Relevant bibliographies by topics / Glial Function

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Glial Function'

Author: Grafiati
Published: 4 June 2021
Last updated: 7 February 2022

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Journal articles on the topic "Glial Function"

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McClain, Jonathon L., and Brian D. Gulbransen. "The acute inhibition of enteric glial metabolism with fluoroacetate alters calcium signaling, hemichannel function, and the expression of key proteins." Journal of Neurophysiology 117, no. 1 (January 1, 2017): 365–75. http://dx.doi.org/10.1152/jn.00507.2016.

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Glia play key roles in the regulation of neurotransmission in the nervous system. Fluoroacetate (FA) is a metabolic poison widely used to study glial functions by disrupting the tricarboxylic acid cycle enzyme aconitase. Despite the widespread use of FA, the effects of FA on essential glial functions such as calcium (Ca2+) signaling and hemichannel function remain unknown. Therefore, our goal was to assess specifically the impact of FA on essential glial cell functions that are involved with neurotransmission in the enteric nervous system. To this end, we generated a new optogenetic mouse model to study specifically the effects of FA on enteric glial Ca2+ signaling by crossing PC::G5-tdTomato mice with Sox10::creER T2 mice. FA did not change the peak glial Ca2+ response when averaged across all glia within a ganglion. However, FA decreased the percent of responding glia by 30% ( P < 0.05) and increased the peak Ca2+ response of the glial cells that still exhibited a response by 26% ( P < 0.01). Disruption of Ca2+ signaling with FA impaired the activity-dependent uptake of ethidium bromide through connexin-43 (Cx43) hemichannels ( P < 0.05) but did not affect baseline Cx43-dependent dye uptake. FA did not cause overt glial or neurodegeneration, but glial cells significantly increased glial fibrillary acid protein by 56% ( P < 0.05) following treatment with FA. Together, these data show that the acute impairment of glial metabolism with FA causes key changes in glial functions associated with their roles in neurotransmission and phenotypic changes indicative of reactive gliosis. NEW & NOTEWORTHY Our study shows that the acute impairment of enteric glial metabolism with fluoroacetate (FA) alters specific glial functions that are associated with the modification of neurotransmission in the gut. These include subtle changes to glial agonist-evoked calcium signaling, the subsequent disruption of connexin-43 hemichannels, and changes in protein expression that are consistent with a transition to reactive glia. These changes in glial function offer a mechanistic explanation for the effects of FA on peripheral neuronal networks.
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Wang, Yu-Feng, and Yong-Jing Gao. "2019 Academic Annual Meeting and the Frontier Seminar on “Glial Cell Function and Disease” (Nantong, China)." ASN Neuro 11 (January 2019): 175909141986357. http://dx.doi.org/10.1177/1759091419863576.

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The contribution of glial activities to the functions, diseases, and repair of the central nervous system has received increasing attention in neuroscience studies. To promote the research of glial cells and increase cooperation with peers, the 2019 Academic Annual Meeting and the Frontier Seminar on “Glial Cell Function and Disease” was held in Nantong City, Jiangsu Province, China from May 24 to 26. The meeting was organized by Drs. Yong-Jing Gao and Jia-Wei Zhou of the Chinese Society of Neuroscience Glia Branch. The conference focused on the physiological and pathological functions of astrocytes, microglia, and oligodendrocytes with 25 speakers in two plenary speeches and five sections of more than 180 participants engaged in glial cell research. In the two plenary lectures, Yutian Wang from the University of British Columbia and Xia Zhang from the University of Ottawa presented “Development of NMDAR (N-methyl-D-aspartic acid receptor)-positive allosteric modulators as novel therapeutics for brain disorders” and “Mechanisms underlying cannabinoid regulation of brain function and disease,” respectively. The five sections included microglia and disease, astrocytes and disease, glioma treatment and glial imaging, oligodendrocytes and disease, and glial–neuronal interactions and disease. This meeting allowed extensive and in-depth academic exchanges on the latest research and experimental techniques, represented the highest achievements of Chinese scholars on glial cells, and promoted the cooperation between peers in the fields of glia studies.
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Bacci, Alberto, Claudia Verderio, Elena Pravettoni, and Michela Matteoli. "The role of glial cells in synaptic function." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 354, no. 1381 (February 28, 1999): 403–9. http://dx.doi.org/10.1098/rstb.1999.0393.

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Glial cells represent the most abundant cell population in the central nervous system and for years they have been thought to provide just structural and trophic support to neurons. Recently, several studies were performed, leading to the identification of an active interaction between glia and neurons. This paper focuses on the role played by glial cells at the level of the synapse, reviewing recent data defining how glia is determinant in synaptogenesis, in the modulation of fully working synaptic contacts and in synaptic plasticity.
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Allen, Nicola J., and David A. Lyons. "Glia as architects of central nervous system formation and function." Science 362, no. 6411 (October 11, 2018): 181–85. http://dx.doi.org/10.1126/science.aat0473.

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Glia constitute roughly half of the cells of the central nervous system (CNS) but were long-considered to be static bystanders to its formation and function. Here we provide an overview of how the diverse and dynamic functions of glial cells orchestrate essentially all aspects of nervous system formation and function. Radial glia, astrocytes, oligodendrocyte progenitor cells, oligodendrocytes, and microglia each influence nervous system development, from neuronal birth, migration, axon specification, and growth through circuit assembly and synaptogenesis. As neural circuits mature, distinct glia fulfill key roles in synaptic communication, plasticity, homeostasis, and network-level activity through dynamic monitoring and alteration of CNS structure and function. Continued elucidation of glial cell biology, and the dynamic interactions of neurons and glia, will enrich our understanding of nervous system formation, health, and function.
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Singhvi, Aakanksha, and Shai Shaham. "Glia-Neuron Interactions in Caenorhabditis elegans." Annual Review of Neuroscience 42, no. 1 (July 8, 2019): 149–68. http://dx.doi.org/10.1146/annurev-neuro-070918-050314.

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Glia are abundant components of animal nervous systems. Recognized 170 years ago, concerted attempts to understand these cells began only recently. From these investigations glia, once considered passive filler material in the brain, have emerged as active players in neuron development and activity. Glia are essential for nervous system function, and their disruption leads to disease. The nematode Caenorhabditis elegans possesses glial types similar to vertebrate glia, based on molecular, morphological, and functional criteria, and has become a powerful model in which to study glia and their neuronal interactions. Facile genetic and transgenic methods in this animal allow the discovery of genes required for glial functions, and effects of glia at single synapses can be monitored by tracking neuron shape, physiology, or animal behavior. Here, we review recent progress in understanding glia-neuron interactions in C. elegans. We highlight similarities with glia in other animals, and suggest conserved emerging principles of glial function.
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Stern, P. R. "Reexamining Glial Function." Science Signaling 3, no. 112 (March 9, 2010): ec76-ec76. http://dx.doi.org/10.1126/scisignal.3112ec76.

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Ceprian, Maria, and Daniel Fulton. "Glial Cell AMPA Receptors in Nervous System Health, Injury and Disease." International Journal of Molecular Sciences 20, no. 10 (May 17, 2019): 2450. http://dx.doi.org/10.3390/ijms20102450.

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Glia form a central component of the nervous system whose varied activities sustain an environment that is optimised for healthy development and neuronal function. Alpha-amino-3-hydroxy-5-methyl-4-isoxazole (AMPA)-type glutamate receptors (AMPAR) are a central mediator of glutamatergic excitatory synaptic transmission, yet they are also expressed in a wide range of glial cells where they influence a variety of important cellular functions. AMPAR enable glial cells to sense the activity of neighbouring axons and synapses, and as such many aspects of glial cell development and function are influenced by the activity of neural circuits. However, these AMPAR also render glia sensitive to elevations of the extracellular concentration of glutamate, which are associated with a broad range of pathological conditions. Excessive activation of AMPAR under these conditions may induce excitotoxic injury in glial cells, and trigger pathophysiological responses threatening other neural cells and amplifying ongoing disease processes. The aim of this review is to gather information on AMPAR function from across the broad diversity of glial cells, identify their contribution to pathophysiological processes, and highlight new areas of research whose progress may increase our understanding of nervous system dysfunction and disease.
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Wang, Sheng-Zhi, Xiao-Dong Liu, Yu-Xin Huang, Qing-Jiu Ma, and Jing-Jie Wang. "Disruption of Glial Function Regulates the Effects of Electro-Acupuncture at Tsusanli on Gastric Activity in Rats." American Journal of Chinese Medicine 37, no. 04 (January 2009): 647–56. http://dx.doi.org/10.1142/s0192415x09007132.

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According to recent evidence, acupuncture at Tsusanli (ST 36) can regulate gastric activity. And this regulation mainly depends upon neural basis or structure and may probably relate to the central neurons in the dorsal vagal complex. However, whether the glias of the dorsal vagal complex participate in the regulation of gastric activity, when electro-acupuncture (EA) at Tsusanli, still remains to be interpreted. In this study, we observed the effect of EA at Tsusanli (ST 36) on regulation of gastric activity. Propentofylline (PPF), a glial metabolic inhibitor, was used to inhibit the function of glial cells. EA at Tsusanli showed that the expressions of glial fibrillary acidic protein (GFAP) and OX42 increased significantly compared to that of the control group, and gastric electric change was obvious, with significantly higher frequency and wave amplitude compared to the control group. The expressions of GFAP and OX42 were decreased markedly when pretreated with PPF group than without PPF pretreatment group. Compared to the Tsusanli group and the control group, the changes of electro gastric graph (EGG) were significantly decreased in PPF pretreatment group. On the other hand, we observed the changes of spontaneous electro-activity of the DVC (dorsal vagal complex) in our previous experiment. The results indicated that EA at Tsusanli could activate glial cells in the dorsal vagal complex and regulate gastric activity. PPF blocked the function of glia, thus the effect of EA at Tsusanli on gastric activity was weakened. Our study suggested that this electro-acupuncture regulation of gastric activity was possibly related with glia of the dorsal vagal complex.
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Dimou, Leda, and Magdalena Götz. "Glial Cells as Progenitors and Stem Cells: New Roles in the Healthy and Diseased Brain." Physiological Reviews 94, no. 3 (July 2014): 709–37. http://dx.doi.org/10.1152/physrev.00036.2013.

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The diverse functions of glial cells prompt the question to which extent specific subtypes may be devoted to a specific function. We discuss this by reviewing one of the most recently discovered roles of glial cells, their function as neural stem cells (NSCs) and progenitor cells. First we give an overview of glial stem and progenitor cells during development; these are the radial glial cells that act as NSCs and other glial progenitors, highlighting the distinction between the lineage of cells in vivo and their potential when exposed to a different environment, e.g., in vitro. We then proceed to the adult stage and discuss the glial cells that continue to act as NSCs across vertebrates and others that are more lineage-restricted, such as the adult NG2-glia, the most frequent progenitor type in the adult mammalian brain, that remain within the oligodendrocyte lineage. Upon certain injury conditions, a distinct subset of quiescent astrocytes reactivates proliferation and a larger potential, clearly demonstrating the concept of heterogeneity with distinct subtypes of, e.g., astrocytes or NG2-glia performing rather different roles after brain injury. These new insights not only highlight the importance of glial cells for brain repair but also their great potential in various aspects of regeneration.
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Yadav, Smita, Susan H. Younger, Linghua Zhang, Katherine L. Thompson-Peer, Tun Li, Lily Y. Jan, and Yuh Nung Jan. "Glial ensheathment of the somatodendritic compartment regulates sensory neuron structure and activity." Proceedings of the National Academy of Sciences 116, no. 11 (February 25, 2019): 5126–34. http://dx.doi.org/10.1073/pnas.1814456116.

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Sensory neurons perceive environmental cues and are important of organismal survival. Peripheral sensory neurons interact intimately with glial cells. While the function of axonal ensheathment by glia is well studied, less is known about the functional significance of glial interaction with the somatodendritic compartment of neurons. Herein, we show that three distinct glia cell types differentially wrap around the axonal and somatodendritic surface of the polymodal dendritic arborization (da) neuron of the Drosophila peripheral nervous system for detection of thermal, mechanical, and light stimuli. We find that glial cell-specific loss of the chromatin modifier gene dATRX in the subperineurial glial layer leads to selective elimination of somatodendritic glial ensheathment, thus allowing us to investigate the function of such ensheathment. We find that somatodendritic glial ensheathment regulates the morphology of the dendritic arbor, as well as the activity of the sensory neuron, in response to sensory stimuli. Additionally, glial ensheathment of the neuronal soma influences dendritic regeneration after injury.
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Dissertations / Theses on the topic "Glial Function"

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Mellor, Robert. "Neurochemical studies on cultured glial cells." Thesis, University of Oxford, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300038.

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Sinclair, Michael S. "Modulation of Peripheral Taste Function by Glial-like Taste Cells." Scholarly Repository, 2012. http://scholarlyrepository.miami.edu/oa_dissertations/715.

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Taste is detected by cells of taste buds in the oral cavity. Mammalian taste buds contain three types of cells: receptor, presynaptic, and glial-like. Of these three, glial-like cells are the least studied. Their only known function is that they clear neurotransmitters from the extracellular space. The present work describes two previously undocumented properties of glial-like cells. First, Oxytocin receptor (OXTR) mRNA was detected by RT-PCR in taste tissue of mice. In the taste buds of Oxtr-YFP knockin mice, YFP was seen in glial-like taste cells and other cells immediately outside the taste bud, but no other cells in oral epithelium. Oxytocin (OXT) elicited Ca2+ responses from cells that resemble glial-like taste cells (by criteria including gene expression and lack of excitability). The EC50 for OXT in these cells was 33 nM, and responses saturated at 1 µM. 500 nM L-371,257 (an OXTR antagonist) significantly inhihited the responses to OXT. In a semi-intact preparation of lingual slices, OXT did not alter bitter tastant-evoked Ca2+ responses. Further, in behavioral studies, OXT (10 mg/kg i.p.) did not alter the responses of mice to aversive salty (NaCl), bitter (quinine), or sour (citric acid) solutions. In contrast, OXT (0.1 mg/kg i.p.) significantly decreased taste behavioral responses to low-to-intermediate concentrations of sucrose. My data suggest that OXT may modulate sweet taste sensitivity in vivo by acting on glial-like cells in taste buds. Second, Renal Outer Medullary K channel (ROMK) mRNA was also detected by RT-PCR in taste buds . Immunostaining revealed that ROMK is localized to the apical tips of glial-like taste cells. In the kidney, ROMK, apically localized in nephron epithelium facilitates a unidirectional flow (i.e. excretion) of K+. I suggest that, analogous to glia in the central nervous system, glial-like taste cells homeostatically redistribute extracellular [K+ ] within taste buds to maintain their sensitivity. The results of this study reveal that glial-like taste cells resemble nervous system glia in more ways than simply clearing neurotransmitters. They may also modulate the sensory output of the taste bud and buffer the extracellular [K+]. A more active role for glial-like cells in the functioning of the taste bud should be investigated.
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Jarjour, Andrew A. "Netrin and netrin receptor function in glial motility and myelination." Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=102513.

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Netrin-1 and its receptors play crucial roles during embryogenesis, guiding axon and neuronal cell migration. Here, roles of netrins and their receptors in glial function were investigated. In the embryonic spinal cord, netrin-1 expressed at the ventral midline orients axon extension. Spinal oligodendrocyte precursor (OP) cells are born close to, and migrate away from, the ventral midline. We find that OPs express DCC and UNC5 netrin receptors and, in an in vitro microchemotaxis assay, are repelled by a netrin-1 gradient. In the absence of netrin-1 or DCC function in vivo, fewer OPs migrate from the ventral to the dorsal embryonic spinal cord, consistent with netrin-1 acting as a repellent guidance cue for these cells.
In the adult CNS, oligodendrocytes continue to express DCC and UNC5 receptors, and upregulate netrin-1 expression. Our findings indicate that netrin-1 and its receptors are localized to paranodal axo-glial junctions, specialized cell-cell adhesions between non-compact myelin loops and axons. In myelinating cerebellar slice cultures derived from neonatal DCC-/- and netrin-1-/- mice, paranodes develop and mature normally but later become disorganized, resulting in loss of domain segregation at the nodal region. These data suggest that netrin-1 and DCC are essential for the maintenance of paranodal junctions, and may be indicative of a wider role in mediating cell-cell contacts in the adult.
Netrin-1, DCC, and UNC5 homologues have also been identified as putative tumor suppressors, and their expression is downregulated in many cancers, including glial tumors. In our studies, netrins were found to act as autocrine factors that restrain human glioblastoma cell migration, slowing cell movement and inhibiting the formation of focal contacts associated with lamellipodial protrusion and membrane extension. DCC and UNC5 homologues have previously been proposed to inhibit tumorigenesis by inducing cell death when unbound by netrin. However, we found no evidence of increased cell death in the absence of netrin function in oligodendrocyte precursors, oligodendrocytes or glioma cells. Instead, we find that netrins act as long-range guidance cues during glial precursor migration during development, while acting at short distances to stabilize cell-cell and cell-matrix interactions of mature glia and glial tumor cells, maintaining tissue organization and preventing inappropriate cell motility.
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Niemiec, Aurore. "Relevance of glial release in mouse retinal development and function." Strasbourg, 2009. http://www.theses.fr/2009STRA6287.

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Le système nerveux central (SNC) est principalement composé de neurones, et de cellules gliales. Parmi celles-ci l'on distingue les microglies, les oligodendrocytes et les astrocytes, ces derniers représentant à eux seuls plus de 50% du nombre total de cellules du cerveau. Longtemps considérées comme un vulgaire tissu de soutien, de nombreuses études ont mis en évidence un rôle beaucoup plus actif des cellules gliales dans le fonctionnement du système nerveux. En plus de maintenir l'homéostasie extracellulaire, d'assurer l'apport énergétique aux neurones et de permettre la formation/migration/différentiation des neurones au cours du développement du SNC il est apparu au cours de ces dernières décennies qu'un dialogue entre neurones et glies existe et que celles-ci peuvent moduler la neurotransmission. Durant ma thèse j'ai étudié certains aspects de ce dialogue entre neurones et cellules gliales. En effet leurs interactions sont depuis peu considérées comme déterminantes dans certains processus neurodégénératifs. L'influence des cellules gliales sur les neurones tient notamment aux molécules qu'elles sécrètent comme les facteurs trophiques, les lipoprotéines ou encore comme certaines molécules dont la libération semble être régulée comme la D-sérine. Notre équipe a montré précédemment que le cholestérol d'origine gliale était un facteur nécessaire pour la différentiation dendritique neuronale et la formation de synapses efficaces dans des cellules ganglionnaires de la rétine in vitro. Mon projet de thèse visait ainsi à étudier le rôle de deux types de sécrétion gliale dans la maturation et le fonctionnement du SNC à un niveau plus intégré, à savoir d'une part la sécrétion de cholestérol via les lipoprotéines et d'autre part la sécrétion régulée impliquant les SNAREs.
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Ingersoll, Sarah. "The role of complement anaphylatoxins in CNS pathology and glial cell function." Diss., University of Iowa, 2010. https://ir.uiowa.edu/etd/823.

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Demyelination in the CNS is known to involve several immune effector mechanisms, including complement proteins. For this dissertation project the central hypothesis that C3 and downstream effector complement proteins exacerbate demyelination through activation of glial cells was tested. To investigate the role of C3 and downstream complement proteins in demyelination and remyelination pathology in vivo we utilized the cuprizone model. We used C3 knockout mice (C3-/-), which are lacking the central C3 protein and subsequently all downstream complement effector proteins, and transgenic mice expressing C3a or C5a under the control of the glial GFAP promoter. Interestingly, we found no changes in demyelination or remyelination pathology between C3-/- and control mice. However, C3a and C5a transgenic mice had exacerbated demyelination and slightly delayed remyelination in the corpus callosum compared to WT mice. Transgenic mice had increased cellularity in the corpus callosum due to increased activation and/or migration of microglia. There was also evidence of T cells in the corpus callosum during demyelination in C5a transgenic mice, suggesting C5a may modulate BBB permeability. During early remyelination oligodendrocytes migrated to the corpus callosum in higher numbers in C3a and C5a transgenic mice, thus enabling these mice to remyelinate as effectively as WT mice by the end of the ten week study. To determine the effects of anaphylatoxins on individual glial subsets, we created murine recombinant C3a and C5a proteins. We found that the MAPK pathway proteins JNK1 and ERK1/2 were activated in glia upon stimulation with recombinant anaphylatoxin proteins. When microglia and mixed glial cultures were stimulated with C3a and/or C5a, we observed an increase in the production of proinflammatory cytokines and chemokines. In contrast, anaphylatoxin-treated primary astrocytes had suppressed cytokine and chemokine production compared to untreated astrocytes. In vitro, primary microglia and astrocytes did not significantly migrate in response to stimulation with C3a or C5a proteins, suggesting migration may not be a primary anaphylatoxin-mediated function in the CNS. Overall, our findings show that anaphylatoxin production in the brain plays a negative proinflammatory role during demyelination and that anaphylatoxin proteins can activate individual subsets of glia, initiating the production of inflammatory mediators.
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Rabah, Yasmine. "Satellite glial cell-proprioceptor interactions in dorsal root ganglia Characterization of transgenic mouse lines for selectively targeting glial cells in dorsal root ganglia Satellite glial cells modulate proprioceptive neuron function." Thesis, Sorbonne Paris Cité, 2018. http://www.theses.fr/2018USPCB208.

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Les neurones propriocepteurs sont nécessaires au contrôle du mouvement et à la locomotion. Ils connectent les fuseaux musculaires et les tendons aux motoneurones de la moelle épinière pour informer le système nerveux central de l’état d’élongation et de contraction des muscles. Leurs corps cellulaires sont localisés dans les ganglions rachidiens dorsaux (GRD), où ils sont intimement entourés de cellules gliales GFAP-positives appelées cellules satellites gliales (CSG). Comme les astrocytes du système nerveux central, les CSG expriment à leur surface des récepteurs couplés aux protéines Gq (Gq RCPG) qui peuvent être activés par les neurotransmetteurs libérés par les corps cellulaires de neurones sensoriels du GRD. Les corps cellulaires des neurones sensoriels expriment aussi un certain nombre de récepteurs et transmetteurs. Ces caractéristiques, ainsi que la proximité physique entre les CSG et les neurones sensoriels a permis d’émettre l’hypothèse que les deux types cellulaires sont capables de communiquer. De récentes données de la littérature suggèrent que les CSG et les neurones sensoriels responsables de la détection de la douleur sont capables de dialoguer. Cependant, à notre connaissance, aucune donnée n’a permis jusqu’à présent de démontrer une interaction entre les CSG et les neurones propriocepteurs. Dans cette étude, nous avons émis l’hypothèse que l’activation des Gq RCPG des CSG permet la modulation de l’activité des propriocepteurs. Pour tester cette hypothèse, nous avons utilisé des approches techniques complémentaires (imagerie calcique bi-photonique, immunohistochimie, biochimie et analyses comportementales) combinées à un outil chemogénétique puissant basé sur la technologie DREADD afin d’activer sélectivement la voie de signalisation Gq RCPG dans les CSG. Nous avons démontré dans une préparation de GRD intacte que les CSG sont capables de moduler l’activité des propriocepteurs via une signalisation purinergique. Pour tester la pertinence de cette communication, nous avons réalisé des expériences de comportement sensorimoteur et mis en évidence que l’activation des cellules gliales GFAP-positives induit des déficits sensorimoteurs. Déterminer si la modulation des propriocepteurs par les CSG affecte la transmission sensorimotrice a de profondes implications pour la compréhension du système sensorimoteur et de ses dérèglements
Proprioceptive neurons (one’s own neurons) are necessary for controlling motor control and locomotion. They arise from muscle spindles and tendons and synapse onto ventral horn motoneurons to deliver information about the length and contraction of muscles. Proprioceptor somata reside within the dorsal root ganglia (DRG) and are tightly enwrapped in a thin sheath of GFAP-expressing glial cells, called satellite glial cells (SGCs). Interestingly, SGCs express a number of Gq protein- coupled receptors (Gq GPCRs), which can be activated by neurotransmitters released by sensory neuron somata. Sensory neuron somata also express a number of receptors and transmitters. Both the expression of receptors and the close contact between SGCs and sensory neurons led to the hypothesis that these two cell types communicate. There is emerging evidence that SGCs and nociceptive sensory neuron (pain-sensing neurons) somata can communicate. Furthermore, to date, there is no study conducted on SGC-proprioceptor interaction. We hypothesized that SGC Gq GPCR signaling induces the release of neuroactive molecules from SGCs, leading to the modulation of proprioceptor activity. The main goal of this project has been to test this hypothesis using complementary technical approaches (2-photon Ca2+ imaging, immunohistochemistry, biochemistry and behavior) combined with a powerful chemogenetic DREADD-based tool to activate SGC Gq GPCR activity. We have demonstrated ex vivo that SGCs modulate proprioceptive neuron activity through a purinergic pathway. In order to test the physiological relevance of this discovery in vivo, we performed sensorimotor behavioral experiments and have shown that activating GFAP-expressing glial cells induces sensorimotor deficits. Determining whether SGC-induced proprioceptor activity has profound implications in the understanding of sensorimotor functions in health and diseases
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Murphy, John Anthony. "The protein kinase C of glia." Thesis, University of York, 1989. http://etheses.whiterose.ac.uk/9762/.

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Wunderlich, Kirsten A. [Verfasser], and Eberhart [Akademischer Betreuer] Zrenner. "Novel Findings about the Role of Glial Cells in Retinal Function, Disease, and Therapy / Kirsten A. Wunderlich ; Betreuer: Eberhart Zrenner." Tübingen : Universitätsbibliothek Tübingen, 2016. http://d-nb.info/1197694161/34.

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Littrell, Ofelia Meagan. "NIGROSTRIATAL DOPAMINE-NEURON FUNCTION FROM NEUROTROPHIC-LIKE PEPTIDE TREATMENT AND NEUROTROPHIC FACTOR DEPLETION." UKnowledge, 2011. http://uknowledge.uky.edu/neurobio_etds/1.

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Trophic factors have shown great promise in their potential to treat neurological disease. In particular, glial cell line-derived neurotrophic factor (GDNF) has been identified as a potent neurotrophic factor for midbrain dopamine (DA) neurons in the substantia nigra (SN), which lose function in Parkinson’s disease (PD). GDNF progressed to phase II clinical trials, which did not meet proposed endpoints. The large size and binding characteristics of GDNF have been suspected to contribute to some of the shortcomings of GDNF related to delivery to target brain regions. Smaller peptides derived from GDNF (Dopamine-Neuron Stimulating Peptides – DNSPs) have been recently investigated and appear to demonstrate trophic-like effects comparable to GDNF. In the described studies, a time course study was conducted to determine in vivo DA-release characteristics 1-, 2- and 4- weeks after peptide treatment. These studies determined the effects on DA terminals within striatal sub-regions using microelectrodes. A heterogeneous effect on striatal sub-regions was apparent with the maximum effect in the dorsal striatum – corresponding to terminals originating from the SN. Dysregulation of GDNF or GDNF signaling is believed to contribute to motor dysfunction in aging and PD. Thus, it is hypothesized that GDNF is necessary for the maintenance and function of neurons. To extend this line of investigation, in vivo functional measures (DA-release and -uptake) and behavioral and cellular alterations were investigated in a transgenic mouse model (Gdnf+/-) with reduced GDNF protein levels. The described studies determined that both DA-uptake and -release properties were altered in middle-aged Gdnf+/- mice with only modest reductions in DA neurochemical levels. GDNF levels in Gdnf+/- mice were restored to levels comparable to wild-type (WT) counterparts by treatment with GDNF. GDNF protein supplementation led to enhanced motor behavior and increased markers for DA neurons in the SN of Gdnf+/- mice. Gdnf+/- mice appeared to show a heightened sensitivity to GDNF treatment compared to WT counterparts. Overall, this body of work examines novel synthetic peptides with potential to enhance DA-neuron function and expands upon the current understanding of GDNF’s role in the nigrostriatal pathway.
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Altas, Bekir [Verfasser], Nils [Akademischer Betreuer] Brose, Judith [Gutachter] Stegmüller, and Dirk [Gutachter] Goerlich. "Roles of the Nedd4 Family E3 Ligases in Glial Function and Nerve Cell Development / Bekir Altas ; Gutachter: Judith Stegmüller, Dirk Goerlich ; Betreuer: Nils Brose." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2017. http://d-nb.info/1131875710/34.

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Books on the topic "Glial Function"

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Matsas, Rebecca, and Marco Tsacopoulos, eds. The Functional Roles of Glial Cells in Health and Disease. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4685-6.

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1957-, Castellano Bernardo, and Nieto-Sampedro Manuel 1944-, eds. Glial cell function. Amsterdam: Elsevier, 2001.

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1957-, Castellano Bernardo, and Nieto-Sampedro Manuel 1944-, eds. Glial cell function. Amsterdam: Elsevier, 2003.

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B. Castellano López (Editor) and M. Nieto-Sampedro (Editor), eds. Glial Cell Function (Paperback) (Progress in Brain Research). Elsevier Science, 2003.

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J, Marangos Paul, Campbell Iain C, and Cohen Robert M, eds. Neuronal and glial proteins: Structure, function, and clinical application. San Diego: Academic Press, 1988.

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Ransom, Bruce R. Neuroglia. Edited by Helmut Kettenmann. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199794591.001.0001.

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This resource is the long-awaited new revision of the most highly regarded reference volume on glial cells, and has been completely revised, greatly enlarged, and enhanced with full color figures throughout. Neglected in research for years, it is now evident that the brain only functions in a concerted action of all the cells, namely glia and neurons. Seventy one chapters comprehensively discuss virtually every aspect of normal glial cell anatomy, physiology, biochemistry and function, and consider the central roles of these cells in neurological diseases including stroke, Alzheimer disease, multiple sclerosis, Parkinson's disease, neuropathy, and psychiatric conditions. With more than 20 new chapters it addresses the massive growth of knowledge about the basic biology of glia and the sophisticated manner in which they partner with neurons in the course of normal brain function.
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Marangos, Paul J., and Iain C. Campbell. Neuronal and Glial Proteins: Structure, Function, and Clinical Application (Neurobiological Research). Academic Pr, 1988.

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Marangos, Paul J., and Iain C. Campbell. Neuronal and Glial Proteins: Structure, Function, and Clinical Application (Neurobiological Research). Academic Pr, 1988.

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Mason, Peggy. Cells of the Nervous System. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190237493.003.0002.

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The nervous system is made up of neurons and glia that derive from neuroectoderm. Since neurons are terminally differentiated and do not divide, primary intracranial tumors do not arise from mature neurons. Tumors outside the nervous system may metastasize inside the brain or may release a substance that negatively affects brain function, termed paraneoplastic disease. Neurons receive information through synaptic inputs onto dendrites and soma and send information to other cells via a synaptic terminal. Most neurons send information to faraway locations and for this, an axon that connects the soma to synaptic terminals is required. Glial cells wrap axons in myelin, which speeds up information transfer. Axonal transport is necessary to maintain neuronal function and health across the long distances separating synaptic terminals and somata. A common mechanism of neurodegeneration arises from impairments in axonal transport that lead to protein aggregation and neuronal death.
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The Functional Roles of Glial Cells in Health and Disease: Dialogue between Glia and Neurons. Springer, 2011.

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Book chapters on the topic "Glial Function"

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Soustelle, Laurent, and Angela Giangrande. "Gene function in glial-neuronal interactions." In Glial ⇔ Neuronal Signaling, 21–52. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-1-4020-7937-5_2.

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Ramírez, José M., Alberto Triviño, Ana I. Ramírez, and Juan J. Salazar. "Organization and Function of Astrocytes in Human Retina." In Understanding Glial Cells, 47–62. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5737-1_3.

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Matute, Carlos, David J. Fogarty, José María García-Barcina, Miroslav Gottlieb, María José Morán, and María Victoria Sánchez-Gómez. "Expression and Function of Neurotransmitter Receptors in Glial Cells of the Central Nervous System." In Understanding Glial Cells, 167–83. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5737-1_9.

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Götz, Magdalena. "Biology and Function of Glial Cells." In Neurosciences - From Molecule to Behavior: a university textbook, 163–77. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-10769-6_9.

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Melcangi, Roberto C., and Luis Miguel Garcia-Segura. "Steroid Metabolism in Glial Cells." In Neuroactive Steroids in Brain Function, Behavior and Neuropsychiatric Disorders, 43–59. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6854-6_2.

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Giuliani, Patricia, Patrizia Ballerini, Silvana Buccella, Renata Ciccarelli, Michel P. Rathbone, Silvia Romano, Iolanda D’Alimonte, Francesco Caciagli, Patrizia Di Iorio, and Mieczyslaw Pokorski. "Guanosine Protects Glial Cells Against 6-Hydroxydopamine Toxicity." In Neurotransmitter Interactions and Cognitive Function, 23–33. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/5584_2014_73.

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Kimelberg, H. K., E. R. O’Connor, and Helmut Kettenmann. "Effects of Swelling on Glial Cell Function." In Advances in Comparative and Environmental Physiology, 157–86. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-77124-8_6.

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Srikanth, Madhulika, Li Yao, and Ramazan Asmatulu. "Advances in the Research of Astrocyte Function in Neural Regeneration." In Glial Cell Engineering in Neural Regeneration, 1–18. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-030-02104-7_1.

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Sontheimer, Harald, and Elizabeth Fernandez-Marques. "Ion channel expression and function in astrocytic scars." In Molecular Signaling and Regulation in Glial Cells, 101–13. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60669-4_10.

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Vernadakis, Antonia, Nikos Sakellaridis, and Dimitra Mangoura. "Glial Cells as Metabolic Regulators of Neurons." In Amino Acid Availability and Brain Function in Health and Disease, 91–100. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73175-4_9.

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Conference papers on the topic "Glial Function"

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Shreiber, David I., Hailing Hao, and Ragi A. I. Elias. "The Effects of Glia on the Tensile Properties of the Spinal Cord." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-190184.

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Glia, the primary non-neuronal cells of the central nervous system, were initially believed to bind or glue neurons together and/or provide a supporting scaffold [1, 2]. It is now recognized that these cells provide specialized and essential biological and regulatory functions. Still, their contributions to the overall mechanical properties would also strongly influence the tissue’s tolerance to loading conditions experienced during trauma and potentially regulate of function and growth in neurons and glia [3, 4]. White matter represents an intriguing tissue to appreciate the role of glia in tissue and cellular mechanics. White matter consists of bundles of axons aligned in parallel, which are myelinated by oligodendrocytes, and a network of astrocytes, which interconnect axons and the vascular supply. In this study, we selectively interfered with the glial network during chick embryo development and evaluated the tensile properties of the spinal cord. Myelination was suppressed by injecting ethidium bromide (EB), which is cytotoxic to dividing cells and kills oligodendrocytes and astrocytes, or an antibody against galactocerebroside (αGalC) with serum complement, which interferes with oligodendrocytes during the myelination process without affecting astrocytes.
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Ventura, P. Britten, Kate Karfilis, Peter Kim, Kelsey Wahl, and Hui Zong. "Abstract A22: Social behaviors in medulloblastoma: Functional analysis of tumor-derived, supportive glial cells." In Abstracts: Second AACR International Conference on Frontiers in Basic Cancer Research--Sep 14-18, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.fbcr11-a22.

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Popkin, Rachel, Fluvio Lobo, and Jack Stubbs. "Multimaterial 3D Printing for the Fabrication of Functional Stethoscopes." In 2019 Design of Medical Devices Conference. American Society of Mechanical Engineers, 2019. http://dx.doi.org/10.1115/dmd2019-3297.

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Stethoscopes are ubiquitous across the healthcare system. For the most part, stethoscopes do not represent a financial burden, mostly throughout the developed world. Further reducing the cost of stethoscopes has both humanitarian and prophylactic goals. The Glia project pioneered the concept of 3D printing stethoscopes for war or poverty-stricken regions of the world. Cross-contamination concerns have led researchers and manufacturers to develop single-use stethoscopes. Our aim is to develop a fully printed, multi-material, functional stethoscope to alleviate these concerns. Our team also seeks to establish a framework for the on-demand manufacturing of medical devices to reduce costs associated with shipping, distribution, and inventory.
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LIU, H., and A. A. SZALAY. "THE GLIAL CELL-LINE DERIVED NEUROTROPHIC FACTOR-LUCIFERASE FUSION IS FULLY FUNCTIONAL UPON SECRETION FROM MAMMALIAN CELLS." In Proceedings of the 11th International Symposium. WORLD SCIENTIFIC, 2001. http://dx.doi.org/10.1142/9789812811158_0108.

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Masand, Shirley, Jian Chen, Melitta Schachner, and David I. Shreiber. "A Bioactive Peptide Grafted Scaffold for Peripheral Nerve Regeneration." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53627.

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Despite this innate regenerative potential of the peripheral nervous system, functional recovery often remains incomplete, especially as the severity of injury increases. This has been attributed to a number of sources including the ingrowth of fibrous scar tissue, lack of mechanical support for emerging neurites, and the malrouted reinnervation of neurites towards inappropriate targets. While research in the field is broad, it is generally accepted that an optimal nerve guidance conduit to encourage regeneration should include both biological and mechanical support for emerging neurites and glia.
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Kim, Jennifer, Jayakumar R. Nair, Melissa M. Hadley, Alan Kozikowski, Robert Miller, and Alejandro Villagra. "Abstract LB-295: A novel regulatory role of HDAC6 in the functional inflammatory phenotype of glia cells." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-lb-295.

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Li, Lulu, Alexander Davidovich, Jennifer Schloss, Uday Chippada, Rene Schloss, Noshir Langrana, and Martin Yarmush. "Control of Neural Lineage Differentiation in an Alginate Encapsulation Microenvironment via Cellular Aggregation." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206496.

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Cell replacement therapies, which utilize renewable stem cell sources, hold tremendous potential to treat a wide range of degenerative diseases. Although many studies have established techniques to successfully differentiate stem cells into different mature cell lineages, their practicality is limited by the lack of control during the differentiation process and low yields of differentiated cells. In order to address these issues, we have previously established a murine embryonic stem cell alginate-poly-L-lysine microencapsulation differentiation system [1]. We demonstrated that ES cell differentiation could be mediated by cell-cell aggregation in the encapsulation microenvironment. We have demonstrated that both cell aggregation and hepatocyte functions, such as urea and albumin secretions, as well as increased expression of cytokeratin 18 and cyp4507a, occur concomitantly with surface E-cadherin expression [2]. In the present studies, we assessed the feasibility of inducing neuronal lineage differentiation in the alginate microenvironment by incorporating soluble inducers, such as retinoic acid, into the permeable microcapsule system. We demonstrated decreased cell aggregation and enhanced neuronal lineage differentiation with the expression of various neuronal specific markers, including neurofilament, A2B5, O1 and glial fibrillary acidic protein (GFAP). In addition, we demonstrated that, by blocking the cell aggregation using anti-E-cadherin antibody, encapsulated cells increased neuronal marker expression at a later stage of the encapsulation, even in the absence of retinoic acid. In conjunction with the mechanical and physical characterizations of the alginate crosslinking network, we show that 2.2% alginate concentration is most conducive to neuronal differentiation from embryonic stem cells in the presence of retinoic acid.
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Baker, J. B., M. P. McGrogan, C. Simonsen, R. L. Gronke, and B. W. Festoff. "STRUCTURE AND PROPERTIES OF PROTEASE NEXIN I." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644765.

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Human foreskin fibroblasts secrete several different serine protease inhibitors which differ in size and protease specificities. These proteins, called protease nexins (PNs) all form SDS-resistant complexes with their protease targets. Fibroblast surface receptors recognize the protease-PN complexes and mediate their delivery to lysosomes. PNI is a 45 kilodalton glycoprotein that rapidly inhibits several arg or lys-specific proteases including trypsin, thrombin, and urokinase (k assoc.∼ 4×l06,∼ 6×105 and ∼ 2×105, m−1s−1 respectively). Like antithrombin III, PNI binds heparin and inhibits thrombin at a vastly accelerated rate in the presence of this glycoaminoglycan. Immunofluorescence studies show that in addition to secreting PNI foreskin fibroblasts carry this inhibitor on their surfaces. PNI cDNA has been cloned and sequenced. A mixed oligonucleotide probe derived from PNI N-terminal sequence was used to probe a foreskin fibroblast cDNA library constructed with λGT10. Identification of PNI cDNAs has been verified by sequencing and by expressing active PNI protein in mammalian cells. The full amino acid sequence of PNI, deduced from cDNA sequencing, is 392 residues long and has 30% homology to antithrombin III. An arg-ser pair 32 residues from the C-terminus of the inhibitor is proposed as the reactive center P1-P1 residues. In the hinge region a lys residue is present in a position occupied by a ginor glu residue in other serpins. PNI mRNA exists in 2 slightly different forms:One (αPNI) yields a thr-arg-ser sequence wherethe other βPNI) yields a thr-thr-gly-ser sequence. The presence of the appropriate splice acceptor sites in the genome indicates that these forms are generated from a single gene by alternative splicing. Expressed aPNI and 0PNI proteins both bind thrombin and urokinase. In foreskin fibroblaststhe α form of PNI mRNA predominates over the β form by about 2:1. In foreskin fibroblast cultures secreted PNI inhibits the mitogenic response to thrombin and regulate secreted urokinase. Purified PNI added to human fibrosarcoma (HT1080) cells inhibitsthe tumor cell-mediated destruction of extracellular matrix and transiently, but dramatically, inhibits tumor cell growth. PNI or PNI-like inhibitors may function at multiple physiological sites. The β form of PNI is virtually identical to a glia-derived neurite promoting factor, the cDNA for which has been recently cloned and sequenced by Gloor et al (1). The neurite outgrowth activity of PNI may result from inhibition of a thrombin-like protease that is associated with neurons, since a number of thrombin inhibitors stimulate neurite extension. Recent immunofluoresence experiments, carried out with D. Hantai (Inserm; Paris) demonstrate that anti-PNI antibody intensely stains neuromuscular synapses. In addition, a PNI-like inhibitor is associated with platelets. At low (0.5 nM <) 125I-thrombin concentrations formation of 125I-thrombin-platelet PNI complexes accounts for most of the specific binding of 125I-thrombin to platelets (2). Although the platelet-associated form of PNI is electrophoretically and immunologically indistinguishable from fibroblast PNI, it does not bind urokinase, suggesting that it may be distinct.(1) Gloor, S., K. Odink, J. Guenther, H. Nick, and D. Monard. (1986) Cell 47:687-693.(2) Gronke, R.S., B.L. Bergman, and J.B. Baker. (1987) J. Biol. Chem. (in press)
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Reports on the topic "Glial Function"

1

Look, A. T. Zebrafish Model of NF1 for Structure-Function Analysis, Mechanisms of Glial Tumorigenesis, and Chemical Biology. Fort Belvoir, VA: Defense Technical Information Center, May 2014. http://dx.doi.org/10.21236/ada609199.

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Look, A. T. Zebrafish Model of NF1 for Structure-Function Analysis, Mechanisms of Glial Tumorigenesis, and Chemical Biology. Fort Belvoir, VA: Defense Technical Information Center, May 2013. http://dx.doi.org/10.21236/ada581661.

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Zong, Hui, and Betty Diamond. Social Behavior in Medulloblastoma: Functional Analysis of Tumor-Supporting Glial Cells. Fort Belvoir, VA: Defense Technical Information Center, July 2014. http://dx.doi.org/10.21236/ada613317.

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Zong, Hui. Social Behavior in Medulloblastoma: Functional Analysis of Tumor-Supporting Glial Cells. Fort Belvoir, VA: Defense Technical Information Center, July 2012. http://dx.doi.org/10.21236/ada566929.

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