those of wild-type littermates. In addition to acting downstream of Sdc2, Sarm1 is expressed earlier than Sdc2, which suggests that it has multiple roles in neuronal morphogenesis. Specifically, it is required for proper initiation and elongation of dendrites, axonal outgrowth, and neuronal polarization. These functions likely involve Sarm1-mediated regulation of microtubule stability, as Sarm1 influenced tubulin acetylation. This study thus reveals the molecular mechanism underlying the action of Sarm1 in neuronal morphogenesis.
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Mishra, Archana, Boris Knerr, Sónia Paixão, Edgar R. Kramer, and Rüdiger Klein. "The Protein Dendrite Arborization and Synapse Maturation 1 (Dasm-1) Is Dispensable for Dendrite Arborization." Molecular and Cellular Biology 28, no. 8 (February 11, 2008): 2782–91. http://dx.doi.org/10.1128/mcb.02102-07.
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ABSTRACT The development of a highly branched dendritic tree is essential for the establishment of functional neuronal connections. The evolutionarily conserved immunoglobulin superfamily member, the protein dendrite arborization and synapse maturation 1 (Dasm-1) is thought to play a critical role in dendrite formation of dissociated hippocampal neurons. RNA interference-mediated Dasm-1 knockdown was previously shown to impair dendrite, but not axonal, outgrowth and branching (S. H. Shi, D. N. Cox, D. Wang, L. Y. Jan, and Y. N. Jan, Proc. Natl. Acad. Sci. USA 101:13341-13345, 2004). Here, we report the generation and analysis of Dasm-1 null mice. We find that genetic ablation of Dasm-1 does not interfere with hippocampal dendrite growth and branching in vitro and in vivo. Moreover, the absence of Dasm-1 does not affect the modulation of dendritic outgrowth induced by brain-derived neurotrophic factor. Importantly, the previously observed impairment in dendrite growth after Dasm-1 knockdown is also observed when the Dasm-1 knockdown is performed in cultured hippocampal neurons from Dasm-1 null mice. These findings indicate that the dendrite arborization phenotype was caused by off-target effects and that Dasm-1 is dispensable for hippocampal dendrite arborization.
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Fujishima, Kazuto, Junko Kurisu, Midori Yamada, and Mineko Kengaku. "βIII spectrin controls the planarity of Purkinje cell dendrites by modulating perpendicular axon-dendrite interactions." Development 147, no. 24 (November 24, 2020): dev194530. http://dx.doi.org/10.1242/dev.194530.
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ABSTRACTThe mechanism underlying the geometrical patterning of axon and dendrite wiring remains elusive, despite its crucial importance in the formation of functional neural circuits. The cerebellar Purkinje cell (PC) arborizes a typical planar dendrite, which forms an orthogonal network with granule cell (GC) axons. By using electrospun nanofiber substrates, we reproduce the perpendicular contacts between PC dendrites and GC axons in culture. In the model system, PC dendrites show a preference to grow perpendicularly to aligned GC axons, which presumably contribute to the planar dendrite arborization in vivo. We show that βIII spectrin, a causal protein for spinocerebellar ataxia type 5, is required for the biased growth of dendrites. βIII spectrin deficiency causes actin mislocalization and excessive microtubule invasion in dendritic protrusions, resulting in abnormally oriented branch formation. Furthermore, disease-associated mutations affect the ability of βIII spectrin to control dendrite orientation. These data indicate that βIII spectrin organizes the mouse dendritic cytoskeleton and thereby regulates the oriented growth of dendrites with respect to the afferent axons.
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Troilo, David, Meijuan Xiong, Justin C. Crowley, and Barbara L. Finlay. "Factors controlling the dendritic arborization of retinal ganglion cells." Visual Neuroscience 13, no. 4 (July 1996): 721–33. http://dx.doi.org/10.1017/s0952523800008609.
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AbstractThe effects of changing retinal ganglion cell (RGC) density and availability of presynaptic sites on the development of RGC dendritic arbor in the developing chick retina were contrasted. Visual form deprivation was used to induce ocular enlargement and expanded retinal area resulting in a 20–30% decrease in RGC density. In these retinas, RGC dendritic arbors increased in a compensatory manner to maintain the inner nuclear layer to RGC convergence ratio in a way that is consistent with simple stretching; RGC dendritic arbors become larger with increased branch lengths, but without change in the total number of branches. In the second manipulation, partial optic nerve section was used to produce areas of RGC depletion of approximately 60% in the central retina. This reduction in density is comparable to the density of locations in the normal peripheral retina. In RGC-depleted retinas, dendritic arbor areas of RGCs in the central retina grow to match the size of normal peripheral arbors. In contrast to the expanded case, two measures of intrinsic arbor structure are changed in RGC-depleted retinas; the branch density of RGC dendrites is greater, and the relative areas of the two arbors of bistratified cells are altered. We discuss the potential roles of retinal growth, local RGC density, and availability of presynaptic terminals in the developmental control of RGC dendritic arbor.
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Jan, Yuh-Nung, and Lily Yeh Jan. "Branching out: mechanisms of dendritic arborization." Nature Reviews Neuroscience 11, no. 5 (May 2010): 316–28. http://dx.doi.org/10.1038/nrn2836.
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Kong, Jiming, Vivian W. Y. Tung, John Aghajanian, and Zuoshang Xu. "Antagonistic Roles of Neurofilament Subunits NF-H and NF-M Against NF-L in Shaping Dendritic Arborization in Spinal Motor Neurons." Journal of Cell Biology 140, no. 5 (March 9, 1998): 1167–76. http://dx.doi.org/10.1083/jcb.140.5.1167.
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Dendrites play important roles in neuronal function. However, the cellular mechanism for the growth and maintenance of dendritic arborization is unclear. Neurofilaments (NFs), a major component of the neuronal cytoskeleton, are composed of three polypeptide subunits, NF-H, NF-M, and NF-L, and are abundant in large dendritic trees. By overexpressing each of the three NF subunits in transgenic mice, we altered subunit composition and found that increasing NF-H and/or NF-M inhibited dendritic arborization, whereas increasing NF-L alleviated this inhibition. Examination of cytoskeletal organization revealed that increasing NF-H and/or NF-M caused NF aggregation and dissociation of the NF network from the microtubule (MT) network. Increasing NF-H or NF-H together with NF-M further reduced NFs from dendrites. However, these changes were reversed by elevating the level of NF-L with either NF-H or NF-M. Thus, NF-L antagonizes NF-H and NF-M in organizing the NF network and maintaining a lower ratio of NF-H and NF-M to NF-L is critical for the growth of complex dendritic trees in motor neurons.
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Keil, Kimberly P., Sunjay Sethi, and Pamela J. Lein. "Sex-Dependent Effects of 2,2′,3,5′,6-Pentachlorobiphenyl on Dendritic Arborization of Primary Mouse Neurons." Toxicological Sciences 168, no. 1 (November 3, 2018): 95–109. http://dx.doi.org/10.1093/toxsci/kfy277.
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AbstractEarly life exposures to environmental contaminants are implicated in the pathogenesis of many neurodevelopmental disorders (NDDs). These disorders often display sex biases, but whether environmental neurotoxicants act in a sex-dependent manner to modify neurodevelopment is largely unknown. Since altered dendritic morphology is associated with many NDDs, we tested the hypothesis that male and female primary mouse neurons are differentially susceptible to the dendrite-promoting activity of 2,2′,3,5′,6-pentachlorobiphenyl (PCB 95). Hippocampal and cortical neuron-glia co-cultures were exposed to vehicle (0.1% dimethylsulfoxide) or PCB 95 (100 fM–1 μM) from day in vitro 7–9. As determined by Sholl analysis, PCB 95-enhanced dendritic growth in female but not male hippocampal and cortical neurons. In contrast, both male and female neurons responded to bicuculline with increased dendritic complexity. Detailed morphometric analyses confirmed that PCB 95 effects on the number and length of primary and nonprimary dendrites varied depending on sex, brain region and PCB concentration, and that female neurons responded more consistently with increased dendritic growth and at lower concentrations of PCB 95 than their male counterparts. Exposure to PCB 95 did not alter cell viability or the ratio of neurons to glia in cultures of either sex. These results demonstrate that cultured female mouse hippocampal and cortical neurons are more sensitive than male neurons to the dendrite-promoting activity of PCB 95, and suggest that mechanisms underlying PCB 95-induced dendritic growth are sex-dependent. These data highlight the importance of sex in neuronal responses to environmental neurotoxicants.
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Keeler, Austin B., Dietmar Schreiner, and Joshua A. Weiner. "Protein Kinase C Phosphorylation of a γ-Protocadherin C-terminal Lipid Binding Domain Regulates Focal Adhesion Kinase Inhibition and Dendrite Arborization." Journal of Biological Chemistry 290, no. 34 (July 2, 2015): 20674–86. http://dx.doi.org/10.1074/jbc.m115.642306.
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The γ-protocadherins (γ-Pcdhs) are a family of 22 adhesion molecules with multiple critical developmental functions, including the proper formation of dendritic arbors by forebrain neurons. The γ-Pcdhs bind to and inhibit focal adhesion kinase (FAK) via a constant C-terminal cytoplasmic domain shared by all 22 proteins. In cortical neurons lacking the γ-Pcdhs, aberrantly high activity of FAK and of PKC disrupts dendrite arborization. Little is known, however, about how γ-Pcdh function is regulated by other factors. Here we show that PKC phosphorylates a serine residue situated within a phospholipid binding motif at the shared γ-Pcdh C terminus. Western blots using a novel phospho-specific antibody against this site suggest that a portion of γ-Pcdh proteins is phosphorylated in the cortex in vivo. We find that PKC phosphorylation disrupts both phospholipid binding and the γ-Pcdh inhibition of (but not binding to) FAK. Introduction of a non-phosphorylatable (S922A) γ-Pcdh construct into wild-type cortical neurons significantly increases dendrite arborization. This same S922A construct can also rescue dendrite arborization defects in γ-Pcdh null neurons cell autonomously. Consistent with these data, introduction of a phosphomimetic (S/D) γ-Pcdh construct or treatment with a PKC activator reduces dendrite arborization in wild-type cortical neurons. Together, these data identify a novel mechanism through which γ-Pcdh control of a signaling pathway important for dendrite arborization is regulated.
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SCHIERWAGEN, ANDREAS K., and JAAP VAN PELT. "SHAPING NEURONAL DENDRITES: INTERPLAY OF TOPOLOGICAL AND METRICAL PARAMETERS." Journal of Biological Systems 03, no. 04 (December 1995): 1193–200. http://dx.doi.org/10.1142/s0218339095001076.
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The functional role of a neuron within a network is influenced by the geometry of its dendrites. In the present study we have used a new model of dendritic arborization to analyze how metrical and topological parameters interact to shape a certain dendritic tree. One of the specific questions addressed is how to change topological variability in a systematic way while preserving the metrical features. The second problem concerns the effect of topology on the relationship between dendritic size and the distribution of dendritic surface area with radial distance from soma. The simulation results reproduce features of dendritic architecture found in neocortical pyramidal cells and cat superior colliculus neurons.
Dissertations / Theses on the topic "Dendritic arborization"
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Garrett, Andrew Weiner Joshua A. "Control of synaptogenesis and dendritic arborization by the [gamma]-Protocadherin family of adhesion molecules." [Iowa City, Iowa] : University of Iowa, 2009. http://ir.uiowa.edu/etd/362.
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Garrett, Andrew. "Control of synaptogenesis and dendritic arborization by the γ-Protocadherin family of adhesion molecules." Diss., University of Iowa, 2009. https://ir.uiowa.edu/etd/362.
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During development, the mammalian nervous system wires into a precise network of unrivaled complexity. The formation of this network is regulated by an assortment of molecular cues, both secreted molecules and cell-surface proteins. The ã-Protocadherins (ã-Pcdhs) are particularly good candidates for involvement in these processes. This family of adhesion molecules consists of 22 members, each with diverse extracellular adhesive domains and shared cytoplasmic domains. Thus, cellular interactions with varied adhesive partners can trigger common cytoplasmic responses. Here we investigated the functions of the ã-Pcdhs in two processes involved in neural network formation: dendrite arborization and synaptogenesis.
We first asked how ã-Pcdhs regulate synaptogenesis in the spinal cord. We found that the ã-Pcdhs are differentially expressed by astrocytes as well as neurons. In astrocytes, the proteins localize to perisynaptic processes where they can mediate contacts between neurons and astrocytes. In an in vitro co-culture system in which either only astrocytes or only neurons were null for the ã-Pcdhs, we found that astrocytic ã-Pcdh is required for an early stage of synaptogenesis in a contact-dependent manner, while neuronal ã-Pcdh is sufficient for later stages. Conversely, if neurons lacked the adhesion molecules, very few synaptic contacts formed at all. By deleting the ã-Pcdhs from astrocytes in vivo, we demonstrated that these contacts are required for the normal progression of synaptogenesis.
We also investigated the function of the ã-Pcdhs in the cerebral cortex. We found that cortical-restricted loss of the adhesion molecules resulted in a severe reduction in thickness of layer 1. By crossing the mutant mice to a line in which scattered layer 5 neurons express YFP, we saw that this thinning resulted from a reduced complexity in the apical tufts of dendrites from layer 5 neurons. Sholl analysis demonstrated that the arbor reduction existed throughout the cell, a phenotype that was recapitulated in vitro. Using the in vitro system, we found that the arborization defect was caused by hyperphosphorylation of the PKC substrate, MARCKS, indicating that the ã-Pcdhs may function by inhibiting PKC activity. Thus, we provide new information about the mechanisms through which the ã-Pcdhs influence neural network development.
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Karakatsani, Andromachi [Verfasser], and Hans [Akademischer Betreuer] Straka. "LRP4 regulates dendritic arborization and synapse formation in the central nervous system neurons / Andromachi Karakatsani ; Betreuer: Hans Straka." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2016. http://d-nb.info/1120301963/34.
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Handara, Gerry [Verfasser], and Stephan [Akademischer Betreuer] Kröger. "The role of transmembrane-agrin and its receptor complex during dendritic arborization and synaptogenesis / Gerry Handara ; Betreuer: Stephan Kröger." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2019. http://d-nb.info/1199265411/34.
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高山, 雄太. "筋萎縮性側索硬化症2型原因遺伝子のショウジョウバエホモログの生体内機能." 京都大学 (Kyoto University), 2014. http://hdl.handle.net/2433/189376.
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Chassefeyre, Romain. "Rôle de CHMP2B et du complexe ESCRT-III dans le remodelage dans membranes cellulaires : cas des épines dendritiques." Thesis, Grenoble, 2013. http://www.theses.fr/2013GRENV049/document.
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CHMP2B est une sous-unité du complexe ESCRT-III, un complexe cytosolique très conservé, responsable du remodelage des membranes biologique, dans divers processus cellulaires. Des mutations de CHMP2B sont associées à une forme familiale de démence frontotemporale. Une étude précédente a mis en évidence que les mutants pathogènes de CHMP2B altèrent la morphologie des épines dendritiques, un phénomène potentiellement à l'origine de la maladie. Ce travail de recherche a pour objectif de décrire le rôle de CHMP2B, et du complexe ESCRT-III, dans la structure et le fonctionnement des épines dendritiques. Dans des lignées cellulaires, nous avons démontré que CHMP2B a la propriété de s'associer préférentiellement à la membrane plasmique, de se polymériser en filaments hélicoïdaux et de former de longs et fins tubes membranaires. Ce résultat indique que CHMP2B est directement impliqué dans le remodelage de la membrane plasmique. Dans les neurones, CHMP2B se concentre dans des régions sous-membranaires proches de la PSD. Une analyse biochimique a montré que CHMP2B et CHMP4B sont associées à d'autres sous-unités, pour former un complexe ESCRT-III postsynaptique particulièrement stable. Nous avons identifié par spectrométrie de masse que ce complexe interagit également avec des protéines d'échafaudage postsynaptiques et des protéines de remodelage du cytosquelette d'actine. La déplétion de CHMP2B par RNAi, dans des neurones en culture, affecte la complexité de l'arborisation dendritique, la morphologie des épines dendritiques et empêche le gonflement des épines associé à la LTP. Des expériences de récupération, avec des mutants pontuels, indiquent que le rôle de CHMP2B dans le maintien de l'arborisation dendritique est dépendant à la fois de de son association avec ESCRT-III et la bicouche phospholipidique. Nous proposons une nouvelle fonctionnalité pour un complexe ESCRT-III contenant CHMP2B, dans les processus de remodelage de la membrane postsynaptique associés à la maturation et à la plasticité des épines dendritiquesCHMP2B is a subunit of ESCRT-III, a highly conserved cytosolic protein machinery, responsible for membrane remodeling in diverse cellular mechanisms. Mutations in CHMP2B are responsible for a familial form of frontotemporal dementia. A previous study highlighted that FTD-related mutants of CHMP2B impair the morphological maturation of dendritic spines, a process that may underlie neurodegeneration in this disease. The goal of this research work id directed towards understanding the role of CHMP2B and ESCRT-III in dendritic spines structure and function. In cell lines, we demonstrated that CHMP2B associates preferentially with the plasma membrane, polymerizes in helical filaments and forms long and thin membrane protrusions. This result indicates that CHMP2B is directly involved in plasma membrane remodeling. In neurons, CHMP2B concentrates in specific sub-membrane microdomains close to the PSD. Biochemical analysis revealed that CHMP2B and CHMP4B associate with other subunits to form a remarkably stable postsynaptic ESCRT-III complex. Mass-spectrometry indicated that this complex also interacts with postsynaptic scaffolds and proteins involved in actin cytoskeleton remodelling. RNAi depletion of CHMP2B, in cultured neurons, alters stability of dendrite branching and morphology of dendritic spines, and impairs spine head growth, normally associated with LTP. Rescue experiments, with point mutants, indicated that CHMP2B activity in dendrite branching is dependent on its capacity to both bind phospholipids and oligomerization with ESCRT-III. We propose a novel functionality for an ESCRT-III complex containing CHMP2B, in maturation-dependent and plasticity-dependent processes of dendritic spine morphogenesis
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Ou, Yimiao. "Molecular mechanisms controlling the arborization of dendrites in «Drosophila»." Thesis, McGill University, 2011. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=96940.
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The assembly and function of neural circuits depend on the patterned outgrowth, guidance and targeting of dendrites into appropriate territories during development. As a hallmark of any neuron, cell type-specific dendrite morphology has a crucial role in determining the sensory or synaptic input a neuron receives. Despite recent advances in exploring the molecular and cellular mechanisms that define dendritic architecture, our understanding of dendrite development is still far from complete. In this thesis research, I have taken a genetic screen approach and a candidate molecule approach to discover novel genes and mechanisms that are involved in dendrite morphogenesis, using Drosophila dendritic arborization (da) neurons as a model system. In three independent but related studies, my research led me to focus on 1) the nuclear receptor for the steroid hormone ecdysone (EcR), 2) the transcription factor Longitudinals Lacking (Lola) and 3) the cell surface recognition molecule Turtle (Tutl). I have found that these three different factors each regulate distinct aspects of dendritic arborization including dendrite branching, distribution and self-avoidance. Through their identification, expression patterns, and a characterization of their effects in loss-of-function and gain-of-function experiments, my findings provide novel insight into the regulatory networks that control dendrite morphogenesis.L'élaboration et le fonctionnement harmonieux des circuits nerveux dépendent de la croissance des dendrites et de leur guidage et ciblage vers les territoires appropriés au cours du développement. La morphologie des dendrites sert de signe distinctif pour chaque neurone, et ainsi, joue un rôle crucial dans la détermination des différents influx (synaptiques ou sensoriels) que reçoit un neurone. Malgré de récentes avancées dans la compréhension des mécanismes moléculaires et cellulaires qui contrôlent l'architecture dendritique, notre connaissance du développement des dendrites reste encore incomplète. Mes travaux de recherche se sont attachés à découvrir de nouveaux gènes et mécanismes impliqués dans la morphogenèse dendritique. Dans ce but, j'ai choisi au cours de ma thèse deux méthodes d'étude: une approche par crible génétique et une approche par gènes candidats, que j'ai appliquées aux neurones appelés dendritic arborization (da) de la drosophile, mon modèle d'étude. Mes recherches m'ont permis de me concentrer sur trois molécules: 1) le récepteur nucléaire de l'hormone stéroïde ecdysone (EcR), 2) le facteur de transcription Longitudinals Lacking (Lola) et enfin, 3) la molécule de surface Turtle (Tutl). J'ai pu montrer que chacun de ces facteurs est implique dans des aspects distincts du processus de morphogenèse dendritique incluant le branchement, la distribution et l'auto-répulsion dendritiques. L'identification de ces molécules, la description de leurs patrons d'expression et la caractérisation des phénotypes associés à leurs pertes ou gains de fonctions, m'ont permis d'apporter de nouvelles connaissances des réseaux de régulation contrôlant la morphogenèse dendritique.
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Mah, Kar Men. "Unique roles for the C3 gamma-protocadherin isoform in WNT signaling and dendrite arborization." Diss., University of Iowa, 2017. https://ir.uiowa.edu/etd/5964.
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A key component of neural circuit formation is the elaboration of complex dendritic arbors, the pattern of which constrains inputs to the neuron and thus, the information it processes. As such, many neurodevelopmental disorders such as autism and Down, Rett, and Fragile X Syndromes are associated with reduced forebrain dendrite arborization. Identifying molecules involved in regulating dendrite arborization and neural circuitry formation therefore, is a start to understanding these disorders.
Nearly 70 cadherin superfamily adhesion molecules are encoded by the Pcdha, Pcdhb, and Pcdhg gene clusters. These so-called clustered protocadherins (Pcdhs) are broadly expressed throughout the nervous system, with lower levels found in a few non-neuronal tissues. Each neuron expresses a limited repertoire of clustered Pcdh genes, a complicated process controlled by differential methylation and promoter choice. The clustered Pcdh proteins interact homophilically in trans as cis-multimers, which has the potential to generate a combinatorially explosive number of distinct adhesive interfaces that may give neurons unique molecular identities important for circuit formation. Functional studies of animals in which clustered Pcdhs have been deleted or disrupted demonstrate that these proteins play critical roles in neuronal survival, axon and dendrite arborization, and synaptogenesis. Additionally, they have been implicated in the progression of several cancers, suggesting that basic studies of their function and signaling pathways will have important future clinical applications.
Recent work has shown that γ-Pcdhs can regulate the Wnt signaling pathway, a common tumorigenic pathway which also play roles in neurodevelopment, but the molecular mechanisms remain unknown. I determined that γ-Pcdhs differentially regulate Wnt signaling: the C3 isoform uniquely inhibits the pathway while 13 other isoforms upregulate Wnt signaling. Focusing on γ-Pcdh-C3, I show that the variable cytoplasmic domain (VCD) is critical for Wnt signaling inhibition. γ-Pcdh-C3, but not other isoforms, physically interacts with Axin1, a key component of the canonical Wnt pathway. The C3 VCD competes with Dishevelled for binding to the DIX domain of Axin1, which stabilizes Axin1 at the membrane and leads to reduced phosphorylation of Wnt co-receptor Lrp6. I also present evidence that the Wnt pathway can be modulated up (by γ-Pcdh-A1) or down (by γ-Pcdh-C3) in the cerebral cortex in vivo, using conditional transgenic alleles.
Studies have implicated γ-Pcdhs as a whole, in many neurodevelopmental processes but little is known if distinct roles exists for individual isoforms. By using a specific C3-isoform knockout mouse line engineered in collaboration with Dr. Robert Burgess of The Jackson Laboratory, I was able to uncover a unique role for the C3-isoform in the regulation of dendrite arborization. Mice without γ-Pcdh-C3 exhibit significantly reduced dendrite complexity in cortical neurons. This phenotype was recapitulated in cultured cortical neurons in vitro, which can be rescued by reintroducing the C3-isoform. The ability of γ-Pcdh-C3 to promote dendrite arborization cell-autonomously was abrogated when Axin1 was depleted with an shRNA, indicating that this process by which γ-Pcdh-C3 regulates dendrite arborization is mediated by its interaction with Axin1, which I had previously demonstrated. Together, these data suggest that γ-Pcdh-C3 has unique roles distinct from other γ-Pcdhs, in the regulation of Wnt signaling and dendrite arborization, both of which are mediated by interaction with Axin1.
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Keeler, Austin Byler. "Branching out by sticking together: elucidating mechanisms of gamma-protocadherin control of dendrite arborization." Diss., University of Iowa, 2015. https://ir.uiowa.edu/etd/2230.
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Growth of a properly complex dendrite arbor is a vital step in neuronal differentiation and a prerequisite for normal neural circuit formation; likewise, overly dense or sparse dendrite arbors are a key feature of abnormal neural circuit formation and characteristic of many neurodevelopmental disorders. Thus, identifying factors involved in aberrant dendrite complexity and therefore aberrant circuit formation, are necessary to understanding these disorders. In my doctoral work I have elucidated both intracellular and extracellular aspects to the gamma-protocadherins (γ-Pcdhs) that regulate dendrite complexity.
Loss of the 22 γ-Pcdhs, adhesion molecules that interact homophilically and are expressed combinatorially in neurons and astrocytes, leads to aberrantly high activity of focal adhesion kinase (FAK) and reduced dendrite complexity in cortical neurons. Little is known, however, about how γ-Pcdh function is regulated by other factors. Here I show that PKC phosphorylates a serine residue situated within the shared γ-Pcdh C-terminus; PKC phosphorylation disrupts the γ-Pcdhs’ inhibition of FAK. Additionally, γ-Pcdh phosphorylation or a phosphomimetic mutant reduce dendritic arbors, while blocking γ-Pcdh phosphorylation increases dendrite complexity. Together, these data identify a novel intracellular mechanism through which γ-Pcdh control of a signaling pathway important for dendrite arborization is regulated.
Although specific interactions between diverse cell surface molecules are proposed to regulate circuit formation, the extent to which these promote dendrite growth and branching is unclear. Here, using transgenic mice to manipulate expression in vivo, I and my colleagues show that the complexity of a cortical neuron’s dendritic arbor is regulated by γ-Pcdh isoform matching with surrounding cells. Expression of the same single γ-Pcdh isoform leads to exuberant or minimal arbor complexity depending on matched expression of surrounding cells. Additionally, loss of γ-Pcdhs in astrocytes, or induced mis-matching between astrocytes and neurons, reduces dendrite complexity in a cell non-autonomous manner. Thus, these data support our proposal that γ-Pcdhs create a rare neuronal identity that, depending on the identities of surrounding cells, specifies the complexity of that neuron’s dendritic arbor.
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Dimitrova, Svetla. "Physiological Roles of Robo Receptor during dendrite development of the multidendritic arborization neurons of the Drosophila peripheral nervous system." Diss., lmu, 2007. http://nbn-resolving.de/urn:nbn:de:bvb:19-78347.
Full textBook chapters on the topic "Dendritic arborization"
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Gogan, P., Suzanne Tyč-Dumont, S. M. Korogod, and L. P. Savtchenko. "Functional Connections Between the Architecture of the Dendritic Arborization and the Microarchitecture of the Dendritic Membrane." In Neurobiology, 293–300. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4615-5899-6_23.
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François, Chantal, Jérôme Yelnik, Patricia Arecchi-Bouchhioua, and Gérard Percheron. "Branching Pattern and Geometrical Properties of Dendritic and Axonal Arborizations in the Striato-Pallido-Thalamic System in Macaques." In Advances in Behavioral Biology, 43–50. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4899-0194-1_6.
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Kwon, Ester J., Takahiro Soda, and Li-Huei Tsai. "Neurodevelopment and Schizophrenia." In Neurobiology of Mental Illness, edited by Pamela Sklar, 327–37. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199934959.003.0025.
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A neurodevelopmental model of schizophrenia postulates that some of the key aspects of brain development that normally occur both pre- and post-natally are not occurring correctly, either in time or space. Complex neural circuitry needs to form and be modulated by experience. Classically, proliferation, migration, arborization and myelination occur prenatally. Elaboration and refining of dendritic trees and synapses as well as myelination of the nervous system continues through the first two-decade of life. There are opportunities for genetic and environmental abnormalities and variation to profoundly influence the trajectories of all of these critical functional processes.
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"The Recent Advancement in Rapid Golgi Method and Result Interpretation." In Protocols used in Molecular Biology, edited by Surya Prakash Pandey, Mallikarjuna Rao Gedda, and Abhishek Pathak, 146–52. BENTHAM SCIENCE PUBLISHERS, 2020. http://dx.doi.org/10.2174/9789811439315120010017.
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The foundation knowledge of recent advancements of neuroscience was based on the Golgi staining observations. This is one of the best approaches to visualise the neuronal cytoarchitecture and complete morphology of neurons with incomparable clarity. This technique is based on the principle of heavy metal impregnation. There are many modifications and advancement occurred to improve the visualization. This chapter will provide the recently used protocols to visuals the neuronal architecture, dendritic arborization and spine density in different brain regions. Along with the manual observation, the present chapter also describes the currently used tools and software for the better understanding and visualisation of neurons.
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Iwasaki, Toshiharu, Kingsley Ibhazehiebo, Junko Kimura-Kuroda, Wataru Miyazaki, Noriaki Shimokawa, and Noriyuki Koibuchi. "Disruption of Thyroid Hormone Receptor-Mediated Transcription, Thyroid Hormone-Induced Purkinje Cell Dendrite Arborization and Granule Cell Neurite Extension by Polybrominated Diphenylethers." In BASIC/TRANSLATIONAL - Endocrine-Disrupting Chemicals, P1–91—P1–91. The Endocrine Society, 2011. http://dx.doi.org/10.1210/endo-meetings.2011.part1.p4.p1-91.
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