Littérature scientifique sur le sujet « Animals, Astrocyte »
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Articles de revues sur le sujet "Animals, Astrocyte"
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Maysinger, Dusica, Mélanie Lalancette-Hébert, Jeff Ji, Katherine Jabbour, Jens Dernedde, Kim Silberreis, Rainer Haag et Jasna Kriz. « Dendritic polyglycerols are modulators of microglia-astrocyte crosstalk ». Future Neurology 14, no 4 (novembre 2019) : FNL31. http://dx.doi.org/10.2217/fnl-2019-0008.
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Aim: To determine the ability of sulfated dendritic polyglycerols (dPGS) to modulate neuroglia activation challenged with lipopolysaccharide (LPS). Materials & methods: Microglia/astrocyte activation in vivo was determined in transgenic animals expressing TLR2-/GFAP-luciferase reporter. Mechanisms implicated in microglia-astrocyte crosstalk were studied in primary mouse brain cultures. Results & discussion: dPGS significantly reduced microglia activation in vivo, and decreased astrocytic LCN2 production. Activated microglia are necessary for astrocyte stimulation and increase in LCN2 abundance. LCN2 production in astrocytes involves signaling via toll-like receptor 4, activation of NF-κB, IL6 and enhancement of reactive oxygen species. Conclusion: dPGS are powerful modulators of microglia-astrocyte crosstalk and LCN2 abundance; dPGS are promising anti-inflammatory dendritic nanostructures.
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Lalo, Ulyana, et Yuriy Pankratov. « Astrocytes as Perspective Targets of Exercise- and Caloric Restriction‐Mimetics ». Neurochemical Research 46, no 10 (7 mars 2021) : 2746–59. http://dx.doi.org/10.1007/s11064-021-03277-2.
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AbstractEnhanced mental and physical activity can have positive effects on the function of aging brain, both in the experimental animals and human patients, although cellular mechanisms underlying these effects are currently unclear. There is a growing evidence that pre-clinical stage of many neurodegenerative diseases involves changes in interactions between astrocytes and neurons. Conversely, astrocytes are strategically positioned to mediate the positive influence of physical activity and diet on neuronal function. Thus, development of therapeutic agents which could improve the astroglia-neuron communications in ageing brain is of crucial importance. Recent advances in studies of cellular mechanisms of brain longevity suggest that astrocyte-neuron communications have a vital role in the beneficial effects of caloric restriction, physical exercise and their pharmacological mimetics on synaptic homeostasis and cognitive function. In particular, our recent data indicate that noradrenaline uptake inhibitor atomoxetine can enhance astrocytic Ca2+-signaling and astroglia-driven modulation of synaptic plasticity. Similar effects were exhibited by caloric restriction-mimetics metformin and resveratrol. The emerged data also suggest that astrocytes could be involved in the modulatory action of caloric restriction and its mimetics on neuronal autophagy. Still, the efficiency of astrocyte-targeting compounds in preventing age-related cognitive decline is yet to be fully explored, in particular in the animal models of neurodegenerative diseases and autophagy impairment.
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Allnoch, Baumgärtner et Hansmann. « Impact of Astrocyte Depletion upon Inflammation and Demyelination in a Murine Animal Model of Multiple Sclerosis ». International Journal of Molecular Sciences 20, no 16 (12 août 2019) : 3922. http://dx.doi.org/10.3390/ijms20163922.
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Astrocytes play a key role in demyelinating diseases, like multiple sclerosis (MS), although many of their functions remain unknown. The aim of this study was to investigate the impact of astrocyte depletion upon de- and remyelination, inflammation, axonal damage, and virus distribution in Theiler`s murine encephalomyelitis (TME). Groups of two to six glial fibrillary acidic protein (GFAP)-thymidine-kinase transgenic SJL mice and SJL wildtype mice were infected with TME virus (TMEV) or mock (vehicle only). Astrocyte depletion was induced by the intraperitoneal administration of ganciclovir during the early and late phase of TME. The animals were clinically investigated while using a scoring system and a rotarod performance test. Necropsies were performed at 46 and 77 days post infection. Cervical and thoracic spinal cord segments were investigated using hematoxylin and eosin (H&E), luxol fast blue-cresyl violet (LFB), immunohistochemistry targeting Amigo2, aquaporin 4, CD3, CD34, GFAP, ionized calcium-binding adapter molecule 1 (Iba1), myelin basic protein (MBP), non-phosphorylated neurofilaments (np-NF), periaxin, S100A10, TMEV, and immunoelectron microscopy. The astrocyte depleted mice showed a deterioration of clinical signs, a downregulation and disorganization of aquaporin 4 in perivascular astrocytes accompanied by vascular leakage. Furthermore, astrocyte depleted mice showed reduced inflammation and lower numbers of TMEV positive cells in the spinal cord. The present study indicates that astrocyte depletion in virus triggered CNS diseases contributes to a deterioration of clinical signs that are mediated by a dysfunction of perivascular astrocytes.
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Chrishtop, V. V., T. A. Rumyantseva et D. A. Pozhilov. « GFAP Expression in the Cerebral Cortex during the Development of Cerebral Hypoxia in Rats Showing Different Results in the Morris Water Maze ». Journal Biomed 16, no 1 (28 février 2020) : 89–98. http://dx.doi.org/10.33647/2074-5982-16-1-89-98.
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The state of cognitive functions in cerebrovascular disorders is one of the most urgent healthcare problems. Recently obtained data convincingly indicate the participation of astrocytes in the formation of cognitive functions of the brain. We conducted a study on 88 Wistar rats. Following the results of testing the rats in a Morris water maze, all animals were divided into two subgroups: those with a high (HLA) and low (LLA) level of spatial situational learning abilities in the Morris water maze test. The animals in the experimental group (48 animals) underwent bilateral ligation of both carotid arteries. The animals were removed from the experiment on the 21st, 60th and 90th day after the operation. Glial fibrillar acidic protein (GFAP), a marker of mature astrocytes, was detected using primary polyclonal rabbit antibodies on histological sections of the precentral gyrus of the brain. Data were obtained on a more pronounced decrease in the numerical density of astrocyte bodies and the number of astrocyte main processes in HLA and LLA animals in earlier (on the 21st day) and later (on the 90th day) stages of the experiment, respectively. The growth of the area occupied by the astrocyte processes occurred earlier in HLA animals (on the 60th day after the simulation) compared to LLA animals (on the 90th day after the simulation). The conducted factor analysis confirmed the presence of two factors associated with the dynamics of the studied parameters. The conclusion is made about alternative variants of changes in the studied groups. The HLA subgroup predominantly demonstrated changes of an alterational character in earlier experimental stages, while adaptive changes were observed in the later stages of the experiment. Conversely, in the LLA subgroup, alterations and adaptations occurred in later and earlier experimental stages, respectively.
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Hofmann, Gabrielle C., Eileen M. Hasser et David D. Kline. « Unilateral vagotomy alters astrocyte and microglial morphology in the nucleus tractus solitarii of the rat ». American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 320, no 6 (1 juin 2021) : R945—R959. http://dx.doi.org/10.1152/ajpregu.00019.2021.
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The nucleus tractus solitarii (nTS) is the initial site of integration of sensory information from the cardiorespiratory system and contributes to reflex responses to hypoxia. Afferent fibers of the bilateral vagus nerves carry input from the heart, lungs, and other organs to the nTS where it is processed and modulated. Vagal afferents and nTS neurons are integrally associated with astrocytes and microglia that contribute to neuronal activity and influence cardiorespiratory control. We hypothesized that vagotomy would alter glial morphology and cardiorespiratory responses to hypoxia. Unilateral vagotomy (or sham surgery) was performed in rats. Prior to and seven days after surgery, baseline and hypoxic cardiorespiratory responses were monitored in conscious and anesthetized animals. The brainstem was sectioned and caudal, mid-area postrema (mid-AP), and rostral sections of the nTS were prepared for immunohistochemistry. Vagotomy increased immunoreactivity (-IR) of astrocytic glial fibrillary acidic protein (GFAP), specifically at mid-AP in the nTS. Similar results were found in the dorsal motor nucleus of the vagus (DMX). Vagotomy did not alter nTS astrocyte number, yet increased astrocyte branching and altered morphology. In addition, vagotomy both increased nTS microglia number and produced morphologic changes indicative of activation. Cardiorespiratory baseline parameters and hypoxic responses remained largely unchanged, but vagotomized animals displayed fewer augmented breaths (sighs) in response to hypoxia. Altogether, vagotomy alters nTS glial morphology, indicative of functional changes in astrocytes and microglia that may affect cardiorespiratory function in health and disease.
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Ramadasan-Nair, Renjini, Jessica Hui, Leslie S. Itsara, Philip G. Morgan et Margaret M. Sedensky. « Mitochondrial Function in Astrocytes Is Essential for Normal Emergence from Anesthesia in Mice ». Anesthesiology 130, no 3 (1 mars 2019) : 423–34. http://dx.doi.org/10.1097/aln.0000000000002528.
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Abstract Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New Background In mice, restriction of loss of the mitochondrial complex I gene Ndufs4 to glutamatergic neurons confers a profound hypersensitivity to volatile anesthetics similar to that seen with global genetic knockout of Ndufs4. Astrocytes are crucial to glutamatergic synapse functioning during excitatory transmission. Therefore, the authors examined the role of astrocytes in the anesthetic hypersensitivity of Ndufs4(KO). Methods A tamoxifen-activated astrocyte-specific Ndufs4(KO) mouse was constructed. The specificity of the astrocyte-specific inducible model was confirmed by using the green fluorescent protein reporter line Ai6. Approximately 120 astrocyte-specific knockout and control mice were used for the experiments. Mice were anesthetized with varying concentrations of isoflurane or halothane; loss of righting reflex and response to a tail clamp were determined and quantified as the induction and emergence EC50s. Because norepinephrine has been implicated in emergence from anesthesia and astrocytes respond to norepinephrine to release gliotransmitters, the authors measured norepinephrine levels in the brains of control and knockout Ndufs4 animals. Results The induction EC50s for tail clamp in both isoflurane and halothane were similar between the control and astrocyte-specific Ndufs4(KO) mice at 3 weeks after 4-hydroxy tamoxifen injection (induction concentration, EC50(ind)—isoflurane: control = 1.27 ± 0.12, astrocyte-specific knockout = 1.21 ± 0.18, P = 0.495; halothane: control = 1.28 ± 0.05, astrocyte-specific knockout = 1.20 ± 0.05, P = 0.017). However, the emergent concentrations in both anesthetics for the astrocyte-specific Ndufs4(KO) mice were less than the controls for tail clamp; (emergence concentration, EC50(em)—isoflurane: control = 1.18 ± 0.10, astrocyte-specific knockout = 0.67 ± 0.11, P < 0.0001; halothane: control = 1.08 ± 0.09, astrocyte-specific knockout = 0.59 ± 0.12, P < 0.0001). The induction EC50s for loss of righting reflex were also similar between the control and astrocyte-specific Ndufs4(KO) mice (EC50(ind)—isoflurane: control = 1.02 ± 0.10, astrocyte-specific knockout = 0.97 ± 0.06, P = 0.264; halothane: control = 1.03 ± 0.05, astrocyte-specific knockout = 0.99 ± 0.08, P = 0.207). The emergent concentrations for loss of righting reflex in both anesthetics for the astrocyte-specific Ndufs4(KO) mice were less than the control (EC50(em)—isoflurane: control = 1.0 ± 0.07, astrocyte-specific knockout = 0.62 ± 0.12, P < 0.0001; halothane: control = 1.0 ± 0.04, astrocyte-specific KO = 0.64 ± 0.09, P < 0.0001); N ≥ 6 for control and astrocyte-specific Ndufs4(KO) mice. For all tests, similar results were seen at 7 weeks after 4-hydroxy tamoxifen injection. The total norepinephrine content of the brain in global or astrocyte-specific Ndufs4(KO) mice was unchanged compared to control mice. Conclusions The only phenotype of the astrocyte-specific Ndufs4(KO) mouse was a specific impairment in emergence from volatile anesthetic-induced general anesthesia. The authors conclude that normal mitochondrial function within astrocytes is essential for emergence from anesthesia.
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Meldolesi, Jacopo. « Astrocytes : News about Brain Health and Diseases ». Biomedicines 8, no 10 (6 octobre 2020) : 394. http://dx.doi.org/10.3390/biomedicines8100394.
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Astrocytes, the most numerous glial cells in the brains of humans and other mammalian animals, have been studied since their discovery over 100 years ago. For many decades, however, astrocytes were believed to operate as a glue, providing only mechanical and metabolic support to adjacent neurons. Starting from a “revolution” initiated about 25 years ago, numerous astrocyte functions have been reconsidered, some previously unknown, others attributed to neurons or other cell types. The knowledge of astrocytes has been continuously growing during the last few years. Based on these considerations, in the present review, different from single or general overviews, focused on six astrocyte functions, chosen due in their relevance in both brain physiology and pathology. Astrocytes, previously believed to be homogeneous, are now recognized to be heterogeneous, composed by types distinct in structure, distribution, and function; their cooperation with microglia is known to govern local neuroinflammation and brain restoration upon traumatic injuries; and astrocyte senescence is relevant for the development of both health and diseases. Knowledge regarding the role of astrocytes in tauopathies and Alzheimer’s disease has grow considerably. The multiple properties emphasized here, relevant for the present state of astrocytes, will be further developed by ongoing and future studies.
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Babaee, Abdolreza, Seyed Hassan Eftekhar Vaghefi, Samereh Dehghani Soltani, Majid Asadi Shekaari, Nader Shahrokhi et Mohsen Basiri. « Hippocampal Astrocyte Response to Melatonin Following Neural Damage Induction in Rats ». Basic and Clinical Neuroscience Journal 12, no 2 (1 mars 2021) : 177–86. http://dx.doi.org/10.32598/bcn.12.2.986.1.
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Introduction: Brain injury induces an almost immediate response from glial cells, especially astrocytes. Activation of astrocytes leads to the production of inflammatory cytokines and reactive oxygen species that may result in secondary neuronal damage. Melatonin is an anti-inflammatory and antioxidant agent, and it has been reported to exert neuroprotection through the prevention of neuronal death in several models of central nervous system injury. This study aimed to investigate the effect of melatonin on astrocyte activation induced by Traumatic Brain Injury (TBI) in rat hippocampus and dentate gyrus. Methods: Animals were randomly divided into 5 groups; Sham group, TBI group, vehicle group, and melatonin‐treated TBI groups (TBI+Mel5, TBI+Mel20). Immunohistochemical method (GFAP marker) and TUNEL assay were used to evaluate astrocyte reactivity and neuronal death, respectively. Results: The results demonstrated that the astrocyte number was reduced significantly in melatonin‐treated groups compared to the vehicle group. Additionally, based on TUNEL results, melatonin administration noticeably reduced the number of apoptotic neurons in the rat hippocampus and dentate gyrus. Conclusion: In general, our findings suggest that melatonin treatment after brain injury reduces astrocyte reactivity as well as neuronal cell apoptosis in rat hippocampus and dentate gyrus.
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Rutka, James T., Masaji Murakami, Peter B. Dirks, Sherri Lynn Hubbard, Laurence E. Becker, Kozo Fukuyama, Shin Jung et Kazuhito Matsuzawa. « Role of glial filaments in cells and tumors of glial origin : a review ». Neurosurgical Focus 3, no 1 (juillet 1997) : E2. http://dx.doi.org/10.3171/foc.1997.3.1.2.
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In the adult human brain, normal astrocytes constitute nearly 40% of the total central nervous system (CNS) cell population and may assume a star-shaped configuration resembling epithelial cells insofar as the astrocytes remain intimately associated, through their cytoplasmic extensions, with the basement membrane of the capillary endothelial cells and the basal lamina of the glial limitans externa. Although their exact function remains unknown, in the past, astrocytes were thought to subserve an important supportive role for neurons, providing a favorable ionic environment, modulating extracellular levels of neurotransmitters, and serving as spacers that organize neurons. In immunohistochemical preparations, normal, reactive, and neoplastic astrocytes may be positively identified and distinguished from other CNS cell types by the expression of the astrocyte-specific intermediate filament glial fibrillary acidic protein (GFAP). This GFAP is a 50-kD intracytoplasmic filamentous protein that constitutes a portion of, and is specific for, the cytoskeleton of the astrocyte. This protein has proved to be the most specific marker for cells of astrocytic origin under normal and pathological conditions. Interestingly, with increasing astrocytic malignancy, there is progressive loss of GFAP production. As the human gene for GFAP has now been cloned and sequenced, this review begins with a summary of the molecular biology of GFAP including the proven utility of the GFAP promoter in targeting genes of interest to the CNS in transgenic animals. Based on the data provided the authors argue cogently for an expanded role of GFAP in complex cellular events such as cytoskeletal reorganization, maintenance of myelination, cell adhesion, and signaling pathways. As such, GFAP may not represent a mere mechanical integrator of cellular space, as has been previously thought. Rather, GFAP may provide docking sites for important kinases that recognize key cellular substrates that enable GFAP to form a dynamic continuum with microfilaments, integrin receptors, and the extracellular matrix.
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Rutka, James T., Masaji Murakami, Peter B. Dirks, Sherri Lynn Hubbard, Laurence E. Becker, Kozo Fukuyama, Shin Jung, Atsushi Tsugu et Kazuhito Matsuzawa. « Role of glial filaments in cells and tumors of glial origin : a review ». Journal of Neurosurgery 87, no 3 (septembre 1997) : 420–30. http://dx.doi.org/10.3171/jns.1997.87.3.0420.
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✓ In the adult human brain, normal astrocytes constitute nearly 40% of the total central nervous system (CNS) cell population and may assume a star-shaped configuration resembling epithelial cells insofar as the astrocytes remain intimately associated, through their cytoplasmic extensions, with the basement membrane of the capillary endothelial cells and the basal lamina of the glial limitans externa. Although their exact function remains unknown, in the past, astrocytes were thought to subserve an important supportive role for neurons, providing a favorable ionic environment, modulating extracellular levels of neurotransmitters, and serving as spacers that organize neurons. In immunohistochemical preparations, normal, reactive, and neoplastic astrocytes may be positively identified and distinguished from other CNS cell types by the expression of the astrocyte-specific intermediate filament glial fibrillary acidic protein (GFAP). Glial fibrillary acidic protein is a 50-kD intracytoplasmic filamentous protein that constitutes a portion of, and is specific for, the cytoskeleton of the astrocyte. This protein has proved to be the most specific marker for cells of astrocytic origin under normal and pathological conditions. Interestingly, with increasing astrocytic malignancy, there is progressive loss of GFAP production. As the human gene for GFAP has now been cloned and sequenced, this review begins with a summary of the molecular biology of GFAP including the proven utility of the GFAP promoter in targeting genes of interest to the CNS in transgenic animals. Based on the data provided the authors argue cogently for an expanded role of GFAP in complex cellular events such as cytoskeletal reorganization, maintenance of myelination, cell adhesion, and signaling pathways. As such, GFAP may not represent a mere mechanical integrator of cellular space, as has been previously thought. Rather, GFAP may provide docking sites for important kinases that recognize key cellular substrates that enable GFAP to form a dynamic continuum with microfilaments, integrin receptors, and the extracellular matrix.
Thèses sur le sujet "Animals, Astrocyte"
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Featherstone, Robert Earle. « Plasticity in the maternal circuit, effects of pup exposure and retention interval on astrocyte numbers in primiparous and multiparous animals ». Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0011/MQ29187.pdf.
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Dutuit, Magali. « Régulations physiologiques et pathologiques des fonctions astrocytaires impliquées dans l'homéostasie du GABA et du glutamate ». Lyon 1, 2000. http://www.theses.fr/2000LYO1T222.
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Basu, Shubhayu. « Effects of three dimensional structure of tissue scaffolds on animal cell culture ». Connect to this title online, 2004. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1092689986.
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Thesis (Ph. D.)--Ohio State University, 2004.Title from first page of PDF file. Document formatted into pages; contains xviii, 236 p.; also includes graphics (some col.). Includes bibliographical references (p. 194-211). Available online via OhioLINK's ETD Center
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Clavreul, Solène. « Développement du réseau astroglial dans le cortex cérébral murin ». Thesis, Sorbonne université, 2018. http://www.theses.fr/2018SORUS540.
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Les astrocytes représentent une des populations cellulaires les plus nombreuses du cerveau. Ces cellules gliales extrêmement ramifiées y jouent un rôle essentiel, notamment dans le cortex cérébral, où elles forment un réseau tridimensionnel continu tout en présentant une hétérogénéité importante au niveau morphologique, moléculaire et fonctionnel. Afin de déterminer comment le réseau astrocytaire est établi au cours du développement cortical murin, des analyses clonales ont été effectuées grâce à une stratégie de marquage multicolore permettant d’étudier simultanément la descendance de nombreux progéniteurs. Les résultats de ces travaux montrent que les clones d’astrocytes corticaux s’imbriquent avec leurs voisins et présentent une variabilité importante au niveau de leur composition en termes de nombre et sous-types cellulaires, leur organisation et leur dispersion spatiale. Le réseau astrocytaire se développe au cours d’une première phase dynamique de prolifération et de dispersion pendant la première semaine postnatale, suivie par une phase de maturation à l’échelle de la cellule avec augmentation du volume des astrocytes et de la complexité de leur arborisation. Ces travaux montrent par ailleurs la contribution non négligeable de progéniteurs postnataux au réseau astrocytaire, qui s’ajoute à celle des cellules souches neurales corticales embryonnaires. La grande variabilité du réseau astrocytaire à l’échelle clonale suggère que son développement repose sur des unités clonales plastiques composées de cellules dont l’organisation spatiale et les caractéristiques finales dépendent probablement de leurs interactions avec leur environnement neuronal via des acteurs moléculaires qui restent à caractériserAstrocytes are one of the most numerous cell types in the brain. They consist in ramified glial cells that play essential roles in neural tissue where they form an uninterrupted tridimensional network, while displaying important local heterogeneity in terms of morphology and molecular marker expression. To determine how this network is established during development, multiclonal lineage tracing was performed to analyzed large numbers of astrocyte clones issued from nearby mouse cortical progenitors. Results show that cortical astrocyte clones intermix with their neighbors, display extensive variability in terms of spatial organization, numbers and subtypes of generated cells, and increase in size towards the upper part of the cortex. Furthermore, this organization develops through two stages that comprise a dynamic phase of proliferation accompanied by spatial dispersion, and a maturation phase where morphological complexity and volume increase at the single cell level. Moreover a significant contribution of subependymal postnatal progenitors to the generation of astrocytes, independent of their subtype and location, was uncovered in addition to prenatal delaminating apical progenitors. Thus cortical astrocyte network development appears unstereotyped at the clonal level. This suggests that the construction of this network relies on plastic clonal units issued from non-specified astrocyte progenitors that differentially expand and mature, and whose descendants probably acquire their final characteristics through interactions with their neuronal environment through molecular mechanisms that still need to be defined
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Marques, Karina de Brito. « Plasticidade sinaptica em motoneuronios alfa medulares de animais submetidos a encefalomielite autoimune experimental ». [s.n.], 2007. http://repositorio.unicamp.br/jspui/handle/REPOSIP/316501.
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Orientador: Alexandre Leite Rodrigues de OliveiraTese (doutorado) - Universidade Estadual de Campinas, Instituto de Biologia
Made available in DSpace on 2018-08-09T22:49:48Z (GMT). No. of bitstreams: 1 Marques_KarinadeBrito_D.pdf: 8050913 bytes, checksum: f9c7d621391d6f3f99413a9c27749530 (MD5) Previous issue date: 2007
Resumo: Durante o curso da encefalomielite autoimmune experimental ocorre uma grave redução das funções motoras e sensitivas. Esses eventos têm sido classicamente atribuídos ao processo desmielinizante da doença. Em ratos, os sinais clínicos da doença desaparecem 5 dias após completa tetraplegia, indicando que o processo desmielinizante não é a única causa da rápida evolução da doença. Assim sendo, investigamos as alterações sinaptológicas e o processo inflamatório induzidos pela encefalomielite autoimune experimental (EAE) em motoneurônios medulares e sua relação com o surto e remissão da doença. Para esse estudo, foram utilizados ratos Lewis, fêmeas de 7 semanas. Os animais foram induzidos à EAE por meio de dose única de proteína básica de mielina emulsificada com adjuvante completo de Freund e sacrificados no 13º dia após indução (surto grau 3) e no 26º dia (remissão da doença). Também, para investigar a possibilidade de que o tratamento com acetato de glatirâmer, uma droga imunomoduladora baseada na estrutura de aminoácidos da proteína básica de mielina, interfira no processo de plasticidade sináptica, os animais foram induzidos à EAE, tratados com AG diariamente e sacrificados após 2 semanas. Os grupos experimentais foram divididos em: estudo da aposição sináptica durante surto e remissão da doença e tratamento dos animais induzidos à EAE com AG. Assim, os espécimes foram processados para análise através de imunohistoquímica e microscopia eletrônica de transmissão. Nossos resultados indicaram que os componentes gliais (astrócitos e microglia), estimulados pela inflamação, desempenham papel ativo no processo de retração sináptica em motoneurônios alfa. Apresentamos evidências de que a eliminação de terminais sinápticos contribui para a perda da função motora observada no curso da doença e que o imunomodulador AG não só possui efeito antiinflamatório, mas também influencia diretamente na plasticidade de elementos neurais no microambiente medular. Reforçam, também, que um processo agudo de inflamação pode colaborar diretamente para a recuperação e sobrevivência neuronal, uma vez que as células inflamatórias produzem citocinas e fatores neurotróficos no microambiente medular
Abstract: During the course of experimental autoimmune encephalomyelitis, a massive loss of motor and sensitive function occurs, which has been classically attributed to the demyelination process. In rats, the clinical signs disappear within 5 days following complete tetraplegia, indicating that demyelination might not be the only cause for the rapid evolution of the disease. The immunomodulador glatiramer acetate (GA) has been shown significantly reduce the seriousness of the symptoms during the exacerbation of the disease. However, little is known about its effects on the spinal motoneurons and on their afferents. The present work investigated the occurrence of experimental autoimmune encephalomyelitis-induced changes of the synaptic covering of spinal motoneurons during exacerbation and after remission and investigated whether GA has a direct influence on synapse plasticity and on the deafferentiation of motoneurons during the course of EAE in rats. Lewis rats were subjected to EAE associated with GA or placebo treatment. The animals were sacrificed after fifteen days of treatment. For the both cases the spinal cords was processed for immunohistochemical analysis (IH) and electron transmission microscopy. The terminals were typed with transmission electron microscopy as C-, F- and Stype. Immunohistochemical analysis of synaptophysin, glial fibrillary acidic protein and the microglia/macrophage marker F4/80 were also used in order to draw a correlation between the synaptic changes and the glial reaction. The ultrastructural analysis showed that, during exacerbation, there was a strong retraction of both F- and S-type terminals. In this sense, both the covering as well as the length of the remaining terminals suffered great reductions. However, the retracted terminals rapidly returned to apposition, although the mean length remained shorter. A certain level of sprouting may have occurred as, after remission, the number of F-terminals was greater than in the control group. The immunohistochemical analysis showed that the peak of synaptic loss was coincident with an increased macro- and microglial reaction. Interestingly, although the GA treatment preserved synaptophysin labelling, it did not significantly reduce the glial reaction, indicating that inflammatory activity was still present. Our results suggest that the major changes occurring in the spinal cord network during the time course of the disease may contribute significantly to the origin of the clinical signs as well as help to explain their rapid recovery and that the immunomodulator GA has a direct influence on the stability of nerve terminals in the spinal cord, which in turn may contribute to its neuroprotective effects during the course of multiple sclerosis
Doutorado
Anatomia
Doutor em Biologia Celular e Estrutural
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Sirisi, Dolcet Sònia. « Bases moleculars de la Leucoeocefalopatia Megalencefàllca amb Quists subcorlicals. Utilització de models animals i cel·lulars ». Doctoral thesis, Universitat de Barcelona, 2014. http://hdl.handle.net/10803/284761.
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La Leucoencefalopatia Megalencefàlica amb quists subcorticals, també anomenada MLC, és un tipus rar de leucodistròfia vacuolitzant. Actualment encara es desconeix el mecanisme fisiopatològic de la malaltia, i per tant ni hi ha cap tractament possible per als pacients.
S’han descrit dos gens implicats en la malaltia MLC. El primer gen descobert s’anomena MLC1 i codifica per una proteïna de membrana que porta el mateix nom. El segon gen s’anomena GLIALCAM i codifica per una proteïna transmembrana de tipus I que també porta el mateix nom. S’ha decrit que la proteïna GlialCAM actua com a subunitat ß de MLC1 ja que es capaç de dirigir-la i concentrar-la a les unions cel•lulars. Per altra banda, GlialCAM també s’ha descrit com a subunitat auxiliar del canal de Cl- ClC-2 ja que és capaç de modificar les propietats d’activació i rectificació del canal.
En la present tesi s’han generat i estudiat diferents models animals i cel•lulars per a l’estudi de la malaltia. En primer lloc, s’ha generat i s’ha caracteritzat un model de ratolí knock-out per a Mlc1. Gràcies a aquest model s’ha observat que la proteïna MLC1 és únicament astrocitària i que la proteïna GlialCAM no es independent de MLC1, ja que en absència d’aquesta es troba deslocalitzada en el cerebel. També s’ha pogut descriure per primer cop la implicació del canal de Cl- ClC-2 en la fisiopatologia, ja que els seus nivells de proteïna disminuixen en el cerebel i el canal es troba gairebé inactiu en els oligodendròcits de l’animal knock-out. Les característiques fenotípiques que presenta el model de ratolí equivalen a les característiques observades en els pacients en fases inicials de la malaltia, ja que l’animal tot i que mostra presència de vacuoles no presenta deteriorament motor i macrocefàlia aparent.
També s’ha generat un model de peix zebra knock-out per a zmlc1. Aquest model presenta avantatges respecte el ratolí, com per exemple el baix cost o l’aplicació de tècniques genètiques a gran escala. Aquest model ha permés observar de nou que realment GlialCAM necessita a MLC1 per a la seva correcta localització. També s’ha observat que l’ortòleg zGlialCAMa conserva la seva funció de entre espécies ja que també es capaç de modificar les corrents de ClC-2.
Aquests resultats obtinguts amb els models s’han pogut comparar amb el cervell d’una pacient. Aquest cervell demostra que MLC1 és necessària per a la correcta localització de GlialCAM en la regió del cerebel.
Per altra banda, s’han desenvolupat diferents models cel•lulars. Primerament s’han estudiat els astròcits del ratolí knock-out. Aquestes cel•lules mancades de MLC1 també presenten vacuoles per tot el citoplasma, però no mostren canvis en la localització ni en els nivells de proteïna de GlialCAM i ClC-2. Aquest fet juntament amb altres estudis del grup van fer pensar si la condició necessària per a que es veguessin afectades aquestes proteïnes estaria relacionada amb el procés del sifoneig de K+.
Estudis realitzats en astròcits de rata demostren que en condicions d’un alt contingut de K+, com per exemple durant una alta activitat neuronal, GlialCAM i ClC-2 és localitzen juntament a les membranes cel•lular i ClC-2 canvia les seves propietat de canal. Paral•lelament, estudis realitzats en oligodendròcits de rata també demostren que aquest fet també succeix en aquest tipus cel•lular.Megalencefalic leukoencephalopathy with subcortical cysts, also known as MLC, is a rare type of leukodystrophy. Currently still unknown pathophysiological mechanism of the disease, and therefore there is no effective treatment possible for patients. There are two genes involved in the MLC disease. Gene was first discovered was MLC1 and this encodes for a membrane protein with the same name. The second gene is called GLIALCAM and encodes for a transmembrane protein type I that also carries the same name. In our group is has been described that GlialCAM acts as a protein ß subunit of MLC1 because it is able to direct and concentrate in the cellular junctions. Moreover, GlialCAM also act as auxiliary subunit of CLC-2 Cl channel as it is capable of modifying the activation and rectification properties of the channel. In this work we have developed two different models to study the physiopathology. The results show that GlialCAM affected by the absence of MLC1. It has been also demonstrated that ClC-2 is implicated in the disease.These results were compared with a patient brian and has been shown that MLC1 is important for the correct location of GlialCAM in the cerbellum. Have also been developed a different cellular models. The results with this models show that GlialCAM and ClC-2 could have a functional role in the process of potassium siphoning.
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Cabarrocas, Julie Marie Cécile. « Etude de l'auto-réactivité dirigée contre un antigène du système nerveux au moyen de souris transgéniques ». Toulouse 3, 2005. http://www.theses.fr/2005TOU30068.
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Dans le cadre de l'étude de l'auto-immunité dirigée contre un antigène du système nerveux, nous avons analysé, au moyen de lignées de souris transgéniques: i) les conséquences cliniques et histologiques de réactions auto-immunes induites par des lymphocytes T (LT) CD8+ spécifiques d'un antigène exprimé par des cellules gliales, les astrocytes et les cellules gliales entériques (CGE) ; ii) le rôle des LT CD8+ dans la surveillance immune du système nerveux central et l'induction de réponses inflammatoires au sein de cet organe ; et iii) les mécanismes d'induction de tolérance affectant des populations de LT CD4+ spécifiques d'un auto-antigène exprimé par les astrocytes et les CGEWe have studied autoimmunity targeting a nervous system-specific antigen with the use of several transgenic mouse lines, and have investigated : i) clinical and histopathological effects of autoimmune processes induced by CD8+ T-cells specific for a glial antigen expressed in astrocytes and enteric glial cells (EGC) ; ii) the role of CD8+ T-cells in the immune surveillance of the central nervous system and the induction of inflammatory lesions in this organ ; and iii) the mechanisms of tolerance affecting populations of astrocytes- and EGC-specific CD4+ T-cells
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Jukkola, Peter I. « The Role of Potassium Ion and Water Channels in an Animal Model ofMultiple Sclerosis ». The Ohio State University, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=osu1397656579.
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Rouleau, Caroline. « Implications du pyruvate dans le métabolisme de lignées astrocytaires spinales spontanément transformées ». Montpellier 1, 2006. http://www.theses.fr/2006MON1T029.
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L'objectif de ce travail est d'explorer en détail le métabolisme de lignées astrocytaires dérivant de la moelle épinière d'embryons de rat. La respiration mitochondriale, certains paramètres de la glycolyse et l'activité de l'oncogène Akt sont étudiés dans les lignées en passages précoces (EP) et dans les lignées en passages tardifs (LP), qui se sont spontanément transformées après avoir été maintenues pendant plus de 35 passages dans le milieu de culture ne contenant pas de pyruvate. Dans les LP, en comparaison avec les EP, il existe une diminution de la glycolyse, une réduction du nombre de mitochondries par cellule et un déficit de la respiration portant sur les complexes I et II+III de la chaîne respiratoire mitochondriale. Le traitement des LP par le pyruvate, pendant 20 passages supplémentaires, ne modifie pas l'état de transformation des cellules. Alors que ce traitement rétablit la glycolyse, aucun effet bénéfique n'est constaté sur le déficit respiratoire. Le traitement des EP par du pyruvate, jusqu'à ce qu'elles soient par définition en passages tardifs, prévient la transformation spontanée. Alors que les EP traitées par le pyruvate ont un déficit modéré de la respiration, elles renferment 2 fois plus de mitochondries par cellule que les EP non traitées. L'augmentation du nombre de mitochondries compense le déficit modéré de la respiration afin de maintenir les capacités d'oxydation dans ces lignées tardives qui ne sont pas transformées. Dans l'ensemble des lignées, l'activité de l'oncogène Akt varie dans le même sens que la glycolyse et que la respiration et est directement stimulée par le pyruvate dans les lignées traitées. En conclusion, ce travail ouvre de nouvelles perspectives quant à la compréhension des mécanismes possiblement associés à la transformation astrocytaire et met en évidence de nouvelles voies thérapeutiques potentielles afin d'améliorer le contrôle des proliférations astrocytaires.
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Guérin-Eysseric, Hélène. « Expression du métabolisme cérébral de l'éthanol : production d'acétaldéhyde et de radicaux libres par les cellules astrocytaires de rat en culture ». Université Joseph Fourier (Grenoble), 1997. http://www.theses.fr/1997GRE10249.
Texte intégralRésumé :
Les mécanismes physiopathologiques responsables des complications neurologiques de l'alcoolisme sont très complexes. Le métabolisme oxydatif de l'éthanol a largement été étudié au niveau du foie, mais beaucoup moins au niveau cérébral. Le but de notre travail a été d'étudier la capacité du cerveau à produire d'une part de l'acétaldéhyde et d'autre part des radicaux libres par métabolisation de l'éthanol en travaillant sur un modèle de culture de cellules astrocytaires de rat. Après avoir mis au point et valide un système d'exposition à l'éthanol des cultures de cellules en permettant d'éviter son évaporation, nous avons pu démontrer que les astrocytes sont capables de métaboliser l'éthanol en acétaldéhyde via la catalase et constituent également un site de production d'un radical libre dérivé de l'éthanol : le radical -hydroxyéthyle. Compte tenu du fait que les astrocytes jouent un rôle primordial dans le développement et le fonctionnement du système nerveux central, la preuve qu'ils sont le siège d'une production d'acétaldéhyde et de radicaux libres présentant tous les deux des effets cytotoxiques, constitue un élément important dans la compréhension des mécanismes de la neurotoxicité de l'éthanol.
Livres sur le sujet "Animals, Astrocyte"
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Takao, Kumazawa, Kruger Lawrence et Mizumura Kazue, dir. The polymodal receptor : A gateway to pathological pain. Amsterdam : Elsevier, 1996.
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Plasticity in the maternal circuit : Effects of pup exposure and retention interval on astrocyte numbers in primiparous and multiparous animals. Ottawa : National Library of Canada = Bibliothèque nationale du Canada, 1999.
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(Editor), T. Kumazawa, L. Kruger (Editor) et K. Mizumura (Editor), dir. The Polymodal Receptor - A Gateway to Pathological Pain (Progress in Brain Research). Elsevier Science, 1996.
Trouver le texte intégralChapitres de livres sur le sujet "Animals, Astrocyte"
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Ahmed, Saifuddin, Toshie Tsuchiya et Rumi Sawada. « In Vitro Cytotoxic Effects of Tin Compounds on Normal Human Astrocytes ». Dans Animal Cell Technology : Basic & ; Applied Aspects, 175–80. Dordrecht : Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-9646-4_28.
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Nakamura, Naohito, et Toshie Tsuchiya. « Effect of biodegradable polymer poly (L-lactic acid) on the cellular function of human astrocytes ». Dans Animal Cell Technology : Basic & ; Applied Aspects, 331–37. Dordrecht : Springer Netherlands, 2006. http://dx.doi.org/10.1007/1-4020-4457-7_45.
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Hallof-Büstrich, Heike, et Barbara Di Benedetto. « Examining the Coverage of Blood Vessels by Astrocyte Endfeet in an Animal Model of Major Depressive Disorder ». Dans Methods in Molecular Biology, 255–63. New York, NY : Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9068-9_18.
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Mersel, M., L. Vitkovic, G. Vincendon et A. N. Malviya. « Modification of Plasma Membrane DT-Diaphorase Activity Upon Transformation : A Comparison between Astrocytes in Primary Culture and C6 Glioblastoma Cells ». Dans Plasma Membrane Oxidoreductases in Control of Animal and Plant Growth, 402. Boston, MA : Springer US, 1988. http://dx.doi.org/10.1007/978-1-4684-8029-0_48.
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V. Pushchina, Evgeniya, Anatoly A. Varaksin et Dmitry K. Obukhov. « Hydrogen Sulfide as a Factor of Neuroprotection during the Constitutive and Reparative Neurogenesis in Fish Brain ». Dans Neuroprotection - New Approaches and Prospects. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.90547.
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The H2S-producing systems were studied in trout telencephalon, tectum, and cerebellum at 1 week after eye injury. The results of ELISA analysis have shown a 1.7-fold increase in the CBS expression at 1 week post-injury, as compared to the intact trout. In the ventricular and subventricular regions of trout telencephalon, CBS+ cells, as well as neuroepithelial and glial types, were detected. As a result of injury, the number of CBS+ neuroepithelial cells in the pallial and subpallial periventricular regions of the telencephalon increases. In the tectum, a traumatic damage leads to an increase in the CBS expression in radial glia with a simultaneous decrease in the number of CBS immunopositive neuroepithelial cells detected in intact animals. In the cerebellum, we revealed neuroglial interrelations, in which H2S is probably released from the astrocyte-like cells with subsequent activation of the neuronal NMDA receptors. The organization of the H2S-producing cell complexes suggests that the amount of glutamate produced in the trout cerebellum and its reuptake is controlled with the involvement of astrocyte-like cells, reducing its excitotoxicity. We believe that the increase in the number of H2S-producing cells constitutes a response to oxidative stress, and the overproduction of H2S neutralizes the reactive oxygen species.
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« Astrocytes as Target Site for Neurotoxicity ». Dans Advances In Animal Alternatives For Safety And Efficacy Testing, 229–42. CRC Press, 1997. http://dx.doi.org/10.1201/9781439805817-30.
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Kuter, Katarzyna. « Astrocytes and microglia in Parkinson's disease and animal models ». Dans Genetics, Neurology, Behavior, and Diet in Parkinson's Disease, 83–99. Elsevier, 2020. http://dx.doi.org/10.1016/b978-0-12-815950-7.00006-0.
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Koepsell, Hermann. « General Overview of Organic Cation Transporters in Brain ». Dans Handbook of Experimental Pharmacology. Berlin, Heidelberg : Springer Berlin Heidelberg, 2021. http://dx.doi.org/10.1007/164_2021_449.
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AbstractInhibitors of Na+/Cl− dependent high affinity transporters for norepinephrine (NE), serotonin (5-HT), and/or dopamine (DA) represent frequently used drugs for treatment of psychological disorders such as depression, anxiety, obsessive-compulsive disorder, attention deficit hyperactivity disorder, and addiction. These transporters remove NE, 5-HT, and/or DA after neuronal excitation from the interstitial space close to the synapses. Thereby they terminate transmission and modulate neuronal behavioral circuits. Therapeutic failure and undesired central nervous system side effects of these drugs have been partially assigned to neurotransmitter removal by low affinity transport. Cloning and functional characterization of the polyspecific organic cation transporters OCT1 (SLC22A1), OCT2 (SLC22A2), OCT3 (SLC22A3) and the plasma membrane monoamine transporter PMAT (SLC29A4) revealed that every single transporter mediates low affinity uptake of NE, 5-HT, and DA. Whereas the organic transporters are all located in the blood brain barrier, OCT2, OCT3, and PMAT are expressed in neurons or in neurons and astrocytes within brain areas that are involved in behavioral regulation. Areas of expression include the dorsal raphe, medullary motoric nuclei, hypothalamic nuclei, and/or the nucleus accumbens. Current knowledge of the transport of monoamine neurotransmitters by the organic cation transporters, their interactions with psychotropic drugs, and their locations in the brain is reported in detail. In addition, animal experiments including behavior tests in wildtype and knockout animals are reported in which the impact of OCT2, OCT3, and/or PMAT on regulation of salt intake, depression, mood control, locomotion, and/or stress effect on addiction is suggested.
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Hryntsova, Nataliia. « STATE OF RAT PINEAL GLAND STRUCTURAL COMPONENTS IN THE CONDITIONS OF DIFFERENT EXTRACELLULAR DEHYDATION TERMS ». Dans Integration of traditional and innovation processes of development of modern science. Publishing House “Baltija Publishing”, 2020. http://dx.doi.org/10.30525/978-9934-26-021-6-30.
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The monograph presents a theoretical generalization and a new solution for the research target to study the state of the pineal gland structural components in sexually mature rats under different terms of extracellular dehydration. The experiment was performed on 24 white sexually mature male rats aged 5-6 months. The animals of the experimental group were simulated extracellular dehydration of mild and heavy severity. Animals were kept and manipulated in compliance with national and international bioethics standards. Different degrees of extracellular dehydration severity caused negative changes in all structural components of the pineal gland in experimental animals: stromal, vascular and parenchymal, with the greatest intensity in animals with heavy severity course. Morphological rearrangements were nonspecific and polymorphic in nature. In the pineal gland of animals with a mild severity course there was a tension of adaptive processes, increased secretory activity by both indole-producing and polypeptide-producing pinealocytes (with predominance of the latter), formation of the gland’s reserve capacity. There was a moderate increase in the expression of heat shock proteins in pinealocytes, which, certainly, made these cells more resistant to apoptotic rearrangements and the subsequent action of extreme factors. With increasing duration of the experiment (severe degree), there was a significant decrease in the size of the gland, thickening and swelling of the stromal component, sharp impairment of hemodynamics in the organ. Blood viscosity increased, its rheological properties were impaired (stasis, sludge), vascular wall permeability increased, processes of accelerated apoptosis in part of pinealocytes developed. The heat shock proteins level and the proliferative activity of astrocytic glia were significantly reduced, indicating a weakening of the mechanisms of anti-apoptotic and anti-stress protection. The 90-day effect of extracellular dehydration on the experimental animals’ body caused the phenomenon of chronic stress “subcompensation”, which was expressed in the depletion of pineal indolamines reserve and their urgent evacuation into the blood to maintain general adaptive capacity of the body. However, disturbances in the morphology of the vascular wall and increased blood viscosity negatively affected the mechanisms of pineal hormones diffusion into the vascular bed, the development of compensatory-adaptive processes in the body as a whole and the course of general adaptation syndrome.
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Peta, Charoula, Emmanouella Tsirimonaki, Constantinos Fedonidis, Xeni Koliou, Nikos Sakellaridis et Dimitra Mangoura. « Two Tails for Neurofibromin : A Tale of Two Microtubule-Associated Proteins ». Dans Neurofibromatosis [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.97574.
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Neurofibromatosis type 1, NF-1, is a common monogenic (NF1) disease, characterized by highly variable clinical presentation and high predisposition for tumors, especially those of astrocytic origin (low- to high-grade gliomas). Unfortunately, very few genotype–phenotype correlations have been possible, and the numerous identified mutations do not offer help for prognosis and patient counselling. Whole gene deletion in animals does not successfully model the disease, as NF-1 cases caused by point mutations could be differentially affected by cell type-specific alternative splice variants of NF1. In this chapter, we will discuss the differential Microtubule-Associated-Protein (MAP) properties of NLS or ΔNLS neurofibromins, produced by the alternatively splicing of exon 51, which also contains a Nuclear Localization Sequence (NLS), in the assembly of the mitotic spindle and in faithful genome transmission. We will also commend on the major theme that emerges about NLS-containing tumor suppressors that function as mitotic MAPs.
Actes de conférences sur le sujet "Animals, Astrocyte"
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Rocha, Andreia, Bruna Bellaver, Luiza Machado, Carolina Soares, Pâmela C. L. Ferreira, Samuel Greggio Gianina T. Venturin, Jaderson C. da Costa, Diogo O. Souza et Eduardo R. Zimmer. « TEMPORAL CHANGES IN ASTROCYTES ON A TRANSGENIC RAT MODEL OF AD ». Dans XIII Meeting of Researchers on Alzheimer's Disease and Related Disorders. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1980-5764.rpda023.
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Background: Recent evidences have pointed to astrocytes as important players in the Alzheimer’s Disease (AD) pathogenesis. Objective: With this in mind, we aim to longitudinally investigate astrocyte changes in a new important AD transgenic model, the TgF344-AD rat, the first animal model harboring human APP/PS1 mutations which presents age-dependent amyloid and tau pathology. Methods: TgF344-AD rats and wild type littermates were evaluated in three time points: 3, 6 and 9 months of age. Rats underwent a [18F]FDG-microPET, a spatial-memory, an astrocytes CSF biomarkers (ELISA multiplex) and a glutamate uptake (ex-vivo slices) analysis. Examination of further time-points are being conducted at the moment. Results: At 9 months of age, TgF344-AD animals presented an increase in the cortical [18F]FDG uptake and a decline in their alternance performance in the Y-maze task. In the CSF analysis, GFAP was elevated at both 6 months and 9 months, while S100B presented a decrease at 6mo. Additionally, the cortical glutamate uptake was increased at 9 months. Conclusion: This study is the first to longitudinally investigate the in vivo brain glucose metabolism in the TgF344-AD rat model. Our results suggest that this model presents an early increase on glucose metabolism which may be related to astrocytes activation and the increase of glutamate uptake by these cells. Furthermore, we also identified a spatial memory impairment at the same age.
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Pak, Rebecca W., Eric Hsu, Gian Molina-Castro, Dwight E. Bergles et Jin U. Kang. « Fluorescence dual-color fiberscope for monitoring neuron and astrocyte concurrent activities in freely-behaving animals ». Dans Neural Imaging and Sensing 2021, sous la direction de Qingming Luo, Jun Ding et Ling Fu. SPIE, 2021. http://dx.doi.org/10.1117/12.2578947.
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