Relevant bibliographies by topics / Glial cells

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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 cells'

Author: Grafiati
Published: 4 June 2021
Last updated: 20 July 2024

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Journal articles on the topic "Glial cells"

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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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Argente-Arizón, Pilar, Santiago Guerra-Cantera, Luis Miguel Garcia-Segura, Jesús Argente, and Julie A. Chowen. "Glial cells and energy balance." Journal of Molecular Endocrinology 58, no. 1 (January 2017): R59—R71. http://dx.doi.org/10.1530/jme-16-0182.

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The search for new strategies and drugs to abate the current obesity epidemic has led to the intensification of research aimed at understanding the neuroendocrine control of appetite and energy expenditure. This intensified investigation of metabolic control has also included the study of how glial cells participate in this process. Glia, the most abundant cell type in the central nervous system, perform a wide spectrum of functions and are vital for the correct functioning of neurons and neuronal circuits. Current evidence indicates that hypothalamic glia, in particular astrocytes, tanycytes and microglia, are involved in both physiological and pathophysiological mechanisms of appetite and metabolic control, at least in part by regulating the signals reaching metabolic neuronal circuits. Glia transport nutrients, hormones and neurotransmitters; they secrete growth factors, hormones, cytokines and gliotransmitters and are a source of neuroprogenitor cells. These functions are regulated, as glia also respond to numerous hormones and nutrients, with the lack of specific hormonal signaling in hypothalamic astrocytes disrupting metabolic homeostasis. Here, we review some of the more recent advances in the role of glial cells in metabolic control, with a special emphasis on the differences between glial cell responses in males and females.
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NEWMAN, ERIC A. "A dialogue between glia and neurons in the retina: modulation of neuronal excitability." Neuron Glia Biology 1, no. 3 (August 2004): 245–52. http://dx.doi.org/10.1017/s1740925x0500013x.

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Bidirectional signaling between neurons and glial cells has been demonstrated in brain slices and is believed to mediate glial modulation of synaptic transmission in the CNS. Our laboratory has characterized similar neuron–glia signaling in the mammalian retina. We find that light-evoked neuronal activity elicits Ca2+ increases in Müller cells, which are specialized retinal glial cells. Neuron to glia signaling is likely mediated by the release of ATP from neurons and is potentiated by adenosine. Glia to neuron signaling has also been observed and is mediated by several mechanisms. Stimulation of glial cells can result in either facilitation or depression of synaptic transmission. Release of D-serine from Müller cells might also potentiate NMDA receptor transmission. Müller cells directly inhibit ganglion cells by releasing ATP, which, following hydrolysis to adenosine, activates neuronal A1 receptors. The existence of bidirectional signaling mechanisms indicates that glial cells participate in information processing in the retina.
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Udolph, G., P. Rath, and W. Chia. "A requirement for Notch in the genesis of a subset of glial cells in the Drosophila embryonic central nervous system which arise through asymmetric divisions." Development 128, no. 8 (April 15, 2001): 1457–66. http://dx.doi.org/10.1242/dev.128.8.1457.

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In the Drosophila central nervous system (CNS) glial cells are known to be generated from glioblasts, which produce exclusively glia or neuroglioblasts that bifurcate to produce both neuronal and glial sublineages. We show that the genesis of a subset of glial cells, the subperineurial glia (SPGs), involves a new mechanism and requires Notch. We demonstrate that the SPGs share direct sibling relationships with neurones and are the products of asymmetric divisions. This mechanism of specifying glial cell fates within the CNS is novel and provides further insight into regulatory interactions leading to glial cell fate determination. Furthermore, we show that Notch signalling positively regulates glial cells missing (gcm) expression in the context of SPG development.
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Johnston, A. R., and D. J. Gooday. "Xenopus temporal retinal neurites collapse on contact with glial cells from caudal tectum in vitro." Development 113, no. 2 (October 1, 1991): 409–17. http://dx.doi.org/10.1242/dev.113.2.409.

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Nasal and temporal retinal neurites were confronted in culture with glial cells from the rostral and caudal parts of the optic tectum and with glial cells from the diencephalon. Twenty of each of the six classes of encounter between individual growth cones and isolated glial cells were analysed by time-lapse videorecording. The results show that growth cones from the temporal retina collapse when they contact glial cells from the caudal tectum, but do not collapse when they contact glia from other areas. Growth cones of nasal retinal fibres do not collapse on contact with any of the glial types examined. This suggests that the inhibitory phenomena described by others are in part due to the cell surface characteristics of glial cells, and that there are differences between glia from the front and back of the optic tectum.
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Horn, Zachi, Hourinaz Behesti, and Mary E. Hatten. "N-cadherin provides a cis and trans ligand for astrotactin that functions in glial-guided neuronal migration." Proceedings of the National Academy of Sciences 115, no. 42 (September 27, 2018): 10556–63. http://dx.doi.org/10.1073/pnas.1811100115.

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Prior studies demonstrate that astrotactin (ASTN1) provides a neuronal receptor for glial-guided CNS migration. Here we report that ASTN1 binds N-cadherin (CDH2) and that the ASTN1:CDH2 interaction supports cell–cell adhesion. To test the function of ASTN1:CDH2 binding in glial-guided neuronal migration, we generated a conditional loss of Cdh2 in cerebellar granule cells and in glia. Granule cell migration was slowed in cerebellar slice cultures after a conditional loss of neuronal Cdh2, and more severe migration defects occurred after a conditional loss of glial Cdh2. Expression in granule cells of a mutant form of ASTN1 that does not bind CDH2 also slowed migration. Moreover, in vitro chimeras of granule cells and glia showed impaired neuron–glia attachment in the absence of glial, but not neuronal, Cdh2. Thus, cis and trans bindings of ASTN1 to neuronal and glial CDH2 form an asymmetric neuron–glial bridge complex that promotes glial-guided neuronal migration.
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Freeman, Marc R., and Chris Q. Doe. "Asymmetric Prospero localization is required to generate mixed neuronal/glial lineages in the Drosophila CNS." Development 128, no. 20 (October 15, 2001): 4103–12. http://dx.doi.org/10.1242/dev.128.20.4103.

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In many organisms, single neural stem cells can generate both neurons and glia. How are these different cell types produced from a common precursor? In Drosophila, glial cells missing (gcm) is necessary and sufficient to induce glial development in the CNS. gcm mRNA has been reported to be asymmetrically localized to daughter cells during precursor cell division, allowing the daughter cell to produce glia while precursor cell generates neurons. We show that (1) gcm mRNA is uniformly distributed during precursor cell divisions; (2) the Prospero transcription factor is asymmetrically localized into the glial-producing daughter cell; (3) Prospero is required to upregulate gcm expression and induce glial development; and (4) mislocalization of Prospero to the precursor cell leads to ectopic gcm expression and the production of extra glia. We propose a novel model for the separation of glia and neuron fates in mixed lineages in which the asymmetric localization of Prospero results in upregulation of gcm expression and initiation of glial development in only precursor daughter cells.
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Koussa, Mounir A., Leslie P. Tolbert, and Lynne A. Oland. "Development of a glial network in the olfactory nerve: role of calcium and neuronal activity." Neuron Glia Biology 6, no. 4 (November 2010): 245–61. http://dx.doi.org/10.1017/s1740925x11000081.

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In adult olfactory nerves of mammals and moths, a network of glial cells ensheathes small bundles of olfactory receptor axons. In the developing antennal nerve (AN) of the moth Manduca sexta, the axons of olfactory receptor neurons (ORNs) migrate from the olfactory sensory epithelium toward the antennal lobe. Here we explore developmental interactions between ORN axons and AN glial cells. During early stages in AN glial-cell migration, glial cells are highly dye coupled, dividing glia are readily found in the nerve and AN glial cells label strongly for glutamine synthetase. By the end of this period, dye-coupling is rare, glial proliferation has ceased, glutamine synthetase labeling is absent, and glial processes have begun to extend to enwrap bundles of axons, a process that continues throughout the remainder of metamorphic development. Whole-cell and perforated-patch recordings in vivo from AN glia at different stages of network formation revealed two potassium currents and an R-like calcium current. Chronic in vivo exposure to the R-type channel blocker SNX-482 halted or greatly reduced AN glial migration. Chronically blocking spontaneous Na-dependent activity by injection of tetrodotoxin reduced the glial calcium current implicating an activity-dependent interaction between ORNs and glial cells in the development of glial calcium currents.
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Tedoldi, Angelo, Liam Argent, and Johanna M. Montgomery. "The role of the tripartite synapse in the heart: how glial cells may contribute to the physiology and pathophysiology of the intracardiac nervous system." American Journal of Physiology-Cell Physiology 320, no. 1 (January 1, 2021): C1—C14. http://dx.doi.org/10.1152/ajpcell.00363.2020.

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One of the major roles of the intracardiac nervous system (ICNS) is to act as the final site of signal integration for efferent information destined for the myocardium to enable local control of heart rate and rhythm. Multiple subtypes of neurons exist in the ICNS where they are organized into clusters termed ganglionated plexi (GP). The majority of cells in the ICNS are actually glial cells; however, despite this, ICNS glial cells have received little attention to date. In the central nervous system, where glial cell function has been widely studied, glia are no longer viewed simply as supportive cells but rather have been shown to play an active role in modulating neuronal excitability and synaptic plasticity. Pioneering studies have demonstrated that in addition to glia within the brain stem, glial cells within multiple autonomic ganglia in the peripheral nervous system, including the ICNS, can also act to modulate cardiovascular function. Clinically, patients with atrial fibrillation (AF) undergoing catheter ablation show high plasma levels of S100B, a protein produced by cardiac glial cells, correlated with decreased AF recurrence. Interestingly, S100B also alters GP neuron excitability and neurite outgrowth in the ICNS. These studies highlight the importance of understanding how glial cells can affect the heart by modulating GP neuron activity or synaptic inputs. Here, we review studies investigating glia both in the central and peripheral nervous systems to discuss the potential role of glia in controlling cardiac function in health and disease, paying particular attention to the glial cells of the ICNS.
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Helm, Conrad, Anett Karl, Patrick Beckers, Sabrina Kaul-Strehlow, Elke Ulbricht, Ioannis Kourtesis, Heidrun Kuhrt, et al. "Early evolution of radial glial cells in Bilateria." Proceedings of the Royal Society B: Biological Sciences 284, no. 1859 (July 19, 2017): 20170743. http://dx.doi.org/10.1098/rspb.2017.0743.

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Bilaterians usually possess a central nervous system, composed of neurons and supportive cells called glial cells. Whereas neuronal cells are highly comparable in all these animals, glial cells apparently differ, and in deuterostomes, radial glial cells are found. These particular secretory glial cells may represent the archetype of all (macro) glial cells and have not been reported from protostomes so far. This has caused controversial discussions of whether glial cells represent a homologous bilaterian characteristic or whether they (and thus, centralized nervous systems) evolved convergently in the two main clades of bilaterians. By using histology, transmission electron microscopy, immunolabelling and whole-mount in situ hybridization, we show here that protostomes also possess radial glia-like cells, which are very likely to be homologous to those of deuterostomes. Moreover, our antibody staining indicates that the secretory character of radial glial cells is maintained throughout their various evolutionary adaptations. This implies an early evolution of radial glial cells in the last common ancestor of Protostomia and Deuterostomia. Furthermore, it suggests that an intraepidermal nervous system—composed of sensory cells, neurons and radial glial cells—was probably the plesiomorphic condition in the bilaterian ancestor.
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Dissertations / Theses on the topic "Glial cells"

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Förster, Bettina Ulrike. "Talin in glial cells." Thesis, University of Cambridge, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.612772.

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Nazareth, Lynn. "Determining Cellular and Molecular Mechanisms Behind Glial Cell Phagocytosis." Thesis, Griffith University, 2021. http://hdl.handle.net/10072/408099.

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Phagocytosis (“cell eating”) is an immunobiological process required for maintenance of systemic homoeostasis under normal physiological conditions (during development and adulthood) and in various pathologies. Phagocytosis is a receptor-mediated event, wherein a phagocytic cell recognizes, engulfs and degrades specific targets that need to be eliminated. The targets can be either “self-targets”, such as dead or damaged cells, or “non-self-targets”, such as microorganisms. In the nervous system, the “first responding” phagocytes are usually the supporting glial cells. Based on the location they are present in, glial cells are classified as either CNS or PNS glia. The key phagocytic glia in the CNS are astrocytes and microglia, and in the PNS, Schwann cells (SCs). Some peripheral nerves, however, have other glial types which mediate this function, such as olfactory ensheathing cells (OECs) in the olfactory nerve. Efficient phagocytosis is essential for regeneration after nervous system injury, but after CNS injury, glial phagocytosis is often inefficient. In contrast, after PNS injury, glia rapidly phagocytose and clear the cellular and myelin debris resulting from the injury. Due to their ability to support nerve growth, particularly via physical support and secretion of growth/guidance factors, while simultaneously performing phagocytosis; transplantation of SCs and OECs have promising potential to treat CNS injuries. However, phagocytosis is a highly specialized function and the key molecular and cellular components in PNS glial phagocytosis are largely unknown. If these could be characterized, new drug targets may be revealed that can further promote glial-mediated neural regeneration (but without causing an excessive inflammatory response). The site of a CNS injury is a complex environment, with cell death occurring via different mechanisms. These include distinct types of necrosis and apoptosis, and glia may respond differently to these distinct “self-targets”. Hence, in this Thesis, I investigated key cellular and molecular mechanisms involved in OEC- and SC-mediated phagocytosis of cells undergoing various forms of death. I discovered that OECs and SCs are indeed competent phagocytes that can recognize, internalize and degrade a range of “self-targets”. Both cell types expressed a number of phagocytic receptors, including phosphatidylserine (PS) recognition receptors, pathogen recognition receptors (PRRs), scavenger receptors, Fcγ receptors (FcγRs) and complement receptors (CRs). OECs and SCs both rapidly recognised and engulfed various cellular targets (within 2 h). Recognition of targets occurred mainly via PS displayed on the dying cell surface, with potential involvement of PRRs. The family of small Rho GTPases (Rac, Cdc42 and Rho) were also important for target engulfment. However, while engulfment was rapid, breakdown was relatively slow, particularly when the targets were necrotic bodies and myelin debris (especially when compared to professional phagocytes, i.e., macrophages). Engulfment of apoptotic targets resulted in anti-inflammatory cytokine production, however, necrotic target uptake led to a proinflammatory response. Overall, OECs phagocytosed larger amounts of targets over time, as well as processed targets faster, than SCs. During the process of phagocytosis, OECs also produced less pro-inflammatory, but more immunomodulatory, factors than SCs. Thus, OECs were more efficient in phagocytosing “self-targets” than SCs, accompanied by a more favourable immune response, suggesting that OECs may be better transplantation candidates than SCs. Two peripheral nerves, the olfactory nerve and the trigeminal nerve (intranasal branches) extend between the nasal cavity and the brain. These nerves are populated by OECs and SCs, respectively. These nerves have been shown to function as a pathway by which certain microbes can enter the brain, leading to CNS infection. The nasal mucosa, and associated nasal-associated lymphoid tissue (NALT) constitute a strong physical and immunological barrier against microorganisms, and those that do manage to penetrate the mucosa are considered to be phagocytosed by OECs and SCs in the nerves. However, microbes that can infect the CNS via these two peripheral nerves have been shown to evade phagocytic destruction and instead infect PNS glia. In this Thesis, I also investigated how OECs and SCs respond to bacterium thought to infect the CNS via nerves - Chlamydia muridarum. I chose this bacterium as it is commonly used to model C. pneumoniae infections in mice. C. pneumoniae CNS infection has been suggested to contribute to the development of late-onset dementia, thus being clinically relevant. I found that C. muridarum, which replicates in intracellular inclusion bodies, infected both OECs and SCs, however, the glia were not as susceptible to infection and intracellular bacterial growth as non-immune cells. Both OECs and SCs mounted a significant immune response to bacterial challenge, with OECs producing the strongest response. Despite this, C. muridarum could manipulate various intracellular and phagocytic machinery pathways to survive inside the glia, including pathways involving small Rho GTPases (Rac, Cdc42 and Rho) and PI3K/Akt. C. muridarum also suppressed lysosomal recruitment by “hijacking” Ras-like small GTPases (Rabs) responsible for intracellular trafficking and host nutrient scavenging. Thus, C. muridarum could escape phagocytosis (degradation) and grow inside glia. This is potentially a key reason by which the bacteria may disseminate through peripheral nerves, leading to CNS infection. The findings presented in this Thesis (including resultant publications), increases our understanding of how PNS glia remove dying and damaged “self”, including key cellular and molecular mechanisms involved in OEC and SC-mediated phagocytosis. The current study also, by characterizing how the glia responded to C. muridarum, explored the crucial dichotomy between phagocytosis vs infection. Internalization of bacteria into a cell can lead to either or both. In the case of OECs and SCs, C. muridarum challenge led to infection but also an immune response, restricted bacterial growth and likely also killing of a proportion of bacteria. This understanding may provide us with tools/drug targets for manipulation of various aspects of the PNS glia-mediated phagocytic processes. This could involve improved clearance of cellular debris without adverse inflammatory events post-transplantation into a nervous system injury site. Tweaking certain aspects of the phagocytic pathway may also prevent infections by microbes that can use the nose-to-brain pathway to infect the CNS, without using antibiotics (thus, not contributing to antimicrobial resistance). Finally, this thesis has also given us some interesting insights into differences between the two types of PNS glia. OECs and SCs, were considered to be quite similar in the past and both are deemed as good transplantation candidates. Overall, OECs were found to be more efficient phagocytes and equipped with additional molecular components of phagocytic pathways than SCs. OECs also produced a more favourable immune response than SCs in response to damaged “self”. In contrast, OECs mounted a stronger bactericidal immune response to C. muridarum than SCs, suggesting that OECs exhibit better antimicrobial protection mechanisms than SCs.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Pharmacy & Med Sci
Griffith Health
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Schuliga, Michael, and michael schuliga@deakin edu au. "Steroidogenesis in cultured mammalian glial cells." Deakin University. School of Biological and Chemical Sciences, 1998. http://tux.lib.deakin.edu.au./adt-VDU/public/adt-VDU20061207.154152.

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A protocol for culturing mammalian type 1 astrocytic cells, using female post-natal rat cerebral cortical tissue, was established and refined for use in steroidogenic metabolic studies incorporating progestin radioisotopes. Cultures were characterised for homogeneity using standard morphological and immunostaining techniques. Qualitative and quantitative studies were conducted to characterise the progesterone (P) metabolic pathways present in astrocytes in vitro. Of particular interest was the formation of the P metabolite, 5á-pregnan-3á-ol-20-one (THP). THP is a GABA(A) receptor agonist, believed to play a vital role in neural functioning and CNS homeostasis. One aim of this study was to observe any modulatory effects selected neuroactive ligands have on the conversion of P into THP, in an attempt to link astrocytic steroidogenesis with neuronal control. In qualitative studies, chromatographic procedures were used to establish the progestin profile of cerebral cortical astrocytes. Tritiated P, DHP (5á-pregnan-3,20-dione) and THP incurbates were preliminary fractionated by either normal phase (NP) or reverse phase (RP) high performance liquid chromatography (HPLC). The radiometabolites associated with each fraction were further chromatographed, before and/or after chemical derivatistation, by the aforemention HPLC procedures and thin layer chromatography (TLC). Steroid radiometabolites were tentatively identified by comparing their chromatographic mobility with authentic steroids. The identity of the main putative 5á-reduced P metabolities, DHP, THP and 5á-pregnan-3á,20á-diol (20áOH-THP) were further confirmed by isotopic dilution analysis. Their conclusive identification, along with the tentative identification of 20á-hydroxypreg-4-en-3-one (20áOH-P) and 20á-hydroxy-5á-pregnan-3-one (20áOH-DHP), verify the localisation of 5á-reductase, 3á-hydroxy steroif oxidoreductase (HSOR), and 20á-HSOR activity in the cultured astrocytes utilised in this study programme. Other minor metabolites detected were tentatively identified, including 5á-pregnan-3á,21-diol-20-one (THDoc), indicating the presence of 21-hydroxylase enzymatic activity. THDoc, like THP, is a GABA(A) receptor agonist. The chemical and physical characterisation of several yet unidentified progestin metabolites, associated with a highly polar RP HPLC fraction (designated RP peak 1*), indicate the presence of one or more extra hydroxylase enzymes. Quantitative analysis included a preliminary study. In this study, the percentage yields of radiometabolites formed in cultures incubated with increasing substrate concentrations of (3)H-P for 24 hours were determined. At the lower concentrations examined (ie 0.5 to 50nM), the metabolites associated with the polar RP HPLC fraction (RP peak 1*) collectively have the highest percentage yield. They are subsequently considered metabolic end products of degradative catabolic P pathways. The percentage yield of THP peaks in the medium concentration ranges (ie 5 to 500nM), whereas DHP remains fairly static at a low level with increasing concentration. Both DHP and THP are considered metabolic pathway intermediates. The percentage yield of 20áOH-THP continues to increase with increasing concentration over 5nM, superseding THP approaching the highest concentration examined (5000nM). This indicated the formation of 20áOH-THP does not occur entirely via THP. 20áOH-THP also possibly serves as the direct intermediate in the formation of the main radiometabolites associated with RP peak 1*. A time/yield study incorporating incubation times from one to 24 hours was also conducted. The full array of radiometabolites (individually or in groups) formed in astrocyte cultures incubated with 50nM tritiated P, DHP of THP, were assayed. Cultures were observed to rapidly convert any DHP into THP, showing astrocytic 3á-HSOR activity is very high. The study also showed 5á-reduction (ie the conversation of P into DHP) is the rate limiting reaction in the two step conversion of P into THP. 5á-Reduction also appears to be a rate limiting step in the formation of 20á-hydroxylated metabolites in astrocytes. Cultures incubated with the tritiated 5á-reduced pregnanes from one to four hours form greater quantities to 20á-hydroxylated radiometabolites compared to cultures incubated with (3)H-P. The time yield/studies also provided further evidence the unidentified polar radiometabolites associated with RP peak 1* are metabolic end products. For the P and DHP incubates, the collective formation of the aforementioned polar radiometabolites initially lags behind the formation of THP. As the formation of the latter begins to plateau with increasing time between four to 24 hours, the net yield of radiometabolites associated with RP peak 1* continues to rise. The time/yield studies also indicate 5á-reduction and perhaps 3á-hydroxylation are pre-requisite steps in the formation of the polar metabolites. Cultures incubated with the 5á-reduced progestins from one to four hours form higher yields of the radiometabolites associated with RP peak 1* compared to cultures incubated with P as substrate. The net yields of the radiometabolites associated with RP peak 1* for cultures incubated with THP were substantially higher compared to cultures incubated with DHP after equivalent times. The effect selected neuroligands have on the yield of radiometabolites formed by cultured astrocytes incubated with 50nM (3)H-P was also examined. Dibutyryl cyclic adenosine monophosphate (DBcAMP), not actually a neuroligand per se, but an analog of the intracellular secondary messenger cAMP, was also utilised in these studies. The inhibitory neurotransmitter ã-amino-nbutyric acid (GABA), DBcAMP and isoproterenol (a â-adrenergic receptor agonist) all quickly induce a transient but substantial increase in 20á-HSOR activity in cultured astrocytes. Cultures pretreated with these three compounds (10, 20 and 1µM respectively) form substantially higher yields of 20á-hydroxylated metabolites, including 20áOH-THP (between 200 to 580% greater), when incubated with 50nM (3)H-P for one to four hours. These increases also coincide with increases in the net yield of metabolites formed (by 16 to 48%). The same pre-treated cultures form significantly lower yields of THP, by 25 to 41%, after one hour. This is most likely due to the increased metabolism of any formed THP into 20áOH-THP. Octopamine (an á-adrenergic agonist) only induces a slight increase in 20á-HSOR activity, having relatively little effect on the yield of 20áOH-THP formed. Pretreatment with octopamine induces a significant increase in the yield of THP for cultures incubated with (3)H-P for four hours (by 24%). The increase in THP formation appears to be due to an increase in 3á-HSOR activity, as judged by the concomitant drop in the yield of the 5á-reduced, 3-keto substrates. An increase in 5á-reductase activity cannot be excluded however. Isoproterenol appears to induce an increase in 5á-reductase activity as isoproterenol appears to induce an increase in 5á-reductase activity as isoproterenol one and four hour incubates have higher yields of DHP. This is in contrast to the other three incubates. After 12 hours, all incubates have higher yields of THP (15-30%).
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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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Stuckey, Crystal Elaine. "Oxidative Stress and Cell Death in Osmotically Swollen Glial Cells." Wright State University / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=wright1208492663.

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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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Nutt, Catherine L. "Mechanisms of drug resistance in glial cells." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq28512.pdf.

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Gao, Yuanqing. "Hypothalamic Glial Cells in Diet Induced Obesity." University of Cincinnati / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1447071648.

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Nieweg, Katja. "Cholesterol biosynthesis in neurons and glial cells." Université Louis Pasteur (Strasbourg) (1971-2008), 2007. https://publication-theses.unistra.fr/public/theses_doctorat/2007/NIEWEG_Katja_2007.pdf.

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Cette étude confirme l’hypothèse d’une dépendance des neurones en cholesterol astrocytaire au stade postnatal. Nos travaux montrent que les neurones ne peuvent assurer leurs besoins en cholestérol: L’accumulation de lanostérol et la lente conversion de stérols intermédiaires indiquent que les neurones produisent du cholesterol de façon moins efficace que les cellules gliales. La diminution le taux de cholestérol dans les neurones n’induit pas d’augmentation de l’expression des enzymes de sa voie de biosynthèse. L’absence de synthèse d’ester de cholesterol et d’organelles de stockage de cholesterol accentue la faible capacité des neurones à produire leur cholesterol. Enfin, l’apport en cholesterol par les cellules gliales induit l’arrêt de sa synthèse par les neurones. Cette étude démontre également que les neurones et astrocytes ont une composition distincte en stérol, qui pourrait être liée à des fonctions cellulaires spécifiques et impliquée lors de processus neurodégénératifs.
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Nieweg, Katja Pfrieger Frank. "Cholesterol biosynthesis in neurons and glial cells." Strasbourg : Université de Strasbourg, 2009. http://eprints-scd-ulp.u-strasbg.fr:8080/1048/01/NIEWEG_Katja_2007.pdf.

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Books on the topic "Glial cells"

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Castellano, Bernardo, Berta González, and Manuel Nieto-Sampedro, eds. Understanding Glial Cells. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5737-1.

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1957-, Castellano Bernardo, González Berta 1955-, and Nieto-Sampedro Manuel 1944-, eds. Understanding glial cells. Boston: Kluwer Academic, 1998.

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E, Lancaster Francine, and National Institute on Alcohol Abuse and Alcoholism (U.S.), eds. Alcohol and glial cells. Bethesda, Md: National Institutes of Health, National Institute on Alcohol Abuse and Alcoholism, 1994.

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R, Laming P., and Syková Eva, eds. Glial cells: Their role in behaviour. Cambridge, U.K: Cambridge University Press, 1998.

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Patro, Ishan, Pankaj Seth, Nisha Patro, and Prakash Narain Tandon, eds. The Biology of Glial Cells: Recent Advances. Singapore: Springer Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-8313-8.

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Jeserich, Gunnar, Hans H. Althaus, Christiane Richter-Landsberg, and Rolf Heumann, eds. Molecular Signaling and Regulation in Glial Cells. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60669-4.

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Bignami, A. Glial cells in the central nervous system. Amsterdam: Published by Elsevier for the Foundation for the Study of the Nervous System, 1992.

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von Bernhardi, Rommy, ed. Glial Cells in Health and Disease of the CNS. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-40764-7.

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Alvarez-Leefmans, Francisco J., and John M. Russell, eds. Chloride Channels and Carriers in Nerve, Muscle, and Glial Cells. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4757-9685-8.

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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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Book chapters on the topic "Glial cells"

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Dobson, Katharine L., and Tomas C. Bellamy. "Glial Cells." In Essentials of Cerebellum and Cerebellar Disorders, 219–23. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-24551-5_27.

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Pais, Teresa Faria. "Glial Cells." In Compendium of Inflammatory Diseases, 527–37. Basel: Springer Basel, 2016. http://dx.doi.org/10.1007/978-3-7643-8550-7_111.

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Kettenmann, Helmut, and Alex Verkhratsky. "Glial Cells." In Neuroscience in the 21st Century, 475–506. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-1997-6_19.

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Pais, Teresa Faria. "Glial Cells." In Encyclopedia of Inflammatory Diseases, 1–12. Basel: Springer Basel, 2015. http://dx.doi.org/10.1007/978-3-0348-0620-6_111-1.

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Williams, Matthew, Claire Macdonald, and Mario Cordero. "Glial Cells." In The Neuropathology of Schizophrenia, 221–41. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-68308-5_12.

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Dobson, Katharine L., and Tomas C. Bellamy. "Glial Cells." In Essentials of Cerebellum and Cerebellar Disorders, 187–90. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-15070-8_28.

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Castejón, Orlando J. "Cerebellar Glial Cells." In Scanning Electron Microscopy of Cerebellar Cortex, 87–95. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0159-6_12.

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Kettenmann, Helmut, and Alex Verkhratsky. "Glial Cells: Neuroglia." In Neuroscience in the 21st Century, 547–78. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3474-4_19.

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Kettenmann, Helmut, and Alexei Verkhratsky. "Glial Cells: Neuroglia." In Neuroscience in the 21st Century, 825–60. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-88832-9_19.

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Kettenmann, Helmut, and Alexei Verkhratsky. "Glial Cells: Neuroglia." In Neuroscience in the 21st Century, 1–36. New York, NY: Springer New York, 2021. http://dx.doi.org/10.1007/978-1-4614-6434-1_19-3.

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Conference papers on the topic "Glial cells"

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Kremer, AE, L. Gebhardt, J. Robering, H. Kühn, K. Wolf, and MMJ Fischer. "Lysophosphatidic acid activates peripheral glial cells." In 35. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0038-1677169.

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Toy, Muhammed Fatih, Burcu Kurt Vatandaslar, and Bilal Ersen Kerman. "Refractive index tomography of myelinating glial cells." In Quantitative Phase Imaging V, edited by Gabriel Popescu and YongKeun Park. SPIE, 2019. http://dx.doi.org/10.1117/12.2512706.

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Salakhutdinov, Ildar F., Pamela VandeVord, Olena Palyvoda, Howard T. W. Matthew, Golam Newaz, and Gregory W. Auner. "Polymer gratings for protein and glial cells adsorption." In Laser Science. Washington, D.C.: OSA, 2008. http://dx.doi.org/10.1364/ls.2008.lthd5.

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Yamanaka, Koji. "Active roles of glial cells in neurodegenrative disease." In 2010 International Conference on Systems in Medicine and Biology (ICSMB). IEEE, 2010. http://dx.doi.org/10.1109/icsmb.2010.5735340.

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Leiss, Lina, Ivana Manini, Marta Calderon, and Per Øyvind Enger. "Abstract LB-345: Hypoxia-induced reprogramming cause normal glia to mimic tumor-associated glial cells." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-lb-345.

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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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Stingl, Andreas, Patricia M. A. Farias, Raquel Milani, Arnaldo Andrade, and Andre Galembeck. "Long term imaging of living brain glial cancer cells." In Neural Imaging and Sensing 2018, edited by Qingming Luo and Jun Ding. SPIE, 2018. http://dx.doi.org/10.1117/12.2290330.

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Bacola, Gregory, Simon Vales, Alice Prigent, Kelsie A. Dougherty, Deanna M. Peperno, Shaian Lashani, Bradley A. Wieland, et al. "Abstract 119: Enteric glial cells promote chemoresistance in ATM-expressing cancer stem cells." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-119.

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Chaplygina, A. V., V. I. Kovalev, D. Y. Zhdanova, and N. V. Bobkova. "CHEMICAL CONVERSION OF PRIMARY NEURONAL CULTURES." In NOVEL TECHNOLOGIES IN MEDICINE, BIOLOGY, PHARMACOLOGY AND ECOLOGY. Institute of information technology, 2022. http://dx.doi.org/10.47501/978-5-6044060-2-1.389-393.

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The paper discusses the use of direct chemical transformation of glial cells into neurons to solve the problems of neurodegenerative diseases. Original experimental data on the success-ful use of a conversion cocktail for astrocyte-neuronal conversion in a primary cell culture of the 5xFAD mouse hippocampus are presented.
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Kolosov, M. S., E. Duz, and A. B. Uzdensky. "Photodynamic damage of glial cells in crayfish ventral nerve cord." In Sartov Fall Meeting 2010, edited by Valery V. Tuchin and Elina A. Genina. SPIE, 2010. http://dx.doi.org/10.1117/12.889355.

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Reports on the topic "Glial cells"

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Kamaruzzaman, Mohd Amir, Muhammad Hibatullah Romli, Razif Abas, Sharmili Vidyadaran, Mohamad Taufik Hidayat Baharuldin, Muhammad Luqman Nasaruddin, Vishnnumukkala Thirupathirao, et al. Impact of Endocannabinoid Mediated Glial Cells on Cognitive Function in Alzheimer’s Disease: A Systematic Review and Meta-Analysis of Animal Studies. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2022. http://dx.doi.org/10.37766/inplasy2022.8.0094.

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Review question / Objective: This review aims to review systematically, and meta-analyse published pre-clinical research about the mechanism of endocannabinoid system modulation on glial cells and their effects on cognitive function in designated Alzheimer’s Disease (AD) in the animal model. Condition being studied: Its been acknowledged that the cure of Alzheimer's disease is still vague. Current medicine is working on symptoms only but never stop the disease progression due to neuronal loss. In recent years, researches have found that cannabinoid which is derived from cannabis sativa plant and its compounds exert neuroprotective effects in vitro and in vivo. In fact, cognitive improvement has been shown in some clinical studies. Therefore, the knowledge of cannabinoids and its interaction with living physiological environment like glial cells is crucial as immunomodulation to strategize the potential target of this substance. The original articles from related study relating endocannabinoid mediated glial cell were extracted to summarize and meta-analyze its impact and possible mechanism against cognitive decline in AD.
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Rothstein, Jeffrey D., and Betty Diamond. The Role of NG2 Glial Cells in ALS Pathogenesis. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada598910.

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Rothstein, Jeffrey D. The Role of NG2 Glial Cells in ALS Pathogenesis. Fort Belvoir, VA: Defense Technical Information Center, December 2014. http://dx.doi.org/10.21236/ada618869.

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Estevez-Ordonez, Dagoberto, Matthew Jarrell, Travis Atchley, Nick Laskay, Mark Hadley, and Mohommad Hamo. Systematic Review of Spinal Glial Tumors. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2023. http://dx.doi.org/10.37766/inplasy2023.4.0085.

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Review question / Objective: Does the extent of resection of intramedullary spinal cord astrocytomas affect oncologic and neurologic outcomes? Condition being studied: Intramedullary spinal cord tumors, which are a class of tumors arising from the cells from within the spinal cord. Study designs to be included: Randomized clinical trials, clinical and observational studies, and case series with available abstracts and published as full-scale original articles, brief reports in peer-reviewed academic journals or descriptive publications on surgical techniques with no restriction on language or time of publication.
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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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Stern, Michael. Signaling Pathways Controlling the Growth and Proliferation of Drosophilae Perineural Glial Cells. Fort Belvoir, VA: Defense Technical Information Center, May 2005. http://dx.doi.org/10.21236/ada437242.

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Stern, Michael. Signaling Pathways Controlling the Growth and Proliferation of Drosophila Perineurial Glial Cells. Fort Belvoir, VA: Defense Technical Information Center, May 2004. http://dx.doi.org/10.21236/ada428460.

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Stern, Michael. Signaling Pathways Controlling the Growth and Proliferation of Drosophilae Perineurial Glial Cells. Fort Belvoir, VA: Defense Technical Information Center, May 2003. http://dx.doi.org/10.21236/ada416605.

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Sterm, Michael. Signaling Pathways Controlling the Growth and Proliferation of Drosophila Perineurial Glial Cells. Fort Belvoir, VA: Defense Technical Information Center, May 2006. http://dx.doi.org/10.21236/ada458973.

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