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1
McClain, Jonathon L., and Brian D. Gulbransen. "The acute inhibition of enteric glial metabolism with fluoroacetate alters calcium signaling, hemichannel function, and the expression of key proteins." Journal of Neurophysiology 117, no. 1 (January 1, 2017): 365–75. http://dx.doi.org/10.1152/jn.00507.2016.
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Glia play key roles in the regulation of neurotransmission in the nervous system. Fluoroacetate (FA) is a metabolic poison widely used to study glial functions by disrupting the tricarboxylic acid cycle enzyme aconitase. Despite the widespread use of FA, the effects of FA on essential glial functions such as calcium (Ca2+) signaling and hemichannel function remain unknown. Therefore, our goal was to assess specifically the impact of FA on essential glial cell functions that are involved with neurotransmission in the enteric nervous system. To this end, we generated a new optogenetic mouse model to study specifically the effects of FA on enteric glial Ca2+ signaling by crossing PC::G5-tdTomato mice with Sox10::creER T2 mice. FA did not change the peak glial Ca2+ response when averaged across all glia within a ganglion. However, FA decreased the percent of responding glia by 30% ( P < 0.05) and increased the peak Ca2+ response of the glial cells that still exhibited a response by 26% ( P < 0.01). Disruption of Ca2+ signaling with FA impaired the activity-dependent uptake of ethidium bromide through connexin-43 (Cx43) hemichannels ( P < 0.05) but did not affect baseline Cx43-dependent dye uptake. FA did not cause overt glial or neurodegeneration, but glial cells significantly increased glial fibrillary acid protein by 56% ( P < 0.05) following treatment with FA. Together, these data show that the acute impairment of glial metabolism with FA causes key changes in glial functions associated with their roles in neurotransmission and phenotypic changes indicative of reactive gliosis. NEW & NOTEWORTHY Our study shows that the acute impairment of enteric glial metabolism with fluoroacetate (FA) alters specific glial functions that are associated with the modification of neurotransmission in the gut. These include subtle changes to glial agonist-evoked calcium signaling, the subsequent disruption of connexin-43 hemichannels, and changes in protein expression that are consistent with a transition to reactive glia. These changes in glial function offer a mechanistic explanation for the effects of FA on peripheral neuronal networks.
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Wang, Yu-Feng, and Yong-Jing Gao. "2019 Academic Annual Meeting and the Frontier Seminar on “Glial Cell Function and Disease” (Nantong, China)." ASN Neuro 11 (January 2019): 175909141986357. http://dx.doi.org/10.1177/1759091419863576.
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The contribution of glial activities to the functions, diseases, and repair of the central nervous system has received increasing attention in neuroscience studies. To promote the research of glial cells and increase cooperation with peers, the 2019 Academic Annual Meeting and the Frontier Seminar on “Glial Cell Function and Disease” was held in Nantong City, Jiangsu Province, China from May 24 to 26. The meeting was organized by Drs. Yong-Jing Gao and Jia-Wei Zhou of the Chinese Society of Neuroscience Glia Branch. The conference focused on the physiological and pathological functions of astrocytes, microglia, and oligodendrocytes with 25 speakers in two plenary speeches and five sections of more than 180 participants engaged in glial cell research. In the two plenary lectures, Yutian Wang from the University of British Columbia and Xia Zhang from the University of Ottawa presented “Development of NMDAR (N-methyl-D-aspartic acid receptor)-positive allosteric modulators as novel therapeutics for brain disorders” and “Mechanisms underlying cannabinoid regulation of brain function and disease,” respectively. The five sections included microglia and disease, astrocytes and disease, glioma treatment and glial imaging, oligodendrocytes and disease, and glial–neuronal interactions and disease. This meeting allowed extensive and in-depth academic exchanges on the latest research and experimental techniques, represented the highest achievements of Chinese scholars on glial cells, and promoted the cooperation between peers in the fields of glia studies.
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Bacci, Alberto, Claudia Verderio, Elena Pravettoni, and Michela Matteoli. "The role of glial cells in synaptic function." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 354, no. 1381 (February 28, 1999): 403–9. http://dx.doi.org/10.1098/rstb.1999.0393.
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Glial cells represent the most abundant cell population in the central nervous system and for years they have been thought to provide just structural and trophic support to neurons. Recently, several studies were performed, leading to the identification of an active interaction between glia and neurons. This paper focuses on the role played by glial cells at the level of the synapse, reviewing recent data defining how glia is determinant in synaptogenesis, in the modulation of fully working synaptic contacts and in synaptic plasticity.
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Allen, Nicola J., and David A. Lyons. "Glia as architects of central nervous system formation and function." Science 362, no. 6411 (October 11, 2018): 181–85. http://dx.doi.org/10.1126/science.aat0473.
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Glia constitute roughly half of the cells of the central nervous system (CNS) but were long-considered to be static bystanders to its formation and function. Here we provide an overview of how the diverse and dynamic functions of glial cells orchestrate essentially all aspects of nervous system formation and function. Radial glia, astrocytes, oligodendrocyte progenitor cells, oligodendrocytes, and microglia each influence nervous system development, from neuronal birth, migration, axon specification, and growth through circuit assembly and synaptogenesis. As neural circuits mature, distinct glia fulfill key roles in synaptic communication, plasticity, homeostasis, and network-level activity through dynamic monitoring and alteration of CNS structure and function. Continued elucidation of glial cell biology, and the dynamic interactions of neurons and glia, will enrich our understanding of nervous system formation, health, and function.
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Singhvi, Aakanksha, and Shai Shaham. "Glia-Neuron Interactions in Caenorhabditis elegans." Annual Review of Neuroscience 42, no. 1 (July 8, 2019): 149–68. http://dx.doi.org/10.1146/annurev-neuro-070918-050314.
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Glia are abundant components of animal nervous systems. Recognized 170 years ago, concerted attempts to understand these cells began only recently. From these investigations glia, once considered passive filler material in the brain, have emerged as active players in neuron development and activity. Glia are essential for nervous system function, and their disruption leads to disease. The nematode Caenorhabditis elegans possesses glial types similar to vertebrate glia, based on molecular, morphological, and functional criteria, and has become a powerful model in which to study glia and their neuronal interactions. Facile genetic and transgenic methods in this animal allow the discovery of genes required for glial functions, and effects of glia at single synapses can be monitored by tracking neuron shape, physiology, or animal behavior. Here, we review recent progress in understanding glia-neuron interactions in C. elegans. We highlight similarities with glia in other animals, and suggest conserved emerging principles of glial function.
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Stern, P. R. "Reexamining Glial Function." Science Signaling 3, no. 112 (March 9, 2010): ec76-ec76. http://dx.doi.org/10.1126/scisignal.3112ec76.
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Ceprian, Maria, and Daniel Fulton. "Glial Cell AMPA Receptors in Nervous System Health, Injury and Disease." International Journal of Molecular Sciences 20, no. 10 (May 17, 2019): 2450. http://dx.doi.org/10.3390/ijms20102450.
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Glia form a central component of the nervous system whose varied activities sustain an environment that is optimised for healthy development and neuronal function. Alpha-amino-3-hydroxy-5-methyl-4-isoxazole (AMPA)-type glutamate receptors (AMPAR) are a central mediator of glutamatergic excitatory synaptic transmission, yet they are also expressed in a wide range of glial cells where they influence a variety of important cellular functions. AMPAR enable glial cells to sense the activity of neighbouring axons and synapses, and as such many aspects of glial cell development and function are influenced by the activity of neural circuits. However, these AMPAR also render glia sensitive to elevations of the extracellular concentration of glutamate, which are associated with a broad range of pathological conditions. Excessive activation of AMPAR under these conditions may induce excitotoxic injury in glial cells, and trigger pathophysiological responses threatening other neural cells and amplifying ongoing disease processes. The aim of this review is to gather information on AMPAR function from across the broad diversity of glial cells, identify their contribution to pathophysiological processes, and highlight new areas of research whose progress may increase our understanding of nervous system dysfunction and disease.
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Wang, Sheng-Zhi, Xiao-Dong Liu, Yu-Xin Huang, Qing-Jiu Ma, and Jing-Jie Wang. "Disruption of Glial Function Regulates the Effects of Electro-Acupuncture at Tsusanli on Gastric Activity in Rats." American Journal of Chinese Medicine 37, no. 04 (January 2009): 647–56. http://dx.doi.org/10.1142/s0192415x09007132.
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According to recent evidence, acupuncture at Tsusanli (ST 36) can regulate gastric activity. And this regulation mainly depends upon neural basis or structure and may probably relate to the central neurons in the dorsal vagal complex. However, whether the glias of the dorsal vagal complex participate in the regulation of gastric activity, when electro-acupuncture (EA) at Tsusanli, still remains to be interpreted. In this study, we observed the effect of EA at Tsusanli (ST 36) on regulation of gastric activity. Propentofylline (PPF), a glial metabolic inhibitor, was used to inhibit the function of glial cells. EA at Tsusanli showed that the expressions of glial fibrillary acidic protein (GFAP) and OX42 increased significantly compared to that of the control group, and gastric electric change was obvious, with significantly higher frequency and wave amplitude compared to the control group. The expressions of GFAP and OX42 were decreased markedly when pretreated with PPF group than without PPF pretreatment group. Compared to the Tsusanli group and the control group, the changes of electro gastric graph (EGG) were significantly decreased in PPF pretreatment group. On the other hand, we observed the changes of spontaneous electro-activity of the DVC (dorsal vagal complex) in our previous experiment. The results indicated that EA at Tsusanli could activate glial cells in the dorsal vagal complex and regulate gastric activity. PPF blocked the function of glia, thus the effect of EA at Tsusanli on gastric activity was weakened. Our study suggested that this electro-acupuncture regulation of gastric activity was possibly related with glia of the dorsal vagal complex.
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Dimou, Leda, and Magdalena Götz. "Glial Cells as Progenitors and Stem Cells: New Roles in the Healthy and Diseased Brain." Physiological Reviews 94, no. 3 (July 2014): 709–37. http://dx.doi.org/10.1152/physrev.00036.2013.
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The diverse functions of glial cells prompt the question to which extent specific subtypes may be devoted to a specific function. We discuss this by reviewing one of the most recently discovered roles of glial cells, their function as neural stem cells (NSCs) and progenitor cells. First we give an overview of glial stem and progenitor cells during development; these are the radial glial cells that act as NSCs and other glial progenitors, highlighting the distinction between the lineage of cells in vivo and their potential when exposed to a different environment, e.g., in vitro. We then proceed to the adult stage and discuss the glial cells that continue to act as NSCs across vertebrates and others that are more lineage-restricted, such as the adult NG2-glia, the most frequent progenitor type in the adult mammalian brain, that remain within the oligodendrocyte lineage. Upon certain injury conditions, a distinct subset of quiescent astrocytes reactivates proliferation and a larger potential, clearly demonstrating the concept of heterogeneity with distinct subtypes of, e.g., astrocytes or NG2-glia performing rather different roles after brain injury. These new insights not only highlight the importance of glial cells for brain repair but also their great potential in various aspects of regeneration.
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Yadav, Smita, Susan H. Younger, Linghua Zhang, Katherine L. Thompson-Peer, Tun Li, Lily Y. Jan, and Yuh Nung Jan. "Glial ensheathment of the somatodendritic compartment regulates sensory neuron structure and activity." Proceedings of the National Academy of Sciences 116, no. 11 (February 25, 2019): 5126–34. http://dx.doi.org/10.1073/pnas.1814456116.
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Sensory neurons perceive environmental cues and are important of organismal survival. Peripheral sensory neurons interact intimately with glial cells. While the function of axonal ensheathment by glia is well studied, less is known about the functional significance of glial interaction with the somatodendritic compartment of neurons. Herein, we show that three distinct glia cell types differentially wrap around the axonal and somatodendritic surface of the polymodal dendritic arborization (da) neuron of the Drosophila peripheral nervous system for detection of thermal, mechanical, and light stimuli. We find that glial cell-specific loss of the chromatin modifier gene dATRX in the subperineurial glial layer leads to selective elimination of somatodendritic glial ensheathment, thus allowing us to investigate the function of such ensheathment. We find that somatodendritic glial ensheathment regulates the morphology of the dendritic arbor, as well as the activity of the sensory neuron, in response to sensory stimuli. Additionally, glial ensheathment of the neuronal soma influences dendritic regeneration after injury.
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Kim, Taejoon, Bokyeong Song, and Im-Soon Lee. "Drosophila Glia: Models for Human Neurodevelopmental and Neurodegenerative Disorders." International Journal of Molecular Sciences 21, no. 14 (July 9, 2020): 4859. http://dx.doi.org/10.3390/ijms21144859.
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Glial cells are key players in the proper formation and maintenance of the nervous system, thus contributing to neuronal health and disease in humans. However, little is known about the molecular pathways that govern glia–neuron communications in the diseased brain. Drosophila provides a useful in vivo model to explore the conserved molecular details of glial cell biology and their contributions to brain function and disease susceptibility. Herein, we review recent studies that explore glial functions in normal neuronal development, along with Drosophila models that seek to identify the pathological implications of glial defects in the context of various central nervous system disorders.
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Delvalle, Ninotchska M., David E. Fried, Gretchen Rivera-Lopez, Luke Gaudette, and Brian D. Gulbransen. "Cholinergic activation of enteric glia is a physiological mechanism that contributes to the regulation of gastrointestinal motility." American Journal of Physiology-Gastrointestinal and Liver Physiology 315, no. 4 (October 1, 2018): G473—G483. http://dx.doi.org/10.1152/ajpgi.00155.2018.
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The reflexive activities of the gastrointestinal tract are regulated, in part, by precise interactions between neurons and glia in the enteric nervous system (ENS). Intraganglionic enteric glia are a unique type of peripheral glia that surround enteric neurons and regulate neuronal function, activity, and survival. Enteric glia express numerous neurotransmitter receptors that allow them to sense neuronal activity, but it is not clear if enteric glia monitor acetylcholine (ACh), the primary excitatory neurotransmitter in the ENS. Here, we tested the hypothesis that enteric glia detect ACh and that glial activation by ACh contributes to the physiological regulation of gut functions. Our results show that myenteric enteric glia express both the M3 and M5 subtypes of muscarinic receptors (MRs) and that muscarine drives intracellular calcium (Ca2+) signaling predominantly through M3R activation. To elucidate the functional effects of activation of glial M3Rs, we used GFAP::hM3Dq mice that express a modified human M3R (hM3Dq) exclusively on glial fibrillary acidic protein (GFAP) positive glia to directly activate glial hM3Dqs using clozapine- N-oxide. Using spatiotemporal mapping analysis, we found that the activation of glial hM3Dq receptors enhances motility reflexes ex vivo. Continuous stimulation of hM3Dq receptors in vivo, drove changes in gastrointestinal motility without affecting neuronal survival in the ENS and glial muscarinic receptor activation did not alter neuron survival in vitro. Our results provide the first evidence that GFAP intraganglionic enteric glia express functional muscarinic receptors and suggest that the activation of glial muscarinic receptors contributes to the physiological regulation of functions. NEW & NOTEWORTHY Enteric glia are emerging as novel regulators of enteric reflex circuits, but little is still known regarding the effects of specific transmitter pathways on glia and the resulting consequences on enteric reflexes. Here, we provide the first evidence that enteric glia monitor acetylcholine in the enteric nervous system and that glial activation by acetylcholine is a physiological mechanism that contributes to the functional regulation of intestinal reflexes.
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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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Parker, Robert J., and Vanessa J. Auld. "Signaling in glial development: differentiation migration and axon guidance." Biochemistry and Cell Biology 82, no. 6 (December 1, 2004): 694–707. http://dx.doi.org/10.1139/o04-119.
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Glial cells have diverse functions that are necessary for the proper development and function of complex nervous systems. During development, a variety of reciprocal signaling interactions between glia and neurons dictate all parts of nervous system development. Glia may provide attractive, repulsive, or contact-mediated cues to steer neuronal growth cones and ensure that neurons find their appropriate synaptic targets. In fact, both neurons and glia may act as migrational substrates for one another at different times during development. Also, the exchange of trophic signals between glia and neurons is essential for the proper bundling, fasciculation, and ensheathement of axons as well as the differentiation and survival of both cell types. The growing number of links between glial malfunction and human disease has generated great interest in glial biology. Because of its relative simplicity and the many molecular genetic tools available, Drosophila is an excellent model organism for studying glial development. This review will outline the roles of glia and their interactions with neurons in the embryonic nervous system of the fly.Key words: glia, axon guidance, migration, EGF receptor.
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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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Araque, Alfonso, and Marta Navarrete. "Glial cells in neuronal network function." Philosophical Transactions of the Royal Society B: Biological Sciences 365, no. 1551 (August 12, 2010): 2375–81. http://dx.doi.org/10.1098/rstb.2009.0313.
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Numerous evidence demonstrates that astrocytes, a type of glial cell, are integral functional elements of the synapses, responding to neuronal activity and regulating synaptic transmission and plasticity. Consequently, they are actively involved in the processing, transfer and storage of information by the nervous system, which challenges the accepted paradigm that brain function results exclusively from neuronal network activity, and suggests that nervous system function actually arises from the activity of neuron–glia networks. Most of our knowledge of the properties and physiological consequences of the bidirectional communication between astrocytes and neurons resides at cellular and molecular levels. In contrast, much less is known at higher level of complexity, i.e. networks of cells, and the actual impact of astrocytes in the neuronal network function remains largely unexplored. In the present article, we summarize the current evidence that supports the notion that astrocytes are integral components of nervous system networks and we discuss some functional properties of intercellular signalling in neuron–glia networks.
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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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Booth, G. E., E. F. Kinrade, and A. Hidalgo. "Glia maintain follower neuron survival during Drosophila CNS development." Development 127, no. 2 (January 15, 2000): 237–44. http://dx.doi.org/10.1242/dev.127.2.237.
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While survival of CNS neurons appears to depend on multiple neuronal and non-neuronal factors, it remains largely unknown how neuronal survival is controlled during development. Here we show that glia regulate neuronal survival during formation of the Drosophila embryonic CNS. When glial function is impaired either by mutation of the glial cells missing gene, which transforms glia toward a neuronal fate, or by targeted genetic glial ablation, neuronal death is induced non-autonomously. Pioneer neurons, which establish the first longitudinal axon fascicles, are insensitive to glial depletion whereas the later extending follower neurons die. This differential requirement of neurons for glia is instructive in patterning and links control of cell number with axon guidance during CNS development.
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Campbell, G., H. Goring, T. Lin, E. Spana, S. Andersson, C. Q. Doe, and A. Tomlinson. "RK2, a glial-specific homeodomain protein required for embryonic nerve cord condensation and viability in Drosophila." Development 120, no. 10 (October 1, 1994): 2957–66. http://dx.doi.org/10.1242/dev.120.10.2957.
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We report the identification of RK2, a glial-specific homeodomain protein. RK2 is localized to the nucleus of virtually all embryonic and imaginal glial cells, with the exception of midline glia. Embryos mutant for the gene encoding RK2 are embryonic lethal but normal for early gliogenesis (birth, initial divisions and migration of glia) and axonogenesis (neuronal pathfinding and fasciculation). However, later in development, there are significantly fewer longitudinal glia that are spatially disorganized; in addition, there is a slight disorganization of axon fascicles and a defective nerve cord condensation. This suggests that RK2 is not required for early glial determination, but rather for aspects of glial differentiation or function that are required for embryonic viability.
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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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Chotard, Carole, and Iris Salecker. "Glial cell development and function in the Drosophila visual system." Neuron Glia Biology 3, no. 1 (February 2007): 17–25. http://dx.doi.org/10.1017/s1740925x07000592.
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AbstractIn the developing nervous system, building a functional neuronal network relies on coordinating the formation, specification and survival to diverse neuronal and glial cell subtypes. The establishment of neuronal connections further depends on sequential neuron–neuron and neuron–glia interactions that regulate cell-migration patterns and axon guidance. The visual system of Drosophila has a highly regular, retinotopic organization into reiterated interconnected synaptic circuits. It is therefore an excellent invertebrate model to investigate basic cellular strategies and molecular determinants regulating the different developmental processes that lead to network formation. Studies in the visual system have provided important insights into the mechanisms by which photoreceptor axons connect with their synaptic partners within the optic lobe. In this review, we highlight that this system is also well suited for uncovering general principles that underlie glial cell biology. We describe the glial cell subtypes in the visual system and discuss recent findings about their development and migration. Finally, we outline the pivotal roles of glial cells in mediating neural circuit assembly, boundary formation, neural proliferation and survival, as well as synaptic function.
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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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Rangarajan, R., Q. Gong, and U. Gaul. "Migration and function of glia in the developing Drosophila eye." Development 126, no. 15 (August 1, 1999): 3285–92. http://dx.doi.org/10.1242/dev.126.15.3285.
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Although glial cells have been implicated widely in the formation of axon tracts in both insects and vertebrates, their specific function appears to be context-dependent, ranging from providing essential guidance cues to playing a merely facilitory role. Here we examine the role of the retinal basal glia (RBG) in photoreceptor axon guidance in Drosophila. The RBG originate in the optic stalk and have been thought to migrate into the eye disc along photoreceptor axons, thus precluding any role in axon guidance. Here we show the following. (1) The RBG can, in fact, migrate into the eye disc even in the absence of photoreceptor axons in the optic stalk; they also migrate to ectopic patches of differentiating photoreceptors without axons providing a continuous physical substratum. This suggests that glial cells are attracted into the eye disc not through haptotaxis along established axons, but through another mechanism, possibly chemotaxis. (2) If no glial cells are present in the eye disc, photoreceptor axons are able to grow and direct their growth posteriorly as in wild type, but are unable to enter the optic stalk. This indicates that the RBG have a crucial role in axon guidance, but not in axonal outgrowth per se. (3) A few glia close to the entry of the optic stalk suffice to guide the axons into the stalk, suggesting that glia instruct axons by local interaction.
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Zhang, Albert, Kentaro Noma, and Dong Yan. "Regulation of Gliogenesis by lin-32/Atoh1 in Caenorhabditis elegans." G3 Genes|Genomes|Genetics 10, no. 9 (September 1, 2020): 3271–78. http://dx.doi.org/10.1534/g3.120.401547.
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Abstract The regulation of gliogenesis is a fundamental process for nervous system development, as the appropriate glial number and identity is required for a functional nervous system. To investigate the molecular mechanisms involved in gliogenesis, we used C. elegans as a model and identified the function of the proneural gene lin-32/Atoh1 in gliogenesis. We found that lin-32 functions during embryonic development to negatively regulate the number of AMsh glia. The ectopic AMsh cells at least partially arise from cells originally fated to become CEPsh glia, suggesting that lin-32 is involved in the specification of specific glial subtypes. Moreover, we show that lin-32 acts in parallel with cnd-1/ NeuroD1 and ngn-1/ Neurog1 in negatively regulating an AMsh glia fate. Furthermore, expression of murine Atoh1 fully rescues lin-32 mutant phenotypes, suggesting lin-32/Atoh1 may have a conserved role in glial specification.
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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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Artiushin, Gregory, and Amita Sehgal. "The Glial Perspective on Sleep and Circadian Rhythms." Annual Review of Neuroscience 43, no. 1 (July 8, 2020): 119–40. http://dx.doi.org/10.1146/annurev-neuro-091819-094557.
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While neurons and circuits are almost unequivocally considered to be the computational units and actuators of behavior, a complete understanding of the nervous system must incorporate glial cells. Far beyond a copious but passive substrate, glial influence is inextricable from neuronal physiology, whether during developmental guidance and synaptic shaping or through the trophic support, neurotransmitter and ion homeostasis, cytokine signaling and immune function, and debris engulfment contributions that this class provides throughout an organism's life. With such essential functions, among a growing literature of nuanced roles, it follows that glia are consequential to behavior in adult animals, with novel genetic tools allowing for the investigation of these phenomena in living organisms. We discuss here the relevance of glia for maintaining circadian rhythms and also for serving functions of sleep.
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Colombo, Jorge. "Interlaminar Glia and Other Glial Themes Revisited: Pending Answers Following Three Decades of Glial Research." Neuroglia 1, no. 1 (March 1, 2018): 7–20. http://dx.doi.org/10.3390/neuroglia1010003.
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This review aims to highlight the various significant matters in glial research stemming from personal work by the author and associates at the Unit of Applied Neurobiology (UNA, CEMIC-CONICET), and some of the pending questions. A reassessment and further comments on interlaminar astrocytes—an astroglial cell type that is specific to humans and other non-human primates, and is not found in rodents, is presented. Tentative hypothesis regarding their function and future possible research lines that could contribute to further the analysis of their development and possible role(s), are suggested. The possibility that they function as a separate entity from the “territorial” astrocytes, is also considered. In addition, the potential significance of our observations on interspecies differences in in vitro glial cell dye coupling, on glial diffusible factors affecting the induction of this glial phenotype, and on their interference with the cellular toxic effects of cerebrospinal fluid obtained from l-DOPA treated patients with Parkinson´s disease, is also considered. The major differences oberved in the cerebral cortex glial layout between human and rodents—the main model for studying glial function and pathology—calls for a careful assessment of known and potential species differences in all aspects of glial cell biology. This is essential to provide a better understanding of the organization and function of human and non-human primate brain, and of the neurobiological basis of their behavior.
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VERKHRATSKY, ALEXEJ, RICHARD K. ORKAND, and HELMUT KETTENMANN. "Glial Calcium: Homeostasis and Signaling Function." Physiological Reviews 78, no. 1 (January 1, 1998): 99–141. http://dx.doi.org/10.1152/physrev.1998.78.1.99.
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Verkhratsky, Alexej, Richard K. Orkand, and Helmut Kettenmann. Glial Calcium: Homeostasis and Signaling Function. Physiol. Rev. 78: 99–141, 1998. — Glial cells respond to various electrical, mechanical, and chemical stimuli, including neurotransmitters, neuromodulators, and hormones, with an increase in intracellular Ca2+ concentration ([Ca2+]i). The increases exhibit a variety of temporal and spatial patterns. These [Ca2+]i responses result from the coordinated activity of a number of molecular cascades responsible for Ca2+ movement into or out of the cytoplasm either by way of the extracellular space or intracellular stores. Transplasmalemmal Ca2+ movements may be controlled by several types of voltage- and ligand-gated Ca2+-permeable channels as well as Ca2+ pumps and a Na+/Ca2+ exchanger. In addition, glial cells express various metabotropic receptors coupled to intracellular Ca2+ stores through the intracellular messenger inositol 1,4,5-trisphosphate. The interplay of different molecular cascades enables the development of agonist-specific patterns of Ca2+ responses. Such agonist specificity may provide a means for intracellular and intercellular information coding. Calcium signals can traverse gap junctions between glial cells without decrement. These waves can serve as a substrate for integration of glial activity. By controlling gap junction conductance, Ca2+ waves may define the limits of functional glial networks. Neuronal activity can trigger [Ca2+]i signals in apposed glial cells, and moreover, there is some evidence that glial [Ca2+]i waves can affect neurons. Glial Ca2+ signaling can be regarded as a form of glial excitability.
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Hong, Hui, Huicheng Chen, Yuxia Zhang, Zhimao Wu, Yingying Zhang, Yingyi Zhang, Zeng Hu, et al. "DYF-4 regulates patched-related/DAF-6-mediated sensory compartment formation in C. elegans." PLOS Genetics 17, no. 6 (June 11, 2021): e1009618. http://dx.doi.org/10.1371/journal.pgen.1009618.
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Coordination of neurite extension with surrounding glia development is critical for neuronal function, but the underlying molecular mechanisms remain poorly understood. Through a genome-wide mutagenesis screen in C. elegans, we identified dyf-4 and daf-6 as two mutants sharing similar defects in dendrite extension. DAF-6 encodes a glia-specific patched-related membrane protein that plays vital roles in glial morphogenesis. We cloned dyf-4 and found that DYF-4 encodes a glia-secreted protein. Further investigations revealed that DYF-4 interacts with DAF-6 and functions in a same pathway as DAF-6 to regulate sensory compartment formation. Furthermore, we demonstrated that reported glial suppressors of daf-6 could also restore dendrite elongation and ciliogenesis in both dyf-4 and daf-6 mutants. Collectively, our data reveal that DYF-4 is a regulator for DAF-6 which promotes the proper formation of the glial channel and indirectly affects neurite extension and ciliogenesis.
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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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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.
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Nasser, Yasmin, Ester Fernandez, Catherine M. Keenan, Winnie Ho, Lorraine D. Oland, Lee Anne Tibbles, Michael Schemann, Wallace K. MacNaughton, Anne Rühl, and Keith A. Sharkey. "Role of enteric glia in intestinal physiology: effects of the gliotoxin fluorocitrate on motor and secretory function." American Journal of Physiology-Gastrointestinal and Liver Physiology 291, no. 5 (November 2006): G912—G927. http://dx.doi.org/10.1152/ajpgi.00067.2006.
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The role of enteric glia in gastrointestinal physiology remains largely unexplored. We examined the actions of the gliotoxin fluorocitrate (FC) on intestinal motility, secretion, and inflammation after assessing its efficacy and specificity in vitro. FC (100 μM) caused a significant decrease in the phosphorylation of the glucose analog 2-[ N-(7-nitrobenz-2-oxa-1,3-diaz-4-yl)amino]-2-deoxyglucose in enteric glial cultures and a reduction in glial uptake of the fluorescent dipeptide Ala-Lys-7-amino-4-methylcoumarin-3-acetic acid in both the ileum and colon. Dipeptide uptake by resident murine macrophages or guinea pig myenteric neurons was unaffected by FC. Incubation of isolated guinea pig ileal segments with FC caused a specific and significant increase in glial expression of the phosphorylated form of ERK-1/2. Disruption of enteric glial function with FC in mice reduced small intestinal motility in vitro, including a significant decrease in basal tone and the amplitude of contractility in response to electrical field stimulation. Mice treated with 10 or 20 μmol/kg FC twice daily for 7 days demonstrated a concentration-dependent decrease in small intestinal transit. In contrast, no changes in colonic transit or ion transport in vitro were observed. There were no changes in glial or neuronal morphology, any signs of inflammation in the FC-treated mice, or any change in the number of myenteric nitric oxide synthase-expressing neurons. We conclude that FC treatment causes enteric glial dysfunction, without causing intestinal inflammation. Our data suggest that enteric glia are involved in the modulation of enteric neural circuits underlying the regulation of intestinal motility.
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McQueen, J. K. "Glial cells and neuroendocrine function." Journal of Endocrinology 143, no. 3 (December 1994): 411–15. http://dx.doi.org/10.1677/joe.0.1430411.
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Miller, Diane B., and James P. O'Callaghan. "Depression, cytokines, and glial function." Metabolism 54, no. 5 (May 2005): 33–38. http://dx.doi.org/10.1016/j.metabol.2005.01.011.
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Newman, Eric A., and Andrea Volterra. "Glial control of synaptic function." Glia 47, no. 3 (2004): 207–8. http://dx.doi.org/10.1002/glia.20085.
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Garcia-Segura, Luis M., and Roberto C. Melcangi. "Steroids and glial cell function." Glia 54, no. 6 (2006): 485–98. http://dx.doi.org/10.1002/glia.20404.
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Nave, Klaus-Armin, and Bruce D. Trapp. "Axon-Glial Signaling and the Glial Support of Axon Function." Annual Review of Neuroscience 31, no. 1 (July 2008): 535–61. http://dx.doi.org/10.1146/annurev.neuro.30.051606.094309.
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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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Adams, Niels C., Toshifumi Tomoda, Margaret Cooper, Gunnar Dietz, and Mary E. Hatten. "Mice that lack astrotactin have slowed neuronal migration." Development 129, no. 4 (February 15, 2002): 965–72. http://dx.doi.org/10.1242/dev.129.4.965.
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The cortical regions of the brain are laminated as a result of directed migration of precursor cells along glia during development. Previously, we have used an assay system to identify astrotactin as a neuronal ligand for migration on glial fibers. To examine the function of astrotactin in vivo, we generated a null mutation by targeted gene disruption. The cerebella of astrotactin null mice are approximately 10% smaller than wild type. In vitro and in vivo cerebellar granule cell assays show a decrease in neuron-glial binding, a reduction in migration rates and abnormal development of Purkinje cells. Consequences of this are poorer balance and coordination. Thus, astrotactin functions in migration along glial processes in vivo, a process required for generating laminar structures and for the development of synaptic partner systems.
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Herculano-Houzel, Suzana, and Sandra Dos Santos. "You Do Not Mess with the Glia." Neuroglia 1, no. 1 (July 17, 2018): 193–219. http://dx.doi.org/10.3390/neuroglia1010014.
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Vertebrate neurons are enormously variable in morphology and distribution. While different glial cell types do exist, they are much less diverse than neurons. Over the last decade, we have conducted quantitative studies of the absolute numbers, densities, and proportions at which non-neuronal cells occur in relation to neurons. These studies have advanced the notion that glial cells are much more constrained than neurons in how much they can vary in both development and evolution. Recent evidence from studies on gene expression profiles that characterize glial cells—in the context of progressive epigenetic changes in chromatin during morphogenesis—supports the notion of constrained variation of glial cells in development and evolution, and points to the possibility that this constraint is related to the late differentiation of the various glial cell types. Whether restricted variation is a biological given (a simple consequence of late glial cell differentiation) or a physiological constraint (because, well, you do not mess with the glia without consequences that compromise brain function to the point of rendering those changes unviable), we predict that the restricted variation in size and distribution of glial cells has important consequences for neural tissue function that is aligned with their many fundamental roles being uncovered.
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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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Anton, E. S., M. A. Marchionni, K. F. Lee, and P. Rakic. "Role of GGF/neuregulin signaling in interactions between migrating neurons and radial glia in the developing cerebral cortex." Development 124, no. 18 (September 15, 1997): 3501–10. http://dx.doi.org/10.1242/dev.124.18.3501.
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During neuronal migration to the developing cerebral cortex, neurons regulate radial glial cell function and radial glial cells, in turn, support neuronal cell migration and differentiation. To study how migrating neurons and radial glial cells influence each others' function in the developing cerebral cortex, we examined the role of glial growth factor (a soluble form of neuregulin), in neuron-radial glial interactions. Here, we show that GGF is expressed by migrating cortical neurons and promotes their migration along radial glial fibers. Concurrently, GGF also promotes the maintenance and elongation of radial glial cells, which are essential for guiding neuronal migration to the cortex. In the absence of GGF signaling via erbB2 receptors, radial glial development is abnormal. Furthermore, GGF's regulation of radial glial development is mediated in part by brain lipid-binding protein (BLBP), a neuronally induced, radial glial molecule, previously shown to be essential for the establishment and maintenance of radial glial fiber system. The ability of GGF to influence both neuronal migration and radial glial development in a mutually dependent manner suggests that it functions as a mediator of interactions between migrating neurons and radial glial cells in the developing cerebral cortex.
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Benveniste, E. N. "Inflammatory cytokines within the central nervous system: sources, function, and mechanism of action." American Journal of Physiology-Cell Physiology 263, no. 1 (July 1, 1992): C1—C16. http://dx.doi.org/10.1152/ajpcell.1992.263.1.c1.
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In recent years, there has been increasing evidence that soluble mediators such as cytokines from activated T lymphocytes and macrophages are able to modulate the growth and function of cells found within the central nervous system (CNS), specifically macroglia and microglia cells. Furthermore, glial cells, upon activation, can secrete immunoregulatory factors that influence lymphoid/mononuclear cells as well as the glial cells themselves. Thus the potential exists for bidirectional communication between lymphoid cells and glial cells within the CNS, which in part is mediated via cytokines. This review describes various neurological disease states in which both immune and glial cells may contribute to inflammation and immunologic events occurring in the CNS. The mechanisms by which glial cells both respond to and synthesize a variety of cytokines within the CNS and the capacity of glial cells to acquire major histocompatibility complex antigens and function as antigen-presenting cells within the CNS are described in detail. The implications of these functions, cytokine secretion and antigen presentation, by glial cells are discussed with respect to neurological diseases associated with autoimmunity and/or inflammation.
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Huda, Rafiq, Donald R. McCrimmon, and Marco Martina. "pH modulation of glial glutamate transporters regulates synaptic transmission in the nucleus of the solitary tract." Journal of Neurophysiology 110, no. 2 (July 15, 2013): 368–77. http://dx.doi.org/10.1152/jn.01074.2012.
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The nucleus of the solitary tract (NTS) is the major site for termination of visceral sensory afferents contributing to homeostatic regulation of, for example, arterial pressure, gastric motility, and breathing. Whereas much is known about how different neuronal populations influence these functions, information about the role of glia remains scant. In this article, we propose that glia may contribute to NTS functions by modulating excitatory neurotransmission. We found that acidification (pH 7.0) depolarizes NTS glia by inhibiting K+-selective membrane currents. NTS glia also showed functional expression of voltage-sensitive glutamate transporters, suggesting that extracellular acidification regulates synaptic transmission by compromising glial glutamate uptake. To test this hypothesis, we evoked glutamatergic slow excitatory potentials (SEPs) in NTS neurons with repetitive stimulation (20 pulses at 10 Hz) of the solitary tract. This SEP depends on accumulation of glutamate following repetitive stimulation, since it was potentiated by blocking glutamate uptake with dl- threo-β-benzyloxyaspartic acid (TBOA) or a glia-specific glutamate transport blocker, dihydrokainate (DHK). Importantly, extracellular acidification (pH 7.0) also potentiated the SEP. This effect appeared to be mediated through a depolarization-induced inhibition of glial transporter activity, because it was occluded by TBOA and DHK. In agreement, pH 7.0 did not directly alter d-aspartate-induced responses in NTS glia or properties of presynaptic glutamate release. Thus acidification-dependent regulation of glial function affects synaptic transmission within the NTS. These results suggest that glia play a modulatory role in the NTS by integrating local tissue signals (such as pH) with synaptic inputs from peripheral afferents.
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Welberg, Leonie. "Glial ankyrins function at the junction." Nature Reviews Neuroscience 15, no. 12 (November 20, 2014): 769. http://dx.doi.org/10.1038/nrn3872.
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Gravanis, Iordanis, and Stella E. Tsirka. "Tissue plasminogen activator and glial function." Glia 49, no. 2 (2004): 177–83. http://dx.doi.org/10.1002/glia.20115.
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Annunziato, Lucio, Francesca Boscia, and Giuseppe Pignataro. "Ionic Transporter Activity in Astrocytes, Microglia, and Oligodendrocytes During Brain Ischemia." Journal of Cerebral Blood Flow & Metabolism 33, no. 7 (April 3, 2013): 969–82. http://dx.doi.org/10.1038/jcbfm.2013.44.
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Glial cells constitute a large percentage of cells in the nervous system. During recent years, a large number of studies have critically attributed to glia a new role which no longer reflects the long-held view that glia constitute solely a silent and passive supportive scaffolding for brain cells. Indeed, it has been hypothesized that glia, partnering neurons, have a much more actively participating role in brain function. Alteration of intraglial ionic homeostasis in response to ischemic injury has a crucial role in inducing and maintaining glial responses in the ischemic brain. Therefore, glial transporters as potential candidates in stroke intervention are becoming promising targets to enhance an effective and additional therapy for brain ischemia. In this review, we will describe in detail the role played by ionic transporters in influencing astrocyte, microglia, and oligodendrocyte activity and the implications that these transporters have in the progression of ischemic lesion.
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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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KARTEN, Barbara, Hideki HAYASHI, Gordon A. FRANCIS, Robert B. CAMPENOT, Dennis E. VANCE, and Jean E. VANCE. "Generation and function of astroglial lipoproteins from Niemann–Pick type C1-deficient mice." Biochemical Journal 387, no. 3 (April 26, 2005): 779–88. http://dx.doi.org/10.1042/bj20041694.
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NPC (Niemann–Pick type C) disease is a progressive neurological disorder characterized by defects in intracellular cholesterol trafficking, accumulation of cholesterol in the endosomal system and impaired cholesterol homoeostasis. Although these alterations appear to occur in all NPC1-deficient cell types, the consequences are most profound in the nervous system. Since glial cells are important mediators of brain cholesterol homoeostasis, we proposed that defective generation and/or function of lipoproteins released by glia might contribute to the neurological abnormalities associated with NPC disease. We found that, as in other cell types, Npc1−/− glia accumulate cholesterol intracellularly. We hypothesized that this sequestration of cholesterol in glia might restrict the availability of cholesterol for lipoprotein production. Cerebellar astroglia were cultured from a murine model of NPC disease to compare the lipoproteins generated by these cells and wild-type glia. The experiments demonstrate that the amount of cholesterol in glia-conditioned medium is not reduced by NPC1 deficiency. Similarly, cholesterol efflux to apo (apolipoprotein) A1 or glial expression of the transporter ATP-binding-cassette transporter A1 was not decreased by NPC1 deficiency. In addition, the ratio of apo E:cholesterol and the density distribution of lipoproteins in Npc1−/− and Npc1+/+ glia-conditioned medium are indistinguishable. Importantly, in a functional assay, apo E-containing lipoproteins generated by Npc1−/− and Npc1+/+ glia each stimulate axonal elongation of neurons by approx. 35%. On the basis of these observations, we speculate that the neuropathology characteristic of NPC disease can quite probably be ascribed to impaired processes within neurons in the brain rather than defective lipoprotein production by astroglia.
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Winder, Danny G., and P. Jeffrey Conn. "Roles of metabotropic glutamate receptors in glial function and glial-neuronal communication." Journal of Neuroscience Research 46, no. 2 (October 15, 1996): 131–37. http://dx.doi.org/10.1002/(sici)1097-4547(19961015)46:2<131::aid-jnr1>3.0.co;2-i.
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