Physiology of Astroglia

Astrocytes are neural cells of ectodermal, neuroepithelial origin that provide for homeostasis and defense of the central nervous system (CNS). Astrocytes are highly heterogeneous in morphological appearance; they express a multitude of receptors, channels, and membrane transporters. This complement underlies their remarkable adaptive plasticity that defines the functional maintenance of the CNS in development and aging. Astrocytes are tightly integrated into neural networks and act within the context of neural tissue; astrocytes control homeostasis of the CNS at all levels of organization from molecular to the whole organ.

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Differential Effects of Three CanonicalToxoplasmaStrains on Gene Expression in Human Neuroepithelial Cells

Infection and Immunity ◽

10.1128/iai.00947-10 ◽

2010 ◽

Vol 79 (3) ◽

pp. 1363-1373 ◽

Cited By ~ 38

Author(s):

Jianchun Xiao ◽

Lorraine Jones-Brando ◽

C. Conover Talbot ◽

Robert H. Yolken

Keyword(s):

Gene Expression ◽

Central Nervous System ◽

Nervous System ◽

Nucleotide Metabolism ◽

Neural Cells ◽

Type I ◽

Type Ii ◽

Type Iii ◽

Neuroepithelial Cells ◽

The Central Nervous System

ABSTRACTStrain type is one of the key factors suspected to play a role in determining the outcome ofToxoplasmainfection. In this study, we examined the transcriptional profile of human neuroepithelioma cells in response to representative strains ofToxoplasmaby using microarray analysis to characterize the strain-specific host cell response. The study of neural cells is of interest in light of the ability ofToxoplasmato infect the brain and to establish persistent infection within the central nervous system. We found that the extents of the expression changes varied considerably among the three strains. Neuroepithelial cells infected withToxoplasmatype I exhibited the highest level of differential gene expression, whereas type II-infected cells had a substantially smaller number of genes which were differentially expressed. Cells infected with type III exhibited intermediate effects on gene expression. The three strains also differed in the individual genes and gene pathways which were altered following cellular infection. For example, gene ontology (GO) analysis indicated that type I infection largely affects genes related to the central nervous system, while type III infection largely alters genes which affect nucleotide metabolism; type II infection does not alter the expression of a clearly defined set of genes. Moreover, Ingenuity Pathways Analysis (IPA) suggests that the three lineages differ in the ability to manipulate their host; e.g., they employ different strategies to avoid, deflect, or subvert host defense mechanisms. These observed differences may explain some of the variation in the neurobiological effects of different strains ofToxoplasmaon infected individuals.

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Biology of Oligodendrocyte and Myelin in the Mammalian Central Nervous System

Physiological Reviews ◽

10.1152/physrev.2001.81.2.871 ◽

2001 ◽

Vol 81 (2) ◽

pp. 871-927 ◽

Cited By ~ 1001

Author(s):

Nicole Baumann ◽

Danielle Pham-Dinh

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Proteolipid Protein ◽

Demyelinating Diseases ◽

Neural Cells ◽

The Central Nervous System ◽

Experimental Demyelination ◽

Pelizaeus Merzbacher Disease ◽

Spontaneous Mutants ◽

Extracellular Environment

Oligodendrocytes, the myelin-forming cells of the central nervous system (CNS), and astrocytes constitute macroglia. This review deals with the recent progress related to the origin and differentiation of the oligodendrocytes, their relationships to other neural cells, and functional neuroglial interactions under physiological conditions and in demyelinating diseases. One of the problems in studies of the CNS is to find components, i.e., markers, for the identification of the different cells, in intact tissues or cultures. In recent years, specific biochemical, immunological, and molecular markers have been identified. Many components specific to differentiating oligodendrocytes and to myelin are now available to aid their study. Transgenic mice and spontaneous mutants have led to a better understanding of the targets of specific dys- or demyelinating diseases. The best examples are the studies concerning the effects of the mutations affecting the most abundant protein in the central nervous myelin, the proteolipid protein, which lead to dysmyelinating diseases in animals and human (jimpy mutation and Pelizaeus-Merzbacher disease or spastic paraplegia, respectively). Oligodendrocytes, as astrocytes, are able to respond to changes in the cellular and extracellular environment, possibly in relation to a glial network. There is also a remarkable plasticity of the oligodendrocyte lineage, even in the adult with a certain potentiality for myelin repair after experimental demyelination or human diseases.

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Are astrocytes executive cells within the central nervous system?

Arquivos de Neuro-Psiquiatria ◽

10.1590/0004-282x20160101 ◽

2016 ◽

Vol 74 (8) ◽

pp. 671-678 ◽

Cited By ~ 5

Author(s):

Roberto E. Sica ◽

Roberto Caccuri ◽

Cecilia Quarracino ◽

Francisco Capani

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Synaptic Activity ◽

Neural Cells ◽

Degenerative Diseases ◽

Human Species ◽

Cerebellar Ataxias ◽

The Central Nervous System ◽

Experimental Findings ◽

Lateral Sclerosis

ABSTRACT Experimental evidence suggests that astrocytes play a crucial role in the physiology of the central nervous system (CNS) by modulating synaptic activity and plasticity. Based on what is currently known we postulate that astrocytes are fundamental, along with neurons, for the information processing that takes place within the CNS. On the other hand, experimental findings and human observations signal that some of the primary degenerative diseases of the CNS, like frontotemporal dementia, Parkinson’s disease, Alzheimer’s dementia, Huntington’s dementia, primary cerebellar ataxias and amyotrophic lateral sclerosis, all of which affect the human species exclusively, may be due to astroglial dysfunction. This hypothesis is supported by observations that demonstrated that the killing of neurons by non-neural cells plays a major role in the pathogenesis of those diseases, at both their onset and their progression. Furthermore, recent findings suggest that astrocytes might be involved in the pathogenesis of some psychiatric disorders as well.

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Effectiveness Of Immunolabeling Gfap For Estimating Astrocytic Shape And Volume

Microscopy and Microanalysis ◽

10.1017/s143192760002002x ◽

1999 ◽

Vol 5 (S2) ◽

pp. 1340-1341

Author(s):

E. Bushong ◽

M. E. Martone ◽

C. Foster ◽

M. H. Ellisman

Keyword(s):

Central Nervous System ◽

Blood Flow ◽

Nervous System ◽

Brain Function ◽

Neural Tissue ◽

Surrounding Tissue ◽

The Central Nervous System ◽

Fine Structures ◽

Transport Of Ions ◽

Labeling Pattern

Each astrocyte forms an extensive network of fine processes within the surrounding neural tissue, interacting extensively with neighboring neurons and blood vessels. Fine glial processes surround synapses and probably modulate synaptic transmission. Glial endfeet on capillaries are responsible for transport of ions and metabolites and possibly control blood flow. Alterations in these fine structures may be of significance in brain function and disease. Glial fibrillary acidic protein (GFAP) is an intermediate filament found in astrocytes of the central nervous system. GFAP is commonly found in the perikarya and processes of protoplasmic and fibrous type astrocytes. Immunohistochemical labeling of GFAP is extensively used as a means of determining the location and shape of astrocytes. However, its labeling pattern varies with brain region (e.g. cortex vs. hippocampus), with cell state (natural vs. reactive astrocytes), and with the specific α- GFAP antibody used. Furthermore, Golgi-stained or dye-filled astrocytes show numerous small appendages or vellate structures that conform to the surrounding tissue and do not stain for GFAP.

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Molecular and Cellular Mechanisms Underlying Somatostatin-Based Signaling in Two Model Neural Networks, the Retina and the Hippocampus

International Journal of Molecular Sciences ◽

10.3390/ijms20102506 ◽

2019 ◽

Vol 20 (10) ◽

pp. 2506 ◽

Cited By ~ 2

Author(s):

Maurizio Cammalleri ◽

Paola Bagnoli ◽

Albertino Bigiani

Keyword(s):

Neural Networks ◽

Central Nervous System ◽

Nervous System ◽

Inhibitory Interneurons ◽

Cellular Mechanisms ◽

Widespread Occurrence ◽

Neural Inhibition ◽

The Central Nervous System ◽

Available Information

Neural inhibition plays a key role in determining the specific computational tasks of different brain circuitries. This functional “braking” activity is provided by inhibitory interneurons that use different neurochemicals for signaling. One of these substances, somatostatin, is found in several neural networks, raising questions about the significance of its widespread occurrence and usage. Here, we address this issue by analyzing the somatostatinergic system in two regions of the central nervous system: the retina and the hippocampus. By comparing the available information on these structures, we identify common motifs in the action of somatostatin that may explain its involvement in such diverse circuitries. The emerging concept is that somatostatin-based signaling, through conserved molecular and cellular mechanisms, allows neural networks to operate correctly.

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Monte Carlo track structure simulation in studies of biological effects induced by accelerated charged particles in the central nervous system

EPJ Web of Conferences ◽

10.1051/epjconf/201920404008 ◽

2019 ◽

Vol 204 ◽

pp. 04008 ◽

Cited By ~ 1

Author(s):

Munkhbaatar Batmunkh ◽

Lkhagvaa Bayarchimeg ◽

Aleksandr N. Bugay ◽

Oidov Lkhagva

Keyword(s):

Central Nervous System ◽

Monte Carlo ◽

Nervous System ◽

Hippocampal Neurons ◽

Biological Effects ◽

Charged Particles ◽

Particle Accelerators ◽

Neural Cells ◽

Granular Cells ◽

The Central Nervous System

Simulating the biological damage induced by charged particles trajectories (tracks) in the central nervous system (CNS) at different levels of its organization (molecular, cellular, and tissue) is a challenge of modern radiobiology studies. According to the recent experimental studies at particle accelerators, the most radiation-sensitive area of the CNS is the hippocampus. In this regards, the development of measurement-based Monte Carlo simulation of radiation-induced alterations in the hippocampus is of great interest to understand the radiobiological effects on the CNS. The present work investigates the influence of charged particles on the hippocampal cells of the rat brain using the Geant4 Monte Carlo radiation transport code. The applied computer simulation provides a method to simulate physics processes and chemical reactions in the developed model of the rat hippocampus, which contains different types of neural cells - pyramidal cells, mature and immature granular cells, mossy cells, and neural stem cells. The distribution of stochastic energy depositions has been obtained and analyzed in critical structures of the hippocampal neurons after irradiation with 600 MeV/u iron particles. The computed energy deposition in irradiated hippocampal neurons following a track of iron ion suggests that most of the energy is accumulated by granular cells. The obtained quantities at the level of molecular targets also assume that NMDA and GABA receptors belong to the most probable targets in the irradiated neural cells.

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Septal deafferentation enhances the neurotrophic effects of rat hippocampus on cultured neural cells from the central nervous system

Neuroscience Letters ◽

10.1016/0304-3940(86)90187-4 ◽

1986 ◽

Vol 66 (2) ◽

pp. 181-186 ◽

Cited By ~ 17

Author(s):

Kazunari Yoshida ◽

Shinichi Kohsaka ◽

Takeshi Idei ◽

Seiji Nii ◽

Mitsuhiro Otani ◽

...

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Rat Hippocampus ◽

Neural Cells ◽

The Central Nervous System

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CLINICAL СASE OF INFLUENZA A(H1N1) COMPLICATED WITH ACUTE DISSEMINATED ENCEPHALOMYELITIS

CHILDREN INFECTIONS ◽

10.22627/2072-8107-2018-17-3-64-68 ◽

2018 ◽

Vol 17 (3) ◽

pp. 64-68

Author(s):

L. N. Mazankova ◽

T. A. Chebotareva ◽

E. P. Koval ◽

M. A. Antsupova ◽

A. V. Belaya

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Influenza A ◽

Cytopathic Effect ◽

Rare Complication ◽

Neural Tissue ◽

Acute Disseminated Encephalomyelitis ◽

Pathological Conditions ◽

Influenza A H1n1 ◽

The Central Nervous System

The defeat of the central nervous system in influenza reflects the properties of both the pathogen itself and the complex pathogenetic mechanisms of the influenza infectious process. Existing modern theories do not fully explain the pathological conditions of influenza in the central nervous system, which is still accompanied by ambiguous clinical arguments about the direct cytopathic effect of the influenza virus on neural tissue with the development of encephalitis. Another rare complication of the flu is acute disseminated encephalomyelitis. The autoimmune mechanism of the development of this disease is universally recognized, despite the continuing difficulties of diagnosis in the absence of oligoclonal antibodies in blood plasma and spinal cerebral fluid in the majority of patients.

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MicroRNA-138-5p targets pro-apoptotic factors and favours neural cell survival

10.21203/rs.3.rs-26501/v1 ◽

2020 ◽

Author(s):

Rodrigo M Maza ◽

Agata Silvan ◽

Teresa Muñoz-Galdeano ◽

David Reigada ◽

Ángela del Águila ◽

...

Keyword(s):

Central Nervous System ◽

Cell Death ◽

Nervous System ◽

Cell Line ◽

Neural Cell ◽

Luciferase Reporter ◽

Neural Cells ◽

Qrt Pcr ◽

The Central Nervous System ◽

Apoptotic Genes

Abstract Background The central nervous system-enriched microRNA miR-138-5p becomes significantly downregulated after spinal cord injury (SCI). miR-138-5p modulates essential biological processes in the Central Nervous System (CNS). It also overcomes apoptosis by inhibiting the expression of proteins, including the effector CASP3, key in different cell death pathways. Therefore, we hypothesize that miR-138-5p downregulation following SCI underlies the overexpression of apoptotic genes and sensitizes neural cells to noxious stimuli. To confirm this hypothesis, this study aims a) to identify and validate miR-138-5p targets among the pro-apoptotic genes overexpressed following SCI; and b) to confirm that the miR-138-5p is able to modulate cell death in neural cells Methods We employed computational tools to identify potential pro-apoptotic targets of miR-138-5p. Dysregulation of selected targets after SCI and its relationship to changes in miR-138-5p expression were analysed through qRT-PCR in a rat SCI model. Validation of the regulation of those apoptotic targets was carried out by luciferase reporter, qRT-PCR, and immunoblot assays in cultures of neural cell lines transfected with a mimetic of the microRNA. The functional effects of modifying the expression of miR-138-5p were later examined in cultures of the rat neural cell line C6 employing enzymatic assays to measure the activity of effector CASP3 and CASP7 together with MTT and flow cytometry assays to estimate cell death. Results Consensus among different algorithms identified 209 potential targets of miR-138-5p. A total of 176 of them become dysregulated after SCI, including proteins basic to apoptosis process such as CASP3 and CASP7, or BAK (Bcl-2 homologous antagonist/killer). Downregulation of miR-138-5p after SCI correlates with the overexpression of these three targets. Cell culture analyses confirm that miR-138-5p targets their 3’UTRs and reduces their expression after microRNA transfection. Transfection of miR-138-5p in C6 cell line results in a reduced effector caspase activity and protects cells from apoptotic stimulation. Conclusions Our results demonstrate that downregulation of miR-138-5p after SCI can be deleterious to spinal neural cells. A mixture of direct effects mediated by the upregulation of apoptotic targets and indirect effects related to the upregulation of cell cycle proteins can be expected.

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Neuromesodermal Lineage Contribution to CNS Development in Invertebrate and Vertebrate Chordates

Genes ◽

10.3390/genes12040592 ◽

2021 ◽

Vol 12 (4) ◽

pp. 592

Author(s):

Clare Hudson ◽

Hitoyoshi Yasuo

Keyword(s):

Central Nervous System ◽

Nervous System ◽

System Development ◽

Neural Tissue ◽

Nervous System Development ◽

Cns Development ◽

Neural Fate ◽

The Central Nervous System ◽

Ascidian Embryos ◽

Anterior Posterior

Ascidians are invertebrate chordates and the closest living relative to vertebrates. In ascidian embryos a large part of the central nervous system arises from cells associated with mesoderm rather than ectoderm lineages. This seems at odds with the traditional view of vertebrate nervous system development which was thought to be induced from ectoderm cells, initially with anterior character and later transformed by posteriorizing signals, to generate the entire anterior-posterior axis of the central nervous system. Recent advances in vertebrate developmental biology, however, show that much of the posterior central nervous system, or spinal cord, in fact arises from cells that share a common origin with mesoderm. This indicates a conserved role for bi-potential neuromesoderm precursors in chordate CNS formation. However, the boundary between neural tissue arising from these distinct neural lineages does not appear to be fixed, which leads to the notion that anterior-posterior patterning and neural fate formation can evolve independently.

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