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Journal articles on the topic 'Glial cells'
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1
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.
2
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.
11
Giesen, K., T. Hummel, A. Stollewerk, S. Harrison, A. Travers, and C. Klambt. "Glial development in the Drosophila CNS requires concomitant activation of glial and repression of neuronal differentiation genes." Development 124, no. 12 (June 15, 1997): 2307–16. http://dx.doi.org/10.1242/dev.124.12.2307.
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Two classes of glial cells are found in the embryonic Drosophila CNS, midline glial cells and lateral glial cells. Midline glial development is triggered by EGF-receptor signalling, whereas lateral glial development is controlled by the gcm gene. Subsequent glial cell differentiation depends partly on the pointed gene. Here we describe a novel component required for all CNS glia development. The tramtrack gene encodes two zinc-finger proteins, one of which, ttkp69, is expressed in all non-neuronal CNS cells. We show that ttkp69 is downstream of gcm and can repress neuronal differentiation. Double mutant analysis and coexpression experiments indicate that glial cell differentiation may depend on a dual process, requiring the activation of glial differentiation by pointed and the concomitant repression of neuronal development by tramtrack.
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Hidalgo, A. "Neuron–glia interactions during axon guidance in Drosophila." Biochemical Society Transactions 31, no. 1 (February 1, 2003): 50–55. http://dx.doi.org/10.1042/bst0310050.
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Axons navigate to trace stereotypic trajectories over an environment often rich in glial cells. Once axonal trajectories are defined, their structuring proceeds through multiple fasciculation and defasciculation events, to finally establish the mature bundles. Fasciculation and ensheathment also proceed in close association between axons and glial cells, and ultimately require glia. The cross-talk between axons and glia during axon guidance is manifested in: (i) axonal fasciculation and bundling, promoted by glia; (ii) growth cone guidance, as glia function as guidepost cells at choice points; (iii) glial migration patterns, which are influenced by neurons; (iv) cell survival control, which constrains position and number of both cell types; and (iv) connectivity, where an axon contacts its final target aided by glial cells. Understanding the reciprocal interactions between neurons and glia during guidance and fasciculation is absolutely necessary to implement repair of axonal trajectories upon damage. Drosophila can be used as a model system for these purposes.
13
Jessen, Kristjan R. "Glial cells." International Journal of Biochemistry & Cell Biology 36, no. 10 (October 2004): 1861–67. http://dx.doi.org/10.1016/j.biocel.2004.02.023.
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Shin, Ji-Yeon, Zhi-Hui Fang, Zhao-Xue Yu, Chuan-En Wang, Shi-Hua Li, and Xiao-Jiang Li. "Expression of mutant huntingtin in glial cells contributes to neuronal excitotoxicity." Journal of Cell Biology 171, no. 6 (December 19, 2005): 1001–12. http://dx.doi.org/10.1083/jcb.200508072.
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Huntington disease (HD) is characterized by the preferential loss of striatal medium-sized spiny neurons (MSNs) in the brain. Because MSNs receive abundant glutamatergic input, their vulnerability to excitotoxicity may be largely influenced by the capacity of glial cells to remove extracellular glutamate. However, little is known about the role of glia in HD neuropathology. Here, we report that mutant huntingtin accumulates in glial nuclei in HD brains and decreases the expression of glutamate transporters. As a result, mutant huntingtin (htt) reduces glutamate uptake in cultured astrocytes and HD mouse brains. In a neuron–glia coculture system, wild-type glial cells protected neurons against mutant htt-mediated neurotoxicity, whereas glial cells expressing mutant htt increased neuronal vulnerability. Mutant htt in cultured astrocytes decreased their protection of neurons against glutamate excitotoxicity. These findings suggest that decreased glutamate uptake caused by glial mutant htt may critically contribute to neuronal excitotoxicity in HD.
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López-Gómez, Laura, Agata Szymaszkiewicz, Marta Zielińska, and Raquel Abalo. "Nutraceuticals and Enteric Glial Cells." Molecules 26, no. 12 (June 21, 2021): 3762. http://dx.doi.org/10.3390/molecules26123762.
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Until recently, glia were considered to be a structural support for neurons, however further investigations showed that glial cells are equally as important as neurons. Among many different types of glia, enteric glial cells (EGCs) found in the gastrointestinal tract, have been significantly underestimated, but proved to play an essential role in neuroprotection, immune system modulation and many other functions. They are also said to be remarkably altered in different physiopathological conditions. A nutraceutical is defined as any food substance or part of a food that provides medical or health benefits, including prevention and treatment of the disease. Following the description of these interesting peripheral glial cells and highlighting their role in physiological and pathological changes, this article reviews all the studies on the effects of nutraceuticals as modulators of their functions. Currently there are only a few studies available concerning the effects of nutraceuticals on EGCs. Most of them evaluated molecules with antioxidant properties in systemic conditions, whereas only a few studies have been performed using models of gastrointestinal disorders. Despite the scarcity of studies on the topic, all agree that nutraceuticals have the potential to be an interesting alternative in the prevention and/or treatment of enteric gliopathies (of systemic or local etiology) and their associated gastrointestinal conditions.
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Van Landeghem, Laurianne, Julien Chevalier, Maxime M. Mahé, Thilo Wedel, Petri Urvil, Pascal Derkinderen, Tor Savidge, and Michel Neunlist. "Enteric glia promote intestinal mucosal healing via activation of focal adhesion kinase and release of proEGF." American Journal of Physiology-Gastrointestinal and Liver Physiology 300, no. 6 (June 2011): G976—G987. http://dx.doi.org/10.1152/ajpgi.00427.2010.
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Wound healing of the gastrointestinal mucosa is essential for the maintenance of gut homeostasis and integrity. Enteric glial cells play a major role in regulating intestinal barrier function, but their role in mucosal barrier repair remains unknown. The impact of conditional ablation of enteric glia on dextran sodium sulfate (DSS)-induced mucosal damage and on healing of diclofenac-induced mucosal ulcerations was evaluated in vivo in GFAP-HSVtk transgenic mice. A mechanically induced model of intestinal wound healing was developed to study glial-induced epithelial restitution. Glial-epithelial signaling mechanisms were analyzed by using pharmacological inhibitors, neutralizing antibodies, and genetically engineered intestinal epithelial cells. Enteric glial cells were shown to be abundant in the gut mucosa, where they associate closely with intestinal epithelial cells as a distinct cell population from myofibroblasts. Conditional ablation of enteric glia worsened mucosal damage after DSS treatment and significantly delayed mucosal wound healing following diclofenac-induced small intestinal enteropathy in transgenic mice. Enteric glial cells enhanced epithelial restitution and cell spreading in vitro. These enhanced repair processes were reproduced by use of glial-conditioned media, and soluble proEGF was identified as a secreted glial mediator leading to consecutive activation of epidermal growth factor receptor and focal adhesion kinase signaling pathways in intestinal epithelial cells. Our study shows that enteric glia represent a functionally important cellular component of the intestinal epithelial barrier microenvironment and that the disruption of this cellular network attenuates the mucosal healing process.
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Vincent, S., J. L. Vonesch, and A. Giangrande. "Glide directs glial fate commitment and cell fate switch between neurones and glia." Development 122, no. 1 (January 1, 1996): 131–39. http://dx.doi.org/10.1242/dev.122.1.131.
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Glial cells constitute the second component of the nervous system and are important during neuronal development. In this paper we describe a gene, glial cell deficient, (glide), that is necessary for glial cell fate commitment in Drosophila melanogaster. Mutations at the glide locus prevent glial cell determination in the embryonic central and peripheral nervous system. Moreover, we show that the absence of glial cells is the consequence of a cell fate switch from glia to neurones. This suggests the existence of a multipotent precursor cells in the nervous system. glide mutants also display defects in axonal navigation, which confirms and extends previous results indicating a role for glial cells in these processes.
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Winberg, M. L., S. E. Perez, and H. Steller. "Generation and early differentiation of glial cells in the first optic ganglion of Drosophila melanogaster." Development 115, no. 4 (August 1, 1992): 903–11. http://dx.doi.org/10.1242/dev.115.4.903.
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We have examined the generation and development of glial cells in the first optic ganglion, the lamina, of Drosophila melanogaster. Previous work has shown that the growth of retinal axons into the developing optic lobes induces the terminal cell divisions that generate the lamina monopolar neurons. We investigated whether photoreceptor ingrowth also influences the development of lamina glial cells, using P element enhancer trap lines, genetic mosaics and birthdating analysis. Enhancer trap lines that mark the differentiating lamina glial cells were found to require retinal innervation for expression. In mutants with only a few photoreceptors, only the few glial cells near ingrowing axons expressed the marker. Genetic mosaic analysis indicates that the lamina neurons and glial cells are readily separable, suggesting that these are derived from distinct lineages. Additionally, BrdU pulse-chase experiments showed that the cell divisions that produce lamina glia, unlike those producing lamina neurons, are not spatially or temporally correlated with the retinal axon ingrowth. Finally, in mutants lacking photoreceptors, cell divisions in the glial lineage appeared normal. We conclude that the lamina glial cells derive from a lineage that is distinct from that of the L-neurons, that glia are generated independently of photoreceptor input, and that completion of the terminal glial differentiation program depends, directly or indirectly, on an inductive signal from photoreceptor axons.
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Morrow, Theresa, Mi-Ryoung Song, and Anirvan Ghosh. "Sequential specification of neurons and glia by developmentally regulated extracellular factors." Development 128, no. 18 (September 15, 2001): 3585–94. http://dx.doi.org/10.1242/dev.128.18.3585.
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Cortical progenitor cells give rise to neurons during embryonic development and to glia after birth. While lineage studies indicate that multipotent progenitor cells are capable of generating both neurons and glia, the role of extracellular signals in regulating the sequential differentiation of these cells is poorly understood. To investigate how factors in the developing cortex might influence cell fate, we developed a cortical slice overlay assay in which cortical progenitor cells are cultured over cortical slices from different developmental stages. We find that embryonic cortical progenitors cultured over embryonic cortical slices differentiate into neurons and those cultured over postnatal cortical slices differentiate into glia, suggesting that the fate of embryonic progenitors can be influenced by developmentally regulated signals. In contrast, postnatal progenitor cells differentiate into glial cells when cultured over either embryonic or postnatal cortical slices. Clonal analysis indicates that the postnatal cortex produces a diffusible factor that induces progenitor cells to adopt glial fates at the expense of neuronal fates. The effects of the postnatal cortical signals on glial cell differentiation are mimicked by FGF2 and CNTF, which induce glial fate specification and terminal glial differentiation respectively. These observations indicate that cell fate specification and terminal differentiation can be independently regulated and suggest that the sequential generation of neurons and glia in the cortex is regulated by a developmental increase in gliogenic signals.
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Magni, Giulia, and Stefania Ceruti. "The Purinergic System and Glial Cells: Emerging Costars in Nociception." BioMed Research International 2014 (2014): 1–13. http://dx.doi.org/10.1155/2014/495789.
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It is now well established that glial cells not only provide mechanical and trophic support to neurons but can directly contribute to neurotransmission, for example, by release and uptake of neurotransmitters and by secreting pro- and anti-inflammatory mediators. This has greatly changed our attitude towards acute and chronic disorders, paving the way for new therapeutic approaches targeting activated glial cells to indirectly modulate and/or restore neuronal functions. A deeper understanding of the molecular mechanisms and signaling pathways involved in neuron-to-glia and glia-to-glia communication that can be pharmacologically targeted is therefore a mandatory step toward the success of this new healing strategy. This holds true also in the field of pain transmission, where the key involvement of astrocytes and microglia in the central nervous system and satellite glial cells in peripheral ganglia has been clearly demonstrated, and literally hundreds of signaling molecules have been identified. Here, we shall focus on one emerging signaling system involved in the cross talk between neurons and glial cells, the purinergic system, consisting of extracellular nucleotides and nucleosides and their membrane receptors. Specifically, we shall summarize existing evidence of novel “druggable” glial purinergic targets, which could help in the development of innovative analgesic approaches to chronic pain states.
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Docampo-Seara, A., E. Candal, and M. A. Rodríguez. "Study of the glial cytoarchitecture of the developing olfactory bulb of a shark using immunochemical markers of radial glia." Brain Structure and Function 227, no. 3 (January 7, 2022): 1067–82. http://dx.doi.org/10.1007/s00429-021-02448-9.
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AbstractDuring development of the olfactory bulb (OB), glial cells play key roles in axonal guiding/targeting, glomerular formation and synaptic plasticity. Studies in mammals have shown that radial glial cells and peripheral olfactory glia (olfactory ensheathing cells, OECs) are involved in the development of the OB. Most studies about the OB glia were carried out in mammals, but data are lacking in most non-mammalian vertebrates. In the present work, we studied the development of the OB glial system in the cartilaginous fish Scyliorhinus canicula (catshark) using antibodies against glial markers, such as glial fibrillary acidic protein (GFAP), brain lipid-binding protein (BLBP), and glutamine synthase (GS). These glial markers were expressed in cells with radial morphology lining the OB ventricle of embryos and this expression continues in ependymal cells (tanycytes) in early juveniles. Astrocyte-like cells were also observed in the granular layer and surrounding glomeruli. Numerous GS-positive cells were present in the primary olfactory pathway of embryos. In the developmental stages analysed, the olfactory nerve layer and the glomerular layer were the regions with higher GFAP, BLBP and GS immuno-reactivity. In addition, numerous BLBP-expressing cells (a marker of mammalian OECs) showing proliferative activity were present in the olfactory nerve layer. Our findings suggest that glial cells of peripheral and central origin coexist in the OB of catshark embryos and early juveniles. These results open the path for future studies about the differential roles of glial cells in the catshark OB during embryonic development and in adulthood.
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Stacey, Stephanie M., Graham B. Thomas, Alain LabbÉ, and Donald J. Van Meyel. "Longitudinal glia in the fly CNS: pushing the envelope on glial diversity and neuron-glial interactions." Neuron Glia Biology 3, no. 1 (February 2007): 27–33. http://dx.doi.org/10.1017/s1740925x07000506.
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AbstractInteractions between neurons and glial cells are crucial for nervous system development and function in all complex organisms, and many functional, morphological and molecular features of glia are well conserved among species. Here we review studies of the longitudinal glia (LG) in the Drosophila CNS. The LG envelop the neuropil in a membrane sheath, and have features resembling both oligodendrocytes and astrocytes. Because of their unique lineage, morphology and molecular features, the LG provide an excellent model to study the genetic mechanisms underlying glial subtype differentiation and diversity, glial morphogenesis and neuron–glial interactions during development. In addition, they are proving useful in understanding how glial cells maintain ion and neurotransmitter homeostasis and protect neurons from environmental insult.
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Suter, Marc R., Yeong-Ray Wen, Isabelle Decosterd, and Ru-Rong Ji. "Do glial cells control pain?" Neuron Glia Biology 3, no. 3 (August 2007): 255–68. http://dx.doi.org/10.1017/s1740925x08000100.
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AbstractManagement of chronic pain is a real challenge, and current treatments that focus on blocking neurotransmission in the pain pathway have resulted in limited success. Activation of glial cells has been widely implicated in neuroinflammation in the CNS, leading to neurodegeneration in conditions such as Alzheimer's disease and multiple sclerosis. The inflammatory mediators released by activated glial cells, such as tumor necrosis factor-α and interleukin-1β not only cause neurodegeneration in these disease conditions, but also cause abnormal pain by acting on spinal cord dorsal horn neurons in injury conditions. Pain can also be potentiated by growth factors such as brain-derived growth factor and basic fibroblast growth factor, which are produced by glia to protect neurons. Thus, glial cells can powerfully control pain when they are activated to produce various pain mediators. We review accumulating evidence that supports an important role for microglial cells in the spinal cord for pain control under injury conditions (e.g. nerve injury). We also discuss possible signaling mechanisms, in particular mitogen-activated protein kinase pathways that are crucial for glial-mediated control of pain. Investigating signaling mechanisms in microglia might lead to more effective management of devastating chronic pain.
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Logan, Mary A., and Marc R. Freeman. "The scoop on the fly brain: glial engulfment functions in Drosophila." Neuron Glia Biology 3, no. 1 (February 2007): 63–74. http://dx.doi.org/10.1017/s1740925x0700049x.
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AbstractGlial cells provide support and protection for neurons in the embryonic and adult brain, mediated in part through the phagocytic activity of glia. Glial cells engulf apoptotic cells and pruned neurites from the developing nervous system, and also clear degenerating neuronal debris from the adult brain after neural trauma. Studies indicate that Drosophila melanogaster is an ideal model system to elucidate the mechanisms of engulfment by glia. The recent studies reviewed here show that many features of glial engulfment are conserved across species and argue that work in Drosophila will provide valuable cellular and molecular insight into glial engulfment activity in mammals.
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Halter, D. A., J. Urban, C. Rickert, S. S. Ner, K. Ito, A. A. Travers, and G. M. Technau. "The homeobox gene repo is required for the differentiation and maintenance of glia function in the embryonic nervous system of Drosophila melanogaster." Development 121, no. 2 (February 1, 1995): 317–32. http://dx.doi.org/10.1242/dev.121.2.317.
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We describe the cloning, expression and phenotypic characterisation of repo, a gene from Drosophila melanogaster that is essential for the differentiation and maintenance of glia function. It is not, however, required for the initial determination of glial cells. In the embryo, the gene, which encodes a homeodomain protein, is expressed exclusively in all developing glia and closely related cells in both the central and peripheral nervous systems. The only observed exceptions in the CNS are the midline glia derived from the mesectoderm and two of three segmental nerve root glial cells. Using a polyclonal antibody we traced the spatial and temporal pattern of the protein expression in detail. Embryos homozygous for null alleles of the protein exhibit late developmental defects in the nervous system, including a reduction in the number of glial cells, disrupted fasciculation of axons, and the inhibition of ventral nerve cord condensation. The expression of an early glial-specific marker is unaffected in such homozygotes. By contrast, the expression of late glial-specific markers is either substantially reduced or absent. The specificity of expression is also observed in the locust Schistocerca gregaria and is thus evolutionarily conserved.
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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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Feng, L., and N. Heintz. "Differentiating neurons activate transcription of the brain lipid-binding protein gene in radial glia through a novel regulatory element." Development 121, no. 6 (June 1, 1995): 1719–30. http://dx.doi.org/10.1242/dev.121.6.1719.
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Formation and maintenance of a radial glial scaffold is fundamental for development of the vertebrate central nervous system. In mammals, radial glia arise in the neuroepithelium immediately prior to differentiation and migration of neurons away from the ventricular zones, and they are maintained until neuronal migration subsides. We have previously shown that expression of the brain lipid-binding protein (BLBP) in radial glia throughout the developing CNS is strictly correlated with the differentiation and migration of neurons upon these cells, and that BLBP function is required to maintain differentiation of primary cerebellar glial cells in vitro (Feng, L., Hatten, M. E. and Heintz, N. (1994). Neuron 12, 895–908). In this study, we demonstrate that BLBP transcription in vivo involves multiple regulatory elements, and that the dynamic temporal and spatial pattern of BLBP expression in radial and Bergmann glial cells throughout the developing CNS is programmed by a single radial glial cell-specific element (RGE). Furthermore, we demonstrate that BLBP expression in primary cerebellar glial cells requires coculture with differentiating neurons, and that this induction is regulated by the radial glia-specific element. The fact that transcription of BLBP in response to neurons in vitro and its dynamic regulation in radial glia throughout the CNS in vivo are both controlled by the RGE provides the first direct evidence supporting a role for differentiating neurons in the epigenetic regulation of radial glial cell function in vivo.
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Losada-Perez, Maria, Neale Harrison, and Alicia Hidalgo. "Molecular mechanism of central nervous system repair by the Drosophila NG2 homologue kon-tiki." Journal of Cell Biology 214, no. 5 (August 22, 2016): 587–601. http://dx.doi.org/10.1083/jcb.201603054.
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Neuron glia antigen 2 (NG2)–positive glia are repair cells that proliferate upon central nervous system (CNS) damage, promoting functional recovery. However, repair is limited because of the failure of the newly produced glial cells to differentiate. It is a key goal to discover how to regulate NG2 to enable glial proliferation and differentiation conducive to repair. Drosophila has an NG2 homologue called kon-tiki (kon), of unknown CNS function. We show that kon promotes repair and identify the underlying mechanism. Crush injury up-regulates kon expression downstream of Notch. Kon in turn induces glial proliferation and initiates glial differentiation by activating glial genes and prospero (pros). Two negative feedback loops with Notch and Pros allow Kon to drive the homeostatic regulation required for repair. By modulating Kon levels in glia, we could prevent or promote CNS repair. Thus, the functional links between Kon, Notch, and Pros are essential for, and can drive, repair. Analogous mechanisms could promote CNS repair in mammals.
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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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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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Kim, Yoo Sung, Juwon Choi, and Bo-Eun Yoon. "Neuron-Glia Interactions in Neurodevelopmental Disorders." Cells 9, no. 10 (September 27, 2020): 2176. http://dx.doi.org/10.3390/cells9102176.
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Recent studies have revealed synaptic dysfunction to be a hallmark of various psychiatric diseases, and that glial cells participate in synapse formation, development, and plasticity. Glial cells contribute to neuroinflammation and synaptic homeostasis, the latter being essential for maintaining the physiological function of the central nervous system (CNS). In particular, glial cells undergo gliotransmission and regulate neuronal activity in tripartite synapses via ion channels (gap junction hemichannel, volume regulated anion channel, and bestrophin-1), receptors (for neurotransmitters and cytokines), or transporters (GLT-1, GLAST, and GATs) that are expressed on glial cell membranes. In this review, we propose that dysfunction in neuron-glia interactions may contribute to the pathogenesis of neurodevelopmental disorders. Understanding the mechanisms of neuron-glia interaction for synapse formation and maturation will contribute to the development of novel therapeutic targets of neurodevelopmental disorders.
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Badenhorst, Paul. "Tramtrack controls glial number and identity in the Drosophila embryonic CNS." Development 128, no. 20 (October 15, 2001): 4093–101. http://dx.doi.org/10.1242/dev.128.20.4093.
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Neurons and glia are often derived from common multipotent stem cells. In Drosophila, neural identity appears to be the default fate of these precursors. Stem cells that generate either neurons or glia transiently express neural stem cell-specific markers. Further development as glia requires the activation of glial-specific regulators. However, this must be accompanied by simultaneous repression of the alternate neural fate. I show that the Drosophila transcriptional repressor Tramtrack is a key repressor of neuronal fates. It is expressed at high levels in all mature glia of the embryonic central nervous system. Analysis of the temporal profile of Tramtrack expression in glia shows that it follows that of existing glial markers. When expressed ectopically before neural stem cell formation, Tramtrack represses the neural stem cell-specific genes asense and deadpan. Surprisingly, Tramtrack protein levels oscillate in a cell cycle-dependent manner in proliferating glia, with expression dropping before replication, but re-initiating after S phase. Overexpression of Tramtrack blocks glial development by inhibiting S-phase and repressing expression of the S-phase cyclin, cyclin E. Conversely, in tramtrack mutant embryos, glia are disrupted and undergo additional rounds of replication. I propose that Tramtrack ensures stable mature glial identity by both repressing neuroblast-specific genes and controlling glial cell proliferation.
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Pose-Méndez, Sol, Michel Rehbock, Alexandra Wolf-Asseburg, and Reinhard W. Köster. "In Vivo Monitoring of Fabp7 Expression in Transgenic Zebrafish." Cells 13, no. 13 (July 2, 2024): 1138. http://dx.doi.org/10.3390/cells13131138.
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In zebrafish, like in mammals, radial glial cells (RGCs) can act as neural progenitors during development and regeneration in adults. However, the heterogeneity of glia subpopulations entails the need for different specific markers of zebrafish glia. Currently, fluorescent protein expression mediated by a regulatory element from the glial fibrillary acidic protein (gfap) gene is used as a prominent glia reporter. We now expand this tool by demonstrating that a regulatory element from the mouse Fatty acid binding protein 7 (Fabp7) gene drives reliable expression in fabp7-expressing zebrafish glial cells. By using three different Fabp7 regulatory element-mediated fluorescent protein reporter strains, we reveal in double transgenic zebrafish that progenitor cells expressing fluorescent proteins driven by the Fabp7 regulatory element give rise to radial glia, oligodendrocyte progenitors, and some neuronal precursors. Furthermore, Bergmann glia represent the almost only glial population of the zebrafish cerebellum (besides a few oligodendrocytes), and the radial glia also remain in the mature cerebellum. Fabp7 regulatory element-mediated reporter protein expression in Bergmann glia progenitors suggests their origin from the ventral cerebellar proliferation zone, the ventricular zone, but not from the dorsally positioned upper rhombic lip. These new Fabp7 reporters will be valuable for functional studies during development and regeneration.
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Gray, G. E., and J. R. Sanes. "Lineage of radial glia in the chicken optic tectum." Development 114, no. 1 (January 1, 1992): 271–83. http://dx.doi.org/10.1242/dev.114.1.271.
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In many parts of the central nervous system, the elongated processes of radial glial cells are believed to guide immature neurons from the ventricular zone to their sites of differentiation. To study the clonal relationships of radial glia to other neural cell types, we used a recombinant retrovirus to label precursor cells in the chick optic tectum with a heritable marker, the E. coli lacZ gene. The progeny of the infected cells were detected at later stages of development with a histochemical stain for the lacZ gene product. Radial glia were identified in a substantial fraction of clones, and these were studied further. Our main results are the following. (a) Clones containing radial glia frequently contained neurons and/or astrocytes, but usually not other radial glia. Thus, radial glia derive from a multipotential progenitor rather than from a committed radial glial precursor. (b) Production of radial glia continues until at least embryonic day (E) 8, after the peak of neuronal birth is over (approximately E5) and after radial migration of immature neurons has begun (E6-7). Radial glial and neuronal lineages do not appear to diverge during this interval, and radial glia are among the last cells that their progenitors produce. (c) As they migrate, many cells are closely apposed to the apical process of their sibling radial glia. Thus, radial glia may frequently guide the migration of their clonal relatives. (d) The population of labelled radial glia declines between E15 and E19-20 (just before hatching), concurrent with a sharp increase in the number of labelled astrocytes. This result suggests that some tectal radial glia transform into astrocytes, as occurs in mammalian cerebral cortex, although others persist after hatching. To reconcile the observations that many radial glia are present early, that radial glia are among the last offspring of a multipotential stem cell, and that most clones contain only a single radial glial cell, we suggest that the stem cell is, or becomes, a radial glial cell.
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Heiman, Maxwell G., and Shai Shaham. "Ancestral roles of glia suggested by the nervous system of Caenorhabditis elegans." Neuron Glia Biology 3, no. 1 (February 2007): 55–61. http://dx.doi.org/10.1017/s1740925x07000609.
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AbstractThe nematode Caenorhabditis elegans has a simple nervous system with glia restricted primarily to sensory organs. Some of the activities that would be provided by glia in the mammalian nervous system are either absent or provided by non-glial cell types in C. elegans, with only a select set of mammalian glial activities being similarly provided by specialized glial cells in this animal. These observations suggest that ancestral roles of glia may be to modulate neuronal morphology and neuronal sensitivity in sensory organs.
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Ojalvo-Sanz, Ana Cristina, and Laura López-Mascaraque. "Gliogenic Potential of Single Pallial Radial Glial Cells in Lower Cortical Layers." Cells 10, no. 11 (November 19, 2021): 3237. http://dx.doi.org/10.3390/cells10113237.
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During embryonic development, progenitor cells are progressively restricted in their potential to generate different neural cells. A specific progenitor cell type, the radial glial cells, divides symmetrically and then asymmetrically to produce neurons, astrocytes, oligodendrocytes, and NG2-glia in the cerebral cortex. However, the potential of individual progenitors to form glial lineages remains poorly understood. To further investigate the cell progeny of single pallial GFAP-expressing progenitors, we used the in vivo genetic lineage-tracing method, the UbC-(GFAP-PB)-StarTrack. After targeting those progenitors in embryonic mice brains, we tracked their adult glial progeny in lower cortical layers. Clonal analyses revealed the presence of clones containing sibling cells of either a glial cell type (uniform clones) or two different glial cell types (mixed clones). Further, the clonal size and rostro-caudal cell dispersion of sibling cells differed depending on the cell type. We concluded that pallial E14 neural progenitors are a heterogeneous cell population with respect to which glial cell type they produce, as well as the clonal size of their cell progeny.
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López-Bayghen, Esther, Sandra Rosas, Francisco Castelán, and Arturo Ortega. "Cerebellar Bergmann glia: an important model to study neuron–glia interactions." Neuron Glia Biology 3, no. 2 (May 2007): 155–67. http://dx.doi.org/10.1017/s1740925x0700066x.
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AbstractThe biochemical effects triggered by the action of glutamate, the main excitatory amino acid, on a specialized type of glia cells, Bergmann glial cells of the cerebellum, are a model system with which to study glia–neuronal interactions. Neuron to Bergmann glia signaling is involved in early stages of development, mainly in cell migration and synaptogenesis. Later, in adulthood, these cells have an important role in the maintenance and proper function of the synapses that they surround. Major molecular targets of this cellular interplay are glial glutamate receptors and transporters, both of which sense synaptic activity. Glutamate receptors trigger a complex network of signaling cascades that involve Ca2+ influx and lead to a differential gene-expression pattern. In contrast, Bergmann glia glutamate transporters participate in the removal of the neurotransmitter from the synaptic cleft and act also as signal transducers that regulate, in the short term, their own activity. These exciting findings strengthen the concept of active participation of glial cells in synaptic transmission and the involvement of neuron–glia circuits in the processing of brain information.
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Perez-Gianmarco, Lucila, and Maria Kukley. "Understanding the Role of the Glial Scar through the Depletion of Glial Cells after Spinal Cord Injury." Cells 12, no. 14 (July 13, 2023): 1842. http://dx.doi.org/10.3390/cells12141842.
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Spinal cord injury (SCI) is a condition that affects between 8.8 and 246 people in a million and, unlike many other neurological disorders, it affects mostly young people, causing deficits in sensory, motor, and autonomic functions. Promoting the regrowth of axons is one of the most important goals for the neurological recovery of patients after SCI, but it is also one of the most challenging goals. A key event after SCI is the formation of a glial scar around the lesion core, mainly comprised of astrocytes, NG2+-glia, and microglia. Traditionally, the glial scar has been regarded as detrimental to recovery because it may act as a physical barrier to axon regrowth and release various inhibitory factors. However, more and more evidence now suggests that the glial scar is beneficial for the surrounding spared tissue after SCI. Here, we review experimental studies that used genetic and pharmacological approaches to ablate specific populations of glial cells in rodent models of SCI in order to understand their functional role. The studies showed that ablation of either astrocytes, NG2+-glia, or microglia might result in disorganization of the glial scar, increased inflammation, extended tissue degeneration, and impaired recovery after SCI. Hence, glial cells and glial scars appear as important beneficial players after SCI.
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Ochoa-Cortes, Fernando, Fabio Turco, Andromeda Linan-Rico, Suren Soghomonyan, Emmett Whitaker, Sven Wehner, Rosario Cuomo, and Fievos L. Christofi. "Enteric Glial Cells." Inflammatory Bowel Diseases 22, no. 2 (February 2016): 433–49. http://dx.doi.org/10.1097/mib.0000000000000667.
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Götz, Magdalena, and Yves-Alain Barde. "Radial Glial Cells." Neuron 46, no. 3 (May 2005): 369–72. http://dx.doi.org/10.1016/j.neuron.2005.04.012.
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Parnavelas, John G., and Bagirathy Nadarajah. "Radial Glial Cells." Neuron 31, no. 6 (September 2001): 881–84. http://dx.doi.org/10.1016/s0896-6273(01)00437-8.
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Pentreath, V. W. "Invertebrate glial cells." Comparative Biochemistry and Physiology Part A: Physiology 93, no. 1 (January 1989): 77–83. http://dx.doi.org/10.1016/0300-9629(89)90194-1.
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Reichenbach, A. "Retinal glial cells." Acta Ophthalmologica 93 (September 23, 2015): n/a. http://dx.doi.org/10.1111/j.1755-3768.2015.0070.
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Baumann, O., and K. Takeyasu. "Polarized distribution of Na,K-ATPase in honeybee photoreceptors is maintained by interaction with glial cells." Journal of Cell Science 105, no. 2 (June 1, 1993): 287–301. http://dx.doi.org/10.1242/jcs.105.2.287.
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Arthropod photoreceptors are polarized cells displaying distinct surface domains. The distribution of the Na,K-ATPase (sodium pump) over these domains was examined in the honeybee photoreceptor using a monoclonal antibody that specifically recognizes the sodium pump alpha-subunit (approximately 100 kDa). We find that the sodium pump is restricted to sites of the nonreceptive photoreceptor surface closely juxtaposed to glial cells; no sodium pumps were detected on the glia-free domains of the nonreceptive surface and on the light-sensitive microvillar membranes. In order to determine the role of photoreceptor-glia contact in maintaining this polarized pump distribution, we assayed the distribution of the Na,K-ATPase after experimentally influencing photoreceptor-glia contact. Sodium pumps were present on the entire nonreceptive photoreceptor surface when photoreceptor-glia contact was removed by isolating the photoreceptors. Remodeling photoreceptor-glia contact by incubation in hyperosmotic saline caused a redistribution of sodium pumps on the photoreceptor surface corresponding to the redistribution of glial cells. We show, further, that both photoreceptor-glia contact and Na,K-ATPase distribution are independent of extracellular Ca2+. No junctional structures were observed at the borders between Na,K-ATPase-positive and Na,K-ATPase-negative membrane domains. Together, these results suggest that adhesion of glial cells to the photoreceptors plays a crucial role in the maintenance of the polarized distribution of Na,K-ATPase in the honeybee photoreceptors. The Ca(2+)-independent adhesion of glial cells to the photoreceptor surface may trap the pump molecules at the sites of photoreceptor-glia contact.
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Putka, Alexandra F., Juan P. Mato, and Hayley S. McLoughlin. "Myelinating Glia: Potential Therapeutic Targets in Polyglutamine Spinocerebellar Ataxias." Cells 12, no. 4 (February 13, 2023): 601. http://dx.doi.org/10.3390/cells12040601.
Full textAbstract:
Human studies, in combination with animal and cellular models, support glial cells as both major contributors to neurodegenerative diseases and promising therapeutic targets. Among glial cells, oligodendrocytes and Schwann cells are the myelinating glial cells of the central and peripheral nervous system, respectively. In this review, we discuss the contributions of these central and peripheral myelinating glia to the pathomechanisms of polyglutamine (polyQ) spinocerebellar ataxia (SCA) types 1, 2, 3, 6, 7, and 17. First, we highlight the function of oligodendrocytes in healthy conditions and how they are disrupted in polyQ SCA patients and diseased model systems. We then cover the role of Schwann cells in peripheral nerve function and repair as well as their possible role in peripheral neuropathy in polyQ SCAs. Finally, we discuss potential polyQ SCA therapeutic interventions in myelinating glial.
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Cafferty, Patrick, and Vanessa J. Auld. "No pun intended: future directions in invertebrate glial cell migration studies." Neuron Glia Biology 3, no. 1 (February 2007): 45–54. http://dx.doi.org/10.1017/s1740925x07000634.
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AbstractGlial cells play a wide range of essential roles in both nervous system development and function and has been reviewed recently (Parker and Auld, 2006). Glia provide an insulating sheath, either form or direct the formation of the blood–brain barrier, contribute to ion and metabolite homeostasis and provide guidance cues. Glial function often depends on the ability of glial cells to migrate toward specific locations during nervous system development. Work in nervous system development in insects, in particular in the fruit fly Drosophila melanogaster and the tobacco hornworm Manduca sexta, has provided significant insight into the roles of glia, although the molecular mechanisms underlying glial cell migration are being determined only now. Indeed, many of the processes and mechanisms discovered in these simpler systems have direct parallels in the development of vertebrate nervous systems. In this review, we first examine the developmental contexts in which invertebrate glial cell migration has been observed, we next discuss the characterized molecules required for proper glial cell migration, and we finally discuss future goals to be addressed in the study of glial cell development.
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Giangrande, A. "Glia in the fly wing are clonally related to epithelial cells and use the nerve as a pathway for migration." Development 120, no. 3 (March 1, 1994): 523–34. http://dx.doi.org/10.1242/dev.120.3.523.
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The Drosophila major wing nerve collects axons from the anterior margin sensory organs. Using the flp recombinase to make clones, I show that all glia present on this nerve are clonally related to wing epithelial cells. Glial cells arise only from regions that also give rise to sensory organs and migrate along the nerve following the direction taken by axons. As in vertebrates, wing glial cells start migrating at a stage at which axons are growing. The migration of wing glial cells is affected by two mutations altering axonogenesis, fused and Notch, which suggests that the two processes are tightly associated.
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Hazel, Thomas, Michael Hefferan, Kateryna Schwartz, Ningpu Yu, Karl Johe, and Michael Levy. "Generation of Human Oligodendrocyte Progenitors for Treatment of Demyelinating Diseases and Spinal Cord Injury." Journal of Experimental Neurology 4, no. 2 (March 31, 2023): 43–54. http://dx.doi.org/10.33696/neurol.4.072.
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Glial cells play a critical role in the development and function of the mammalian central nervous system (CNS). Among other roles, these cells provide the myelin sheath needed for the efficient propagation of impulses along nerve fibers, provide trophic support for neuronal cells, and remove toxins and excess neurotransmitters from the interstitial space. Transplantation of glial cells or glial progenitors into the diseased or injured CNS can provide therapeutic benefits. However, generation of therapeutically useful quantities of glia, in particular oligodendrocytes, is technically challenging. Furthermore, generation of glial precursors from sources such as embryonic stem (ES) cells and induced pluripotent stem (iPS) cells poses potential safety risks due to the tumorigenic potential of undifferentiated cells. Here we report a method that enables the efficient generation and expansion of glial precursors from tissue-restricted neural stem cells (NSC). NSC-derived glial precursors can be expanded extensively in culture and retain the capacity to differentiate into oligodendrocytes and astrocytes in vitro and in vivo. Upon transplantation into different animal models of demyelination a substantial proportion of these cells become oligodendrocytes with the capacity to myelinate host axons. These results demonstrate that tissue-restricted human neural stem cells can serve as an efficient source for myelinating oligodendrocytes with therapeutic potential.
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Maysinger, Dusica, and Jeff Ji. "Nanostructured Modulators of Neuroglia." Current Pharmaceutical Design 25, no. 37 (December 17, 2019): 3905–16. http://dx.doi.org/10.2174/1381612825666190912163339.
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Biological and synthetic nanostructures can influence both glia and neurons in the central nervous system. Neurons represent only a small proportion (about 10%) of cells in the brain, whereas glial cells are the most abundant cell type. Non-targeted nanomedicines are mainly internalized by glia, in particular microglia, and to a lesser extent by astrocytes. Internalized nanomedicines by glia indirectly modify the functional status of neurons. The mechanisms of biochemical, morphological and functional changes of neural cells exposed to nanomedicines are still not well-understood. This minireview provides a cross-section of morphological and biochemical changes in glial cells and neurons exposed to different classes of hard and soft nanostructures.
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Minamihata, Tomoki, Katsura Takano-Kawabe, and Mitsuaki Moriyama. "Inhibition of Sphingosine Kinase 1 Reduces Sphingosine-1-Phosphate and Exacerbates Amyloid-Beta-Induced Neuronal Cell Death in Mixed-Glial-Cell Culture." Neurology International 16, no. 4 (July 4, 2024): 709–30. http://dx.doi.org/10.3390/neurolint16040054.
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In Alzheimer’s disease (AD) pathology, the accumulation of amyloid-beta (Aβ), a main component of senile plaques, activates glial cells and causes neuroinflammation. Excessive neuroinflammation results in neuronal dropouts and finally produces the symptoms of AD. Recent studies suggest that disorder in sphingosine-1-phosphate (S1P) metabolism, especially the decreased expression of sphingosine kinase (SK)1, followed by the reduction in the amount of S1P, can be a promotive factor in AD onset. Thus, we explored the possibility that dysregulated S1P metabolism affects AD through the altered function in glial cells. We evaluated the effect of PF-543, a pharmacological inhibitor of SK1, on the inflammatory responses by lipopolysaccharide (LPS)-activated glial cells, microglia, and astrocytes. The treatment with PF-543 decreased the intracellular S1P content in glial cells. The PF-543 treatment enhanced the nitric oxide (NO) production in the LPS-treated neuron/glia mixed culture. Furthermore, we found that the augmented production of NO and reactive oxygen species (ROS) in the PF-543-treated astrocytes affected the microglial inflammatory responses through humoral factors in the experiment using an astrocyte-conditioned medium. The PF-543 treatment also decreased the microglial Aβ uptake and increased the number of injured neurons in the Aβ-treated neuron/glia mixed culture. These results suggest that a decrease in the glial S1P content can exacerbate neuroinflammation and neurodegeneration through altered glial cell functions.