Journal articles on the topic 'Dendritic cell'
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1
Christie, J. M., and G. L. Westbrook. "Regulation of Backpropagating Action Potentials in Mitral Cell Lateral Dendrites by A-Type Potassium Currents." Journal of Neurophysiology 89, no. 5 (May 1, 2003): 2466–72. http://dx.doi.org/10.1152/jn.00997.2002.
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Dendrodendritic synapses, distributed along mitral cell lateral dendrites, provide powerful and extensive inhibition in the olfactory bulb. Activation of inhibition depends on effective penetration of action potentials into dendrites. Although action potentials backpropagate with remarkable fidelity in apical dendrites, this issue is controversial for lateral dendrites. We used paired somatic and dendritic recordings to measure action potentials in proximal dendritic segments (0–200 μm from soma) and action potential-generated calcium transients to monitor activity in distal dendritic segments (200–600 μm from soma). Somatically elicited action potentials were attenuated in proximal lateral dendrites. The attenuation was not due to impaired access resistance in dendrites or to basal synaptic activity. However, a single somatically elicited action potential was sufficient to evoke a calcium transient throughout the lateral dendrite, suggesting that action potentials reach distal dendritic compartments. Block of A-type potassium channels ( I A) with 4-aminopyridine (10 mM) prevented action potential attenuation in direct recordings and significantly increased dendritic calcium transients, particularly in distal dendritic compartments. Our results suggest that I A may regulate inhibition in the olfactory bulb by controlling action potential amplitudes in lateral dendrites.
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Ligon, Cheryl, Eunju Seong, Ethan J. Schroeder, Nicholas W. DeKorver, Li Yuan, Tammy R. Chaudoin, Yu Cai, Shilpa Buch, Stephen J. Bonasera, and Jyothi Arikkath. "δ-Catenin engages the autophagy pathway to sculpt the developing dendritic arbor." Journal of Biological Chemistry 295, no. 32 (June 17, 2020): 10988–1001. http://dx.doi.org/10.1074/jbc.ra120.013058.
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The development of the dendritic arbor in pyramidal neurons is critical for neural circuit function. Here, we uncovered a pathway in which δ-catenin, a component of the cadherin–catenin cell adhesion complex, promotes coordination of growth among individual dendrites and engages the autophagy mechanism to sculpt the developing dendritic arbor. Using a rat primary neuron model, time-lapse imaging, immunohistochemistry, and confocal microscopy, we found that apical and basolateral dendrites are coordinately sculpted during development. Loss or knockdown of δ-catenin uncoupled this coordination, leading to retraction of the apical dendrite without altering basolateral dendrite dynamics. Autophagy is a key cellular pathway that allows degradation of cellular components. We observed that the impairment of the dendritic arbor resulting from δ-catenin knockdown could be reversed by knockdown of autophagy-related 7 (ATG7), a component of the autophagy machinery. We propose that δ-catenin regulates the dendritic arbor by coordinating the dynamics of individual dendrites and that the autophagy mechanism may be leveraged by δ-catenin and other effectors to sculpt the developing dendritic arbor. Our findings have implications for the management of neurological disorders, such as autism and intellectual disability, that are characterized by dendritic aberrations.
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Chen, Wei R., Gongyu Y. Shen, Gordon M. Shepherd, Michael L. Hines, and Jens Midtgaard. "Multiple Modes of Action Potential Initiation and Propagation in Mitral Cell Primary Dendrite." Journal of Neurophysiology 88, no. 5 (November 1, 2002): 2755–64. http://dx.doi.org/10.1152/jn.00057.2002.
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The mitral cell primary dendrite plays an important role in transmitting distal olfactory nerve input from olfactory glomerulus to the soma-axon initial segment. To understand how dendritic active properties are involved in this transmission, we have combined dual soma and dendritic patch recordings with computational modeling to analyze action-potential initiation and propagation in the primary dendrite. In response to depolarizing current injection or distal olfactory nerve input, fast Na+ action potentials were recorded along the entire length of the primary dendritic trunk. With weak-to-moderate olfactory nerve input, an action potential was initiated near the soma and then back-propagated into the primary dendrite. As olfactory nerve input increased, the initiation site suddenly shifted to the distal primary dendrite. Multi-compartmental modeling indicated that this abrupt shift of the spike-initiation site reflected an independent thresholding mechanism in the distal dendrite. When strong olfactory nerve excitation was paired with strong inhibition to the mitral cell basal secondary dendrites, a small fast prepotential was recorded at the soma, which indicated that an action potential was initiated in the distal primary dendrite but failed to propagate to the soma. As the inhibition became weaker, a “double-spike” was often observed at the dendritic recording site, corresponding to a single action potential at the soma. Simulation demonstrated that, in the course of forward propagation of the first dendritic spike, the action potential suddenly jumps from the middle of the dendrite to the axonal spike-initiation site, leaving the proximal part of primary dendrite unexcited by this initial dendritic spike. As Na+conductances in the proximal dendrite are not activated, they become available to support the back-propagation of the evoked somatic action potential to produce the second dendritic spike. In summary, the balance of spatially distributed excitatory and inhibitory inputs can dynamically switch the mitral cell firing among four different modes: axo-somatic initiation with back-propagation, dendritic initiation either with no forward propagation, forward propagation alone, or forward propagation followed by back-propagation.
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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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Kalb, R. G. "Regulation of motor neuron dendrite growth by NMDA receptor activation." Development 120, no. 11 (November 1, 1994): 3063–71. http://dx.doi.org/10.1242/dev.120.11.3063.
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Spinal motor neurons undergo great changes in morphology, electrophysiology and molecular composition during development. Some of this maturation occurs postnatally when limbs are employed for locomotion, suggesting that neuronal activity may influence motor neuron development. To identify features of motor neurons that might be regulated by activity we first examined the structural development of the rat motor neuron cell body and dendritic tree labeled with cholera toxin-conjugated horseradish peroxidase. The motor neuron cell body and dendrites in the radial and rostrocaudal axes grew progressively over the first month of life. In contrast, the growth of the dendritic arbor/cell and number of dendritic branches was biphasic with overabundant growth followed by regression until the adult pattern was achieved. We next examined the influence of neurotransmission on the development of these motor neuron features. We found that antagonism of the N-methyl-D-aspartate (NMDA) subtype of glutamate receptor inhibited cell body growth and dendritic branching in early postnatal life but had no effect on the maximal extent of dendrite growth in the radial and rostrocaudal axes. The effects of NMDA receptor antagonism on motor neurons and their dendrites was temporally restricted; all of our anatomic measures of dendrite structure were resistant to NMDA receptor antagonism in adults. These results suggest that the establishment of mature motor neuron dendritic architecture results in part from dendrite growth in response to afferent input during a sensitive period in early postnatal life.
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Nithianandam, Vanitha, and Cheng-Ting Chien. "Actin blobs prefigure dendrite branching sites." Journal of Cell Biology 217, no. 10 (July 24, 2018): 3731–46. http://dx.doi.org/10.1083/jcb.201711136.
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The actin cytoskeleton provides structural stability and adaptability to the cell. Neuronal dendrites frequently undergo morphological changes by emanating, elongating, and withdrawing branches. However, the knowledge about actin dynamics in dendrites during these processes is limited. By performing in vivo imaging of F-actin markers, we found that F-actin was highly dynamic and heterogeneously distributed in dendritic shafts with enrichment at terminal dendrites. A dynamic F-actin population that we named actin blobs propagated bidirectionally at an average velocity of 1 µm/min. Interestingly, these actin blobs stalled at sites where new dendrites would branch out in minutes. Overstabilization of F-actin by the G15S mutant abolished actin blobs and dendrite branching. We identified the F-actin–severing protein Tsr/cofilin as a regulator of dynamic actin blobs and branching activity. Hence, actin blob localization at future branching sites represents a dendrite-branching mechanism to account for highly diversified dendritic morphology.
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Sharp, D. J., W. Yu, and P. W. Baas. "Transport of dendritic microtubules establishes their nonuniform polarity orientation." Journal of Cell Biology 130, no. 1 (July 1, 1995): 93–103. http://dx.doi.org/10.1083/jcb.130.1.93.
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The immature processes that give rise to both axons and dendrites contain microtubules (MTs) that are uniformly oriented with their plus-ends distal to the cell body, and this pattern is preserved in the developing axon. In contrast, developing dendrites gradually acquire nonuniform MT polarity orientation due to the addition of a subpopulation of oppositely oriented MTs (Baas, P. W., M. M. Black, and G. A. Banker. 1989. J. Cell Biol. 109:3085-3094). In theory, these minus-end-distal MTs could be locally nucleated and assembled within the dendrite itself, or could be transported into the dendrite after their nucleation within the cell body. To distinguish between these possibilities, we exposed cultured hippocampal neurons to nanomolar levels of vinblastine after one of the immature processes had developed into the axon but before the others had become dendrites. At these levels, vinblastine acts as a kinetic stabilizer of MTs, inhibiting further assembly while not substantially depolymerizing existing MTs. This treatment did not abolish dendritic differentiation, which occurred in timely fashion over the next two to three days. The resulting dendrites were flatter and shorter than controls, but were identifiable by their ultrastructure, chemical composition, and thickened tapering morphology. The growth of these dendrites was accompanied by a diminution of MTs from the cell body, indicating a net transfer of MTs from one compartment into the other. During this time, minus-end-distal microtubules arose in the experimental dendrites, indicating that new MT assembly is not required for the acquisition of nonuniform MT polarity orientation in the dendrite. Minus-end-distal microtubules predominated in the more proximal region of experimental dendrites, indicating that most of the MTs at this stage of development are transported into the dendrite with their minus-ends leading. These observations indicate that transport of MTs from the cell body is an essential feature of dendritic development, and that this transport establishes the nonuniform polarity orientation of MTs in the dendrite.
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Grueber, Wesley B., Lily Y. Jan, and Yuh Nung Jan. "Tiling of the Drosophila epidermis by multidendritic sensory neurons." Development 129, no. 12 (June 15, 2002): 2867–78. http://dx.doi.org/10.1242/dev.129.12.2867.
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Insect dendritic arborization (da) neurons provide an opportunity to examine how diverse dendrite morphologies and dendritic territories are established during development. We have examined the morphologies of Drosophila da neurons by using the MARCM (mosaic analysis with a repressible cell marker) system. We show that each of the 15 neurons per abdominal hemisegment spread dendrites to characteristic regions of the epidermis. We place these neurons into four distinct morphological classes distinguished primarily by their dendrite branching complexities. Some class assignments correlate with known proneural gene requirements as well as with central axonal projections. Our data indicate that cells within two morphological classes partition the body wall into distinct, non-overlapping territorial domains and thus are organized as separate tiled sensory systems. The dendritic domains of cells in different classes, by contrast, can overlap extensively. We have examined the cell-autonomous roles of starry night (stan) (also known as flamingo (fmi)) and sequoia (seq) in tiling. Neurons with these genes mutated generally terminate their dendritic fields at normal locations at the lateral margin and segment border, where they meet or approach the like dendrites of adjacent neurons. However, stan mutant neurons occasionally send sparsely branched processes beyond these territories that could potentially mix with adjacent like dendrites. Together, our data suggest that widespread tiling of the larval body wall involves interactions between growing dendritic processes and as yet unidentified signals that allow avoidance by like dendrites.
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Lin, Chin-Hsien, Hsun Li, Yi-Nan Lee, Ying-Ju Cheng, Ruey-Meei Wu, and Cheng-Ting Chien. "Lrrk regulates the dynamic profile of dendritic Golgi outposts through the golgin Lava lamp." Journal of Cell Biology 210, no. 3 (July 27, 2015): 471–83. http://dx.doi.org/10.1083/jcb.201411033.
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Constructing the dendritic arbor of neurons requires dynamic movements of Golgi outposts (GOPs), the prominent component in the dendritic secretory pathway. GOPs move toward dendritic ends (anterograde) or cell bodies (retrograde), whereas most of them remain stationary. Here, we show that Leucine-rich repeat kinase (Lrrk), the Drosophila melanogaster homologue of Parkinson’s disease–associated Lrrk2, regulates GOP dynamics in dendrites. Lrrk localized at stationary GOPs in dendrites and suppressed GOP movement. In Lrrk loss-of-function mutants, anterograde movement of GOPs was enhanced, whereas Lrrk overexpression increased the pool size of stationary GOPs. Lrrk interacted with the golgin Lava lamp and inhibited the interaction between Lva and dynein heavy chain, thus disrupting the recruitment of dynein to Golgi membranes. Whereas overexpression of kinase-dead Lrrk caused dominant-negative effects on GOP dynamics, overexpression of the human LRRK2 mutant G2019S with augmented kinase activity promoted retrograde movement. Our study reveals a pathogenic pathway for LRRK2 mutations causing dendrite degeneration.
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Leung, Donald Y. M., Harold S. Nelson, Stanley J. Szefler, and William W. Busse. "Langerhans cell–like dendritic cells and inflammatory dendritic epidermal cell–like dendritic cells induce distinct T-cell responses." Journal of Allergy and Clinical Immunology 113, no. 5 (May 2004): 803. http://dx.doi.org/10.1016/j.jaci.2004.03.025.
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Golding, Nace L., William L. Kath, and Nelson Spruston. "Dichotomy of Action-Potential Backpropagation in CA1 Pyramidal Neuron Dendrites." Journal of Neurophysiology 86, no. 6 (December 1, 2001): 2998–3010. http://dx.doi.org/10.1152/jn.2001.86.6.2998.
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In hippocampal CA1 pyramidal neurons, action potentials are typically initiated in the axon and backpropagate into the dendrites, shaping the integration of synaptic activity and influencing the induction of synaptic plasticity. Despite previous reports describing action-potential propagation in the proximal apical dendrites, the extent to which action potentials invade the distal dendrites of CA1 pyramidal neurons remains controversial. Using paired somatic and dendritic whole cell recordings, we find that in the dendrites proximal to 280 μm from the soma, single backpropagating action potentials exhibit <50% attenuation from their amplitude in the soma. However, in dendritic recordings distal to 300 μm from the soma, action potentials in most cells backpropagated either strongly (26–42% attenuation; n = 9/20) or weakly (71–87% attenuation; n = 10/20) with only one cell exhibiting an intermediate value (45% attenuation). In experiments combining dual somatic and dendritic whole cell recordings with calcium imaging, the amount of calcium influx triggered by backpropagating action potentials was correlated with the extent of action-potential invasion of the distal dendrites. Quantitative morphometric analyses revealed that the dichotomy in action-potential backpropagation occurred in the presence of only subtle differences in either the diameter of the primary apical dendrite or branching pattern. In addition, action-potential backpropagation was not dependent on a number of electrophysiological parameters (input resistance, resting potential, voltage sensitivity of dendritic spike amplitude). There was, however, a striking correlation of the shape of the action potential at the soma with its amplitude in the dendrite; larger, faster-rising, and narrower somatic action potentials exhibited more attenuation in the distal dendrites (300–410 μm from the soma). Simple compartmental models of CA1 pyramidal neurons revealed that a dichotomy in action-potential backpropagation could be generated in response to subtle manipulations of the distribution of either sodium or potassium channels in the dendrites. Backpropagation efficacy could also be influenced by local alterations in dendritic side branches, but these effects were highly sensitive to model parameters. Based on these findings, we hypothesize that the observed dichotomy in dendritic action-potential amplitude is conferred primarily by differences in the distribution, density, or modulatory state of voltage-gated channels along the somatodendritic axis.
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A, Bajaji. "Adjunctive and Transformed Immunity: Histiocytic & Dendritic Cell Neoplasm." Gastroenterology & Hepatology International Journal 3, no. 1 (March 23, 2022): 1–10. http://dx.doi.org/10.23880/ghij-16000139.
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Exceptional malignancies of the lymph nodes or soft tissue comprising of < 1% of the tumour incidence are the Histiocytic and Dendritic cell neoplasm. A definitive appearance/biology/ Hematology/ histopathology / exclusive therapeutic options describe the condition. Morphology and Immune reactive appraisal may be mandated to distinguish the neoplasm. Preface: Histiocytic and Dendritic neoplasms are infrequent disorders which incriminate the accessory immune system or mesenchymal cells. Subject to the origin of the neoplasm, from the bone marrow precursors or the mesenchye, the lesions may be categorized as. i) The Histiocytic sarcoma (HS), Langerhans cell histiocytosis(LCH) and the Inter-digitizing dendritic cell sarcoma (IDCS) may commence from the bone marrow precursors and ii) The Follicular dendritic cell sarcoma (FDCS), Intermediate dendritic cell sarcoma (INDCS), Fibroblastic reticular cell tumour (FRCT) and Disseminated juvenile xanthogranuloma(DJX) may emanate from the Stromal or the mesenchymal cell. Divergent differentiation of the bone marrow precursors is a usual manifestation, though hybrid or trans-differentiating malignant lymphoid clones may also materialize in Inter-digitizing dendritic cell sarcoma (IDCS), Histolytic sarcoma (HS) and Follicular dendritic cell sarcoma (FDCS). Together, Histolytic and Dendritic cell tumors constitute < 1% of the lymph node or soft tissue neoplasm. The tumors may be misinterpreted as Non Hodgkin’s Lymphoma or adjunct Lymph-Proliferative disorders. The rare malignancies may be a challenge to discern and medicate. Debatable Histolytic and Dendritic neoplasm mandate a referral. The disorder may be ascertained by the combined analysis on Histology and Immunehistochemistry
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Feng, Chengye, Pankajam Thyagarajan, Matthew Shorey, Dylan Y. Seebold, Alexis T. Weiner, Richard M. Albertson, Kavitha S. Rao, Alvaro Sagasti, Daniel J. Goetschius, and Melissa M. Rolls. "Patronin-mediated minus end growth is required for dendritic microtubule polarity." Journal of Cell Biology 218, no. 7 (May 10, 2019): 2309–28. http://dx.doi.org/10.1083/jcb.201810155.
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Microtubule minus ends are thought to be stable in cells. Surprisingly, in Drosophila and zebrafish neurons, we observed persistent minus end growth, with runs lasting over 10 min. In Drosophila, extended minus end growth depended on Patronin, and Patronin reduction disrupted dendritic minus-end-out polarity. In fly dendrites, microtubule nucleation sites localize at dendrite branch points. Therefore, we hypothesized minus end growth might be particularly important beyond branch points. Distal dendrites have mixed polarity, and reduction of Patronin lowered the number of minus-end-out microtubules. More strikingly, extra Patronin made terminal dendrites almost completely minus-end-out, indicating low Patronin normally limits minus-end-out microtubules. To determine whether minus end growth populated new dendrites with microtubules, we analyzed dendrite development and regeneration. Minus ends extended into growing dendrites in the presence of Patronin. In sum, our data suggest that Patronin facilitates sustained microtubule minus end growth, which is critical for populating dendrites with minus-end-out microtubules.
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Mitchell, Josephine W., Ipek Midillioglu, Ethan Schauer, Bei Wang, Chun Han, and Jill Wildonger. "Coordination of Pickpocket ion channel delivery and dendrite growth in Drosophila sensory neurons." PLOS Genetics 19, no. 11 (November 9, 2023): e1011025. http://dx.doi.org/10.1371/journal.pgen.1011025.
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Sensory neurons enable an organism to perceive external stimuli, which is essential for survival. The sensory capacity of a neuron depends on the elaboration of its dendritic arbor and the localization of sensory ion channels to the dendritic membrane. However, it is not well understood when and how ion channels localize to growing sensory dendrites and whether their delivery is coordinated with growth of the dendritic arbor. We investigated the localization of the DEG/ENaC/ASIC ion channel Pickpocket (Ppk) in the peripheral sensory neurons of developing fruit flies. We used CRISPR-Cas9 genome engineering approaches to tag endogenous Ppk1 and visualize it live, including monitoring Ppk1 membrane localization via a novel secreted split-GFP approach. Fluorescently tagged endogenous Ppk1 localizes to dendrites, as previously reported, and, unexpectedly, to axons and axon terminals. In dendrites, Ppk1 is present throughout actively growing dendrite branches and is stably integrated into the neuronal cell membrane during the expansive growth of the arbor. Although Ppk channels are dispensable for dendrite growth, we found that an over-active channel mutant severely reduces dendrite growth, likely by acting at an internal membrane and not the dendritic membrane. Our data reveal that the molecular motor dynein and recycling endosome GTPase Rab11 are needed for the proper trafficking of Ppk1 to dendrites. Based on our data, we propose that Ppk channel transport is coordinated with dendrite morphogenesis, which ensures proper ion channel density and distribution in sensory dendrites.
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Schutter, Erik De. "Dendritic Voltage and Calcium-Gated Channels Amplify the Variability of Postsynaptic Responses in a Purkinje Cell Model." Journal of Neurophysiology 80, no. 2 (August 1, 1998): 504–19. http://dx.doi.org/10.1152/jn.1998.80.2.504.
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De Schutter, Erik. Dendritic voltage and calcium-gated channels amplify the variability of postsynaptic responses in a Purkinje cell model. J. Neurophysiol. 80: 504–519, 1998. The dendrites of most neurons express several types of voltage and Ca2+-gated channels. These ionic channels can be activated by subthreshold synaptic input, but the functional role of such activations in vivo is unclear. The interaction between dendritic channels and synaptic background input as it occurs in vivo was studied in a realistic computer model of a cerebellar Purkinje cell. It previously was shown using this model that dendritic Ca2+ channels amplify the somatic response to synchronous excitatory inputs. In this study, it is shown that dendritic ion channels also increased the somatic membrane potential fluctuations generated by the background input. This amplification caused a highly variable somatic excitatory postsynaptic potential (EPSP) in response to a synchronous excitatory input. The variability scaled with the size of the response in the model with excitable dendrite, resulting in an almost constant coefficient of variation, whereas in a passive model the membrane potential fluctuations simply added onto the EPSP. Although the EPSP amplitude in the active dendrite model was quite variable for different patterns of background input, it was insensitive to changes in the timing of the synchronous input by a few milliseconds. This effect was explained by slow changes in dendritic excitability. This excitability was determined by how the background input affected the dendritic membrane potentials in the preceding 10–20 ms, causing changes in activation of voltage and Ca2+-gated channels. The most important model variables determining the excitability at the time of a synchronous input were the Ca2+-activation of K+ channels and the inhibitory synaptic conductance, although many other model variables could be influential for particular background patterns. Experimental evidence for the amplification of postsynaptic variability by active dendrites is discussed. The amplification of the variability of EPSPs has important functional consequences in general and for cerebellar Purkinje cells specifically. Subthreshold, background input has a much larger effect on the responses to coherent input of neurons with active dendrites compared with passive dendrites because it can change the effective threshold for firing. This gives neurons with dendritic calcium channels an increased information processing capacity and provides the Purkinje cell with a gating function.
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Çelenk, Fatih. "Follicular dendritic cell sarcoma of the palatine tonsil." Praxis of Otorhinolaryngology 1, no. 2 (October 25, 2013): 81–84. http://dx.doi.org/10.5606/kbbu.2013.36844.
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Arroyo Hornero, Rebeca, and Juliana Idoyaga. "Plasmacytoid dendritic cells: A dendritic cell in disguise." Molecular Immunology 159 (July 2023): 38–45. http://dx.doi.org/10.1016/j.molimm.2023.05.007.
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Alizzi, Rebecca A., Derek Xu, Conrad M. Tenenbaum, Wei Wang, and Elizabeth R. Gavis. "The ELAV/Hu protein Found in neurons regulates cytoskeletal and ECM adhesion inputs for space-filling dendrite growth." PLOS Genetics 16, no. 12 (December 28, 2020): e1009235. http://dx.doi.org/10.1371/journal.pgen.1009235.
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Dendritic arbor morphology influences how neurons receive and integrate extracellular signals. We show that the ELAV/Hu family RNA-binding protein Found in neurons (Fne) is required for space-filling dendrite growth to generate highly branched arbors of Drosophila larval class IV dendritic arborization neurons. Dendrites of fne mutant neurons are shorter and more dynamic than in wild-type, leading to decreased arbor coverage. These defects result from both a decrease in stable microtubules and loss of dendrite-substrate interactions within the arbor. Identification of transcripts encoding cytoskeletal regulators and cell-cell and cell-ECM interacting proteins as Fne targets using TRIBE further supports these results. Analysis of one target, encoding the cell adhesion protein Basigin, indicates that the cytoskeletal defects contributing to branch instability in fne mutant neurons are due in part to decreased Basigin expression. The ability of Fne to coordinately regulate the cytoskeleton and dendrite-substrate interactions in neurons may shed light on the behavior of cancer cells ectopically expressing ELAV/Hu proteins.
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Velte, Toby J., and Richard H. Masland. "Action Potentials in the Dendrites of Retinal Ganglion Cells." Journal of Neurophysiology 81, no. 3 (March 1, 1999): 1412–17. http://dx.doi.org/10.1152/jn.1999.81.3.1412.
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Action potentials in the dendrites of retinal ganglion cells. The somas and dendrites of intact retinal ganglion cells were exposed by enzymatic removal of the overlying endfeet of the Müller glia. Simultaneous whole cell patch recordings were made from a ganglion cell’s dendrite and the cell’s soma. When a dendrite was stimulated with depolarizing current, impulses often propagated to the soma, where they appeared as a mixture of small depolarizations and action potentials. When the soma was stimulated, action potentials always propagated back through the dendrite. The site of initiation of action potentials, as judged by their timing, could be shifted between soma and dendrite by changing the site of stimulation. Applying QX-314 to the soma could eliminate somatic action potentials while leaving dendritic impulses intact. The absolute amplitudes of the dendritic action potentials varied somewhat at different distances from the soma, and it is not clear whether these variations are real or technical. Nonetheless, the qualitative experiments clearly suggest that the dendrites of retinal ganglion cells generate regenerative Na+ action potentials, at least in response to large direct depolarizations.
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Fernandez, Fernando R., W. Hamish Mehaffey, and Ray W. Turner. "Dendritic Na+ Current Inactivation Can Increase Cell Excitability By Delaying a Somatic Depolarizing Afterpotential." Journal of Neurophysiology 94, no. 6 (December 2005): 3836–48. http://dx.doi.org/10.1152/jn.00653.2005.
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Many central neurons support active dendritic spike backpropagation mediated by voltage-gated currents. Active spikes in dendrites have been shown capable of providing feedback to the soma to influence somatic excitability and firing dynamics through a depolarizing afterpotential (DAP). In pyramidal cells of the electrosensory lobe of weakly electric fish, Na+ spikes in dendrites undergo a frequency-dependent broadening that enhances the DAP to increase somatic firing frequency. We use a combination of dynamical analysis and electrophysiological recordings to demonstrate that spike broadening in dendrites is primarily caused by a cumulative inactivation of dendritic Na+ current. We further show that a reduction in dendritic Na+ current increases excitability by decreasing the interspike interval and promoting burst firing. This process arises when inactivation of dendritic Na+ current shifts the latency of the dendritic spike to delay the arrival of the DAP sufficiently to increase its impact on somatic membrane potential despite a reduction in dendritic excitability. Furthermore, the relationship between dendritic Na+ current density and somatic excitability is nonmonotonic, as intermediate levels of dendritic Na+ current exert the greatest excitatory influence. These results reveal that temporal shifts in dendritic spike firing provide a novel means for backpropagating spikes to influence the final output of a cell.
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Kato, Mizuki, and Erik De Schutter. "Models of Purkinje cell dendritic tree selection during early cerebellar development." PLOS Computational Biology 19, no. 7 (July 24, 2023): e1011320. http://dx.doi.org/10.1371/journal.pcbi.1011320.
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We investigate the relationship between primary dendrite selection of Purkinje cells and migration of their presynaptic partner granule cells during early cerebellar development. During postnatal development, each Purkinje cell grows more than three dendritic trees, from which a primary tree is selected for development, whereas the others completely retract. Experimental studies suggest that this selection process is coordinated by physical and synaptic interactions with granule cells, which undergo a massive migration at the same time. However, technical limitations hinder continuous experimental observation of multiple cell populations. To explore possible mechanisms underlying this selection process, we constructed a computational model using a new computational framework, NeuroDevSim. The study presents the first computational model that simultaneously simulates Purkinje cell growth and the dynamics of granule cell migrations during the first two postnatal weeks, allowing exploration of the role of physical and synaptic interactions upon dendritic selection. The model suggests that interaction with parallel fibers is important to establish the distinct planar morphology of Purkinje cell dendrites. Specific rules to select which dendritic trees to keep or retract result in larger winner trees with more synaptic contacts than using random selection. A rule based on afferent synaptic activity was less effective than rules based on dendritic size or numbers of synapses.
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Kilo, Lukas, Tomke Stürner, Gaia Tavosanis, and Anna B. Ziegler. "Drosophila Dendritic Arborisation Neurons: Fantastic Actin Dynamics and Where to Find Them." Cells 10, no. 10 (October 16, 2021): 2777. http://dx.doi.org/10.3390/cells10102777.
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Neuronal dendrites receive, integrate, and process numerous inputs and therefore serve as the neuron’s “antennae”. Dendrites display extreme morphological diversity across different neuronal classes to match the neuron’s specific functional requirements. Understanding how this structural diversity is specified is therefore important for shedding light on information processing in the healthy and diseased nervous system. Popular models for in vivo studies of dendrite differentiation are the four classes of dendritic arborization (c1da–c4da) neurons of Drosophila larvae with their class-specific dendritic morphologies. Using da neurons, a combination of live-cell imaging and computational approaches have delivered information on the distinct phases and the time course of dendrite development from embryonic stages to the fully developed dendritic tree. With these data, we can start approaching the basic logic behind differential dendrite development. A major role in the definition of neuron-type specific morphologies is played by dynamic actin-rich processes and the regulation of their properties. This review presents the differences in the growth programs leading to morphologically different dendritic trees, with a focus on the key role of actin modulatory proteins. In addition, we summarize requirements and technological progress towards the visualization and manipulation of such actin regulators in vivo.
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Kloosterman, Fabian, Pascal Peloquin, and L. Stan Leung. "Apical and Basal Orthodromic Population Spikes in Hippocampal CA1 In Vivo Show Different Origins and Patterns of Propagation." Journal of Neurophysiology 86, no. 5 (November 1, 2001): 2435–44. http://dx.doi.org/10.1152/jn.2001.86.5.2435.
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There is controversy concerning whether orthodromic action potentials originate from the apical or basal dendrites of CA1 pyramidal cells in vivo. The participation of the dendrites in the initialization and propagation of population spikes in CA1 of urethan-anesthetized rats in vivo was studied using simultaneously recorded field potentials and current source density (CSD) analysis. CSD analysis revealed that the antidromic population spike, evoked by stimulation of the alveus, invaded in succession, the axon initial segment (stratum oriens), cell body and ∼200 μm of the proximal apical dendrites. Excitation of the basal dendrites of CA1, following stimulation of CA3 stratum oriens, evoked an orthodromic spike that started near the cell body or initial segment and then propagated ∼200 μm into the proximal apical dendrites. In contrast, the population spike that followed excitation of the apical dendrites of CA1 initiated at the proximal apical dendrites, 50–100 μm distal to the cell body layer, and then propagated centripetally to the cell body and the proximal basal dendrites. A late apical dendritic spike may arise in the mid-apical dendrites (250–300 μm from the cell layer) and propagated distally. The origin or the pattern of propagation of each population spike type was similar for near-threshold to supramaximal stimulus intensities. In summary, population spikes following apical dendritic and basal dendritic excitation in vivo appeared to originate from different locations. Apical dendritic excitation evoked a population spike that initiated in the proximal apical dendrites while basal dendritic excitation evoked a spike that started near the initial segment or cell body. An original finding of this study is the propagation of the population spike from basal to apical dendrites in vivo or vice versa. This backpropagation from one dendritic tree to the other may play an important role in the synaptic plasticity among a network of CA3 to CA1 neurons.
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Hong, Li, Tonya J. Webb, and David S. Wilkes. "Dendritic cell–T cell interactions: CD8αα expressed on dendritic cells regulates T cell proliferation." Immunology Letters 108, no. 2 (February 2007): 174–78. http://dx.doi.org/10.1016/j.imlet.2006.12.003.
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Zagha, Edward, Satoshi Manita, William N. Ross, and Bernardo Rudy. "Dendritic Kv3.3 Potassium Channels in Cerebellar Purkinje Cells Regulate Generation and Spatial Dynamics of Dendritic Ca2+ Spikes." Journal of Neurophysiology 103, no. 6 (June 2010): 3516–25. http://dx.doi.org/10.1152/jn.00982.2009.
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Purkinje cell dendrites are excitable structures with intrinsic and synaptic conductances contributing to the generation and propagation of electrical activity. Voltage-gated potassium channel subunit Kv3.3 is expressed in the distal dendrites of Purkinje cells. However, the functional relevance of this dendritic distribution is not understood. Moreover, mutations in Kv3.3 cause movement disorders in mice and cerebellar atrophy and ataxia in humans, emphasizing the importance of understanding the role of these channels. In this study, we explore functional implications of this dendritic channel expression and compare Purkinje cell dendritic excitability in wild-type and Kv3.3 knockout mice. We demonstrate enhanced excitability of Purkinje cell dendrites in Kv3.3 knockout mice, despite normal resting membrane properties. Combined data from local application pharmacology, voltage clamp analysis of ionic currents, and assessment of dendritic Ca2+ spike threshold in Purkinje cells suggest a role for Kv3.3 channels in opposing Ca2+ spike initiation. To study the physiological relevance of altered dendritic excitability, we measured [Ca2+]i changes throughout the dendritic tree in response to climbing fiber activation. Ca2+ signals were specifically enhanced in distal dendrites of Kv3.3 knockout Purkinje cells, suggesting a role for dendritic Kv3.3 channels in regulating propagation of electrical activity and Ca2+ influx in distal dendrites. These findings characterize unique roles of Kv3.3 channels in dendrites, with implications for synaptic integration, plasticity, and human disease.
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Komendantov, Alexander O., and Giorgio A. Ascoli. "Dendritic Excitability and Neuronal Morphology as Determinants of Synaptic Efficacy." Journal of Neurophysiology 101, no. 4 (April 2009): 1847–66. http://dx.doi.org/10.1152/jn.01235.2007.
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The ability to trigger neuronal spiking activity is one of the most important functional characteristics of synaptic inputs and can be quantified as a measure of synaptic efficacy (SE). Using model neurons with both highly simplified and real morphological structures (from a single cylindrical dendrite to a hippocampal granule cell, CA1 pyramidal cell, spinal motoneuron, and retinal ganglion neurons) we found that SE of excitatory inputs decreases with the distance from the soma and active nonlinear properties of the dendrites can counterbalance this global effect of attenuation. This phenomenon is frequency dependent, with a more prominent gain in SE observed at lower levels of background input–output neuronal activity. In contrast, there are no significant differences in SE between passive and active dendrites under higher frequencies of background activity. The influence of the nonuniform distribution of active properties on SE is also more prominent at lower background frequencies. In models with real morphologies, the effect of active dendritic conductances becomes more dramatic and inverts the SE relationship between distal and proximal locations. In active dendrites, distal synapses have higher efficacy than that of proximal ones because of arising dendritic spiking in thin branches with high-input resistance. Lower levels of dendritic excitability can make SE independent of the distance from the soma. Although increasing dendritic excitability may boost SE of distal synapses in real neurons, it may actually reduce overall SE. The results are robust with respect to morphological variation and biophysical properties of the model neurons. The model of CA1 pyramidal cell with realistic distributions of dendritic conductances demonstrated important roles of hyperpolarization-activated (h-) current and A-type K+ current in controlling the efficacy of single synaptic inputs and overall SE differently in basal and apical dendrites.
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Li, Haimin, Gang Chen, Bing Zhou, and Shumin Duan. "Actin Filament Assembly by Myristoylated, Alanine-rich C Kinase Substrate–Phosphatidylinositol-4,5-diphosphate Signaling Is Critical for Dendrite Branching." Molecular Biology of the Cell 19, no. 11 (November 2008): 4804–13. http://dx.doi.org/10.1091/mbc.e08-03-0294.
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Dendrites undergo extensive growth and branching at early stages, but relatively little is known about the molecular mechanisms underlying these processes. Here, we show that increasing the level of myristoylated, alanine-rich C kinase substrate (MARCKS), a prominent substrate of protein kinase C and a phosphatidylinositol-4,5-diphosphate [PI(4,5)P2] sequestration protein highly expressed in the brain, enhanced branching and growth of dendrites both in vitro and in vivo. Conversely, knockdown of endogenous MARCKS by RNA interference reduced dendritic arborization. Results from expression of different mutants indicated that membrane binding is essential for MARCKS-induced dendritic morphogenesis. Furthermore, MARCKS increased the number and length of filamentous actin-based filopodia along neurites, as well as the motility of filopodia, in a PI(4,5)P2-dependent manner. Time-lapse imaging showed that MARCKS increased frequency of filopodia initiation but did not affect filopodia longevity, suggesting that MARCKS may increase dendritic branching through its action on filopodia initiation. These findings demonstrate a critical role for MARCKS–PI(4,5)P2 signaling in regulating dendrite development.
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Ljunggren, Hans-Gustaf. "Dendritic cells, dendritic cell-based vaccines and Ralph Steinman." Journal of Internal Medicine 271, no. 2 (December 30, 2011): 174–76. http://dx.doi.org/10.1111/j.1365-2796.2011.02495.x.
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Yuan, Q., and T. Knöpfel. "Olfactory Nerve Stimulation-Induced Calcium Signaling in the Mitral Cell Distal Dendritic Tuft." Journal of Neurophysiology 95, no. 4 (April 2006): 2417–26. http://dx.doi.org/10.1152/jn.00964.2005.
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Olfactory receptor neuron axons form the olfactory nerve (ON) and project to the glomerular layer of the olfactory bulb, where they form excitatory synapses with terminal arborizations of the mitral cell (MC) tufted primary dendrite. Clusters of MC dendritic tufts define olfactory glomeruli, where they involve in complex synaptic interactions. The computational function of these cellular interactions is not clear. We used patch-clamp electrophysiology combined with whole field or two-photon Ca2+ imaging to study ON stimulation-induced Ca2+ signaling at the level of individual terminal branches of the MC primary dendrite in mice. ON-evoked subthreshold excitatory postsnaptic potentials induced Ca2+ transients in the MC tuft dendrites that were spatially inhomogeneous, exhibiting discrete “hot spots.” In contrast, Ca2+ transients induced by backpropagating action potentials occurred throughout the dendritic tuft, being larger in the thin terminal dendrites than in the base of the tuft. Single ON stimulation-induced Ca2+ transients were depressed by the NMDA receptor antagonist d-aminophosphonovaleric acid (d-APV), increased with increasing stimulation intensity, and typically showed a prolonged rising phase. The synaptically induced Ca2+ signals reflect, at least in part, dendrodendritic interactions that support intraglomerular coupling of MCs and generation of an output that is common to all MCs associated with one glomerulus.
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Foley, J. F. "From Dendrite to Dendritic." Science Signaling 1, no. 17 (April 29, 2008): ec152-ec152. http://dx.doi.org/10.1126/stke.117ec152.
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Sharp, David J., Wenqian Yu, Lotfi Ferhat, Ryoko Kuriyama, David C. Rueger, and Peter W. Baas. "Identification of a Microtubule-associated Motor Protein Essential for Dendritic Differentiation." Journal of Cell Biology 138, no. 4 (August 25, 1997): 833–43. http://dx.doi.org/10.1083/jcb.138.4.833.
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The quintessential feature of the dendritic microtubule array is its nonuniform pattern of polarity orientation. During the development of the dendrite, a population of plus end–distal microtubules first appears, and these microtubules are subsequently joined by a population of oppositely oriented microtubules. Studies from our laboratory indicate that the latter microtubules are intercalated within the microtubule array by their specific transport from the cell body of the neuron during a critical stage in development (Sharp, D.J., W. Yu, and P.W. Baas. 1995. J. Cell Biol. 130:93– 104). In addition, we have established that the mitotic motor protein termed CHO1/MKLP1 has the appropriate properties to transport microtubules in this manner (Sharp, D.J., R. Kuriyama, and P.W. Baas. 1996. J. Neurosci. 16:4370–4375). In the present study we have sought to determine whether CHO1/MKLP1 continues to be expressed in terminally postmitotic neurons and whether it is required for the establishment of the dendritic microtubule array. In situ hybridization analyses reveal that CHO1/MKLP1 is expressed in postmitotic cultured rat sympathetic and hippocampal neurons. Immunofluorescence analyses indicate that the motor is absent from axons but is enriched in developing dendrites, where it appears as discrete patches associated with the microtubule array. Treatment of the neurons with antisense oligonucleotides to CHO1/MKLP1 suppresses dendritic differentiation, presumably by inhibiting the establishment of their nonuniform microtubule polarity pattern. We conclude that CHO1/MKLP1 transports microtubules from the cell body into the developing dendrite with their minus ends leading, thereby establishing the nonuniform microtubule polarity pattern of the dendrite.
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Rolland, Alexandre, Lydie Guyon, Michelle Gill, Yi-Hong Cai, Jacques Banchereau, Kenneth McClain, and A. Karolina Palucka. "Increased Blood Myeloid Dendritic Cells and Dendritic Cell-Poietins in Langerhans Cell Histiocytosis." Journal of Immunology 174, no. 5 (February 22, 2005): 3067–71. http://dx.doi.org/10.4049/jimmunol.174.5.3067.
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Göbel, Werner, and Fritjof Helmchen. "New Angles on Neuronal Dendrites In Vivo." Journal of Neurophysiology 98, no. 6 (December 2007): 3770–79. http://dx.doi.org/10.1152/jn.00850.2007.
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Imaging technologies are well suited to study neuronal dendrites, which are key elements for synaptic integration in the CNS. Dendrites are, however, frequently oriented perpendicular to tissue surfaces, impeding in vivo imaging approaches. Here we introduce novel laser-scanning modes for two-photon microscopy that enable in vivo imaging of spatiotemporal activity patterns in dendrites. First, we developed a method to image planes arbitrarily oriented in 3D, which proved particularly beneficial for calcium imaging of parallel fibers and Purkinje cell dendrites in rat cerebellar cortex. Second, we applied free linescans—either through multiple dendrites or along a single vertically oriented dendrite—to reveal fast dendritic calcium dynamics in neocortical pyramidal neurons. Finally, we invented a ribbon-type 3D scanning method for imaging user-defined convoluted planes enabling simultaneous measurements of calcium signals along multiple apical dendrites. These novel scanning modes will facilitate optical probing of dendritic function in vivo.
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Szakal, A. K., R. L. Gieringer, M. H. Kosco, and J. G. Tew. "Isolated follicular dendritic cells: cytochemical antigen localization, Nomarski, SEM, and TEM morphology." Journal of Immunology 134, no. 3 (March 1, 1985): 1349–59. http://dx.doi.org/10.4049/jimmunol.134.3.1349.
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Abstract The objectives of the present study were to determine the cytological features of isolated follicular dendritic cells (FDC), which distinguish them from other leukocytes or dendritic cell types. Consequently, we have developed methods for the fixation, peroxidase cytochemistry, and visualization of FDC, which are applicable to cytological evaluations by Nomarski optics, scanning, and transmission electron microscopy. A functionally supported identification of FDC in vitro was made possible by utilizing, in conjunction with the dendritic morphology, the cytochemically identifiable antigen, horseradish peroxidase (HRP), and the known capacity of FDC to sequester immune complexes (i.e. HRP-anti-HRP) on their plasma membranes. The observations showed that FDC constitute a relatively pleomorphic, nonphagocytic group, distinct from other dendritic type cells such as lymphoid dendritic cells, Langerhans cells, and interdigitating cells (LDC, LC, and IDC), as well as typical leukocytes. Morphologically distinct FDC were identified as cells either with filiform dendrites or with "beaded" dendrites. FDC possessed a single or sometimes a double, lymphocyte-size cell body, which contained an irregular, lobated nucleus, Golgi apparatus, numerous small vesicles, and some mitochondria. Mitochondria were not abundant in the dendritic processes. Filiform dendrites tended to branch and anastomose near the cell body and form a radiating "sunburst"-like pattern. On the average, dendrites measured 15-20 microns in length and 0.1-0.3 micron in diameter. Occasional dendrites were extremely elongated, reached several hundred microns in length, and terminated in an enlargement measuring nearly a micron in diameter. Other filiform dendrites usually had a club-shaped terminal enlargement. The microspheres of "beaded" dendrites ranged between 0.3 and 0.6 micron in diameter. The dendritic processes were also shown to have a highly ordered pattern of immune complex attachment on their surface, suggestive of a periodic arrangement of receptor sites.
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Hamze, Kassem, Sabine Autret, Krzysztof Hinc, Soumaya Laalami, Daria Julkowska, Romain Briandet, Margareth Renault, et al. "Single-cell analysis in situ in a Bacillus subtilis swarming community identifies distinct spatially separated subpopulations differentially expressing hag (flagellin), including specialized swarmers." Microbiology 157, no. 9 (September 1, 2011): 2456–69. http://dx.doi.org/10.1099/mic.0.047159-0.
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The non-domesticated Bacillus subtilis strain 3610 displays, over a wide range of humidity, hyper-branched, dendritic, swarming-like migration on a minimal agar medium. At high (70 %) humidity, the laboratory strain 168 sfp + (producing surfactin) behaves very similarly, although this strain carries a frameshift mutation in swrA, which another group has shown under their conditions (which include low humidity) is essential for swarming. We reconcile these different results by demonstrating that, while swrA is essential for dendritic migration at low humidity (30–40 %), it is dispensable at high humidity. Dendritic migration (flagella- and surfactin-dependent) of strains 168 sfp + swrA and 3610 involves elongation of dendrites for several hours as a monolayer of cells in a thin fluid film. This enabled us to determine in situ the spatiotemporal pattern of expression of some key players in migration as dendrites develop, using gfp transcriptional fusions for hag (encoding flagellin), comA (regulation of surfactin synthesis) as well as eps (exopolysaccharide synthesis). Quantitative (single-cell) analysis of hag expression in situ revealed three spatially separated subpopulations or cell types: (i) networks of chains arising early in the mother colony (MC), expressing eps but not hag; (ii) largely immobile cells in dendrite stems expressing intermediate levels of hag; and (iii) a subpopulation of cells with several distinctive features, including very low comA expression but hyper-expression of hag (and flagella). These specialized cells emerge from the MC to spearhead the terminal 1 mm of dendrite tips as swirling and streaming packs, a major characteristic of swarming migration. We discuss a model for this swarming process, emphasizing the importance of population density and of the complementary roles of packs of swarmers driving dendrite extension, while non-mobile cells in the stems extend dendrites by multiplication.
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M.D. Pathology, Vishal Dhingra. "Follicular Dendritic Cell Sarcoma in Colon: A Rare Case Report." Journal of Medical Science And clinical Research 05, no. 04 (April 8, 2017): 20035–38. http://dx.doi.org/10.18535/jmscr/v5i4.50.
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Lam, Y. W., C. L. Cox, C. Varela, and S. Murray Sherman. "Morphological Correlates of Triadic Circuitry in the Lateral Geniculate Nucleus of Cats and Rats." Journal of Neurophysiology 93, no. 2 (February 2005): 748–57. http://dx.doi.org/10.1152/jn.00256.2004.
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We used an in vitro slice preparation of the lateral geniculate nucleus in cats and rats to study morphological correlates of triadic circuitry in relay cells. The three triadic elements involve a retinal synapse onto a GABAergic dendritic terminal of an interneuron, a synapse from the same retinal terminal onto a relay cell dendrite, and a synapse from the same interneuron terminal onto the same relay cell dendrite. We made whole cell recordings and labeled cells with biocytin. Previous methods were used to identify triadic circuitry based on evidence that the retinal terminal activates a metabotropic glutamate receptor on the interneuronal terminal. Thus application of (±)-1-aminocyclopentane- trans-1,3-dicarboxylic acid (an agonist to that receptor) increases the rate of spontaneous inhibitory postsynaptic currents (sIPSCs) recorded in the relay cell, and if some of this increase remains with further addition of TTX (a TTX-insensitive response), a triad is indicated. We quantified the extent of the TTX-insensitive response and sought morphological correlates. In both rats and cats, this response correlated (negatively) with the number of primary dendrites and (positively) with polarity of the dendritic arbor. There was no correlation with cell size. Curiously, in cats, this response correlated with the presence of appendages at primary dendritic branches, but there was no such correlation in rats. These observations in cats map onto the X/Y classification, with X cells having triads, but it is not clear from our results if a comparable classification exists for rats.
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Yap, Chan Choo, Laura Digilio, Lloyd P. McMahon, A. Denise R. Garcia, and Bettina Winckler. "Degradation of dendritic cargos requires Rab7-dependent transport to somatic lysosomes." Journal of Cell Biology 217, no. 9 (June 15, 2018): 3141–59. http://dx.doi.org/10.1083/jcb.201711039.
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Neurons are large and long lived, creating high needs for regulating protein turnover. Disturbances in proteostasis lead to aggregates and cellular stress. We characterized the behavior of the short-lived dendritic membrane proteins Nsg1 and Nsg2 to determine whether these proteins are degraded locally in dendrites or centrally in the soma. We discovered a spatial heterogeneity of endolysosomal compartments in dendrites. Early EEA1-positive and late Rab7-positive endosomes are found throughout dendrites, whereas the density of degradative LAMP1- and cathepsin (Cat) B/D–positive lysosomes decreases steeply past the proximal segment. Unlike in fibroblasts, we found that the majority of dendritic Rab7 late endosomes (LEs) do not contain LAMP1 and that a large proportion of LAMP1 compartments do not contain CatB/D. Second, Rab7 activity is required to mobilize distal predegradative LEs for transport to the soma and terminal degradation. We conclude that the majority of dendritic LAMP1 endosomes are not degradative lysosomes and that terminal degradation of dendritic cargos such as Nsg1, Nsg2, and DNER requires Rab7-dependent transport in LEs to somatic lysosomes.
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Moulin, V., M. E. Morgan, D. Eleveld-Trancikova, J. B. A. G. Haanen, E. Wielders, M. W. G. Looman, R. A. J. Janssen, C. G. Figdor, B. J. H. Jansen, and G. J. Adema. "Targeting dendritic cells with antigen via dendritic cell-associated promoters." Cancer Gene Therapy 19, no. 5 (February 24, 2012): 303–11. http://dx.doi.org/10.1038/cgt.2012.2.
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Jacobs, B., M. Wuttke, C. Papewalis, J. Seissler, and M. Schott. "Dendritic Cell Subtypes and In Vitro Generation of Dendritic Cells." Hormone and Metabolic Research 40, no. 2 (February 2008): 99–107. http://dx.doi.org/10.1055/s-2007-1022561.
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Chen, Keqiang, Ji Ming Wang, Ruoxi Yuan, Xiang Yi, Liangzhu Li, Wanghua Gong, Tianshu Yang, Liwu Li, and Shaobo Su. "Tissue-resident dendritic cells and diseases involving dendritic cell malfunction." International Immunopharmacology 34 (May 2016): 1–15. http://dx.doi.org/10.1016/j.intimp.2016.02.007.
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Audiger, Cindy, and Sylvie Lesage. "Merocytic dendritic cell: a new subset of conventional dendritic cells." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 118.11. http://dx.doi.org/10.4049/jimmunol.202.supp.118.11.
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Abstract Conventional dendritic cells (cDC) are potent antigen-presenting cells that induce the activation of naïve T cells in response to pathogens. cDC activity is mediated primarily by two cDC subsets, namely cDC1 and cDC2, each bearing unique properties. Recently, another DC subset, termed merocytic dendritic cells (mcDC), was defined. In contrast to both cDC1 and cDC2, mcDC are able to reverse T cell anergy, even in non-inflammatory conditions, properties that could be exploited to potentiate cancer treatments. Here, we further characterize mcDC to determine their relationship to cDCs. First, we demonstrate that mcDC express key cDC traits, namely they express the cDC-restricted transcription factor, Zbtb46, and are very potent inducers of mixed lymphocyte reactions. Second, transcriptomic studies reveal that mcDC are more closely related to cDC1 than to cDC2. In contrast, similar to cDC2, mcDC are dependent on IRF4, but not IRF8 and BATF3, two major transcription factors required for cDC1 differentiation. Third, investigating mcDC population dynamics in reconstitution kinetics studies and in parabiotic mice, we demonstrate that, as for cDC1 and cDC2, mcDCs are terminally differentiated cells. Altogether, these data demonstrate that mcDC compose novel cDC subset. Defining the properties of mcDC in mice may help identify a functionally equivalent subset in humans leading to the development of novel cancer immunotherapies.
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Kelliher, Michael T., Yang Yue, Ashley Ng, Daichi Kamiyama, Bo Huang, Kristen J. Verhey, and Jill Wildonger. "Autoinhibition of kinesin-1 is essential to the dendrite-specific localization of Golgi outposts." Journal of Cell Biology 217, no. 7 (May 4, 2018): 2531–47. http://dx.doi.org/10.1083/jcb.201708096.
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Neuronal polarity relies on the selective localization of cargo to axons or dendrites. The molecular motor kinesin-1 moves cargo into axons but is also active in dendrites. This raises the question of how kinesin-1 activity is regulated to maintain the compartment-specific localization of cargo. Our in vivo structure–function analysis of endogenous Drosophila melanogaster kinesin-1 reveals a novel role for autoinhibition in enabling the dendrite-specific localization of Golgi outposts. Mutations that disrupt kinesin-1 autoinhibition result in the axonal mislocalization of Golgi outposts. Autoinhibition also regulates kinesin-1 localization. Uninhibited kinesin-1 accumulates in axons and is depleted from dendrites, correlating with the change in outpost distribution and dendrite growth defects. Genetic interaction tests show that a balance of kinesin-1 inhibition and dynein activity is necessary to localize Golgi outposts to dendrites and keep them from entering axons. Our data indicate that kinesin-1 activity is precisely regulated by autoinhibition to achieve the selective localization of dendritic cargo.
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Shibata, A., M. V. Wright, S. David, L. McKerracher, P. E. Braun, and S. B. Kater. "Unique Responses of Differentiating Neuronal Growth Cones to Inhibitory Cues Presented by Oligodendrocytes." Journal of Cell Biology 142, no. 1 (July 13, 1998): 191–202. http://dx.doi.org/10.1083/jcb.142.1.191.
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During central nervous system development, neurons differentiate distinct axonal and dendritic processes whose outgrowth is influenced by environmental cues. Given the known intrinsic differences between axons and dendrites and that little is known about the response of dendrites to inhibitory cues, we tested the hypothesis that outgrowth of differentiating axons and dendrites of hippocampal neurons is differentially influenced by inhibitory environmental cues. A sensitive growth cone behavior assay was used to assess responses of differentiating axonal and dendritic growth cones to oligodendrocytes and oligodendrocyte- derived, myelin-associated glycoprotein (MAG). We report that >90% of axonal growth cones collapsed after contact with oligodendrocytes. None of the encounters between differentiating, MAP-2 positive dendritic growth cones and oligodendrocytes resulted in growth cone collapse. The insensitivity of differentiating dendritic growth cones appears to be acquired since they develop from minor processes whose growth cones are inhibited (nearly 70% collapse) by contact with oligodendrocytes. Recombinant MAG(rMAG)-coated beads caused collapse of 72% of axonal growth cones but only 29% of differentiating dendritic growth cones. Unlike their response to contact with oligodendrocytes, few growth cones of minor processes were inhibited by rMAG-coated beads (20% collapsed). These results reveal the capability of differentiating growth cones of the same neuron to partition the complex molecular terrain they navigate by generating unique responses to particular inhibitory environmental cues.
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Curti, Antonio, Elisa Ferri, Simona Pandolfi, Alessandro Isidori, and Roberto M. Lemoli. "Dendritic Cell Differentiation." Journal of Immunology 172, no. 1 (December 19, 2003): 3–4. http://dx.doi.org/10.4049/jimmunol.172.1.3.
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&NA;. "Dendritic cell vaccines." Reactions Weekly &NA;, no. 1231 (December 2008): 12. http://dx.doi.org/10.2165/00128415-200812310-00035.
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Mosca, Paul, J. "Dendritic cell vaccines." Frontiers in Bioscience 12, no. 8-12 (2007): 4050. http://dx.doi.org/10.2741/2371.
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Proudfoot, Owen, Dodie Pouniotis, Kuo-Ching Sheng, Bruce E. Loveland, and Geoffrey A. Pietersz. "Dendritic cell vaccination." Expert Review of Vaccines 6, no. 4 (August 2007): 617–33. http://dx.doi.org/10.1586/14760584.6.4.617.
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Pitzer, Ashley L., and Annet Kirabo. "Dendritic Cell A20." Circulation Research 125, no. 12 (December 6, 2019): 1067–69. http://dx.doi.org/10.1161/circresaha.119.316198.
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Vyas, Jatin M. "The dendritic cell." Virulence 3, no. 7 (November 15, 2012): 601–2. http://dx.doi.org/10.4161/viru.22975.
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