Relevant bibliographies by topics / Microglie – Physiologie

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  2. Dissertations / Theses
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  5. Conference papers

Academic literature on the topic 'Microglie – Physiologie'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Microglie – Physiologie"

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Lyons, Susan A., Andrea Pastor, Carsten Ohlemeyer, Oliver Kann, Frank Wiegand, Konstantin Prass, Felix Knapp, Helmut Kettenmann, and Ulrich Dirnagl. "Distinct Physiologic Properties of Microglia and Blood-Borne Cells in Rat Brain Slices After Permanent Middle Cerebral Artery Occlusion." Journal of Cerebral Blood Flow & Metabolism 20, no. 11 (November 2000): 1537–49. http://dx.doi.org/10.1097/00004647-200011000-00003.

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The authors investigated the time course of leukocyte infiltration compared with microglial activation in adult rat brain slices after permanent middle cerebral artery occlusion (MCAO). To distinguish peripheral leukocytes from microglia, the blood cells were prelabeled in vivo with Rhodamine 6G (Rhod6G) IV before induction of ischemia. At specific times after infarct, invading leukocytes, microglia, and endothelial cells were labeled in situ with isolectin (IL)B4-FITC (ILB4). Six hours after MCAO only a few of the ILB4+ cells were colabeled by Rhod6G. These cells expressed the voltage-gated inwardly and outwardly rectifying K+ currents characteristic of macrophages. The majority of the ILB4+ cells were Rhod6G− and expressed a lack of voltage-gated channels, recently described for ramified microglial cells in brain slices, or exhibited only an inward rectifier current, a unique marker for cultured (but unstimulated) microglia. Forty-eight hours after MCAO, all blood-borne and the majority of Rhod6G− cells expressed outward and inward currents indicating that the intrinsic microglial population exhibited physiologic features of stimulated, cultured microglia. The ILB4+/Rhod6G− intrinsic microglial population was more abundant in the border zone of the infarct and their morphology changed from radial to ameboid. Within this zone, the authors observed rapidly migrating cells and recorded this movement by time-lapse microscopy. The current findings indicate that microglial cells acquire physiologic features of leukocytes at a later time point after MCAO.
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Eyo, Ukpong B., and Long-Jun Wu. "Bidirectional Microglia-Neuron Communication in the Healthy Brain." Neural Plasticity 2013 (2013): 1–10. http://dx.doi.org/10.1155/2013/456857.

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Unlike other resident neural cells that are of neuroectodermal origin, microglia are resident neural cells of mesodermal origin. Traditionally recognized for their immune functions during disease, new roles are being attributed to these cells in the development and maintenance of the central nervous system (CNS) including specific communication with neurons. In this review, we highlight some of the recent findings on the bidirectional interaction between neurons and microglia. We discuss these interactions along two lines. First, we review data that suggest that microglial activity is modulated by neuronal signals, focusing on evidence that (i) neurons are capable of regulating microglial activation state and influence basal microglial activities; (ii) classic neurotransmitters affect microglial behavior; (iii) chemotactic signals attract microglia during acute neuronal injury. Next, we discuss some of the recent data on how microglia signal to neurons. Signaling mechanisms include (i) direct physical contact of microglial processes with neuronal elements; (ii) microglial regulation of neuronal synapse and circuit by fractalkine, complement, and DAP12 signaling. In addition, we discuss the use of microglial depletion strategies in studying the role of microglia in neuronal development and synaptic physiology. Deciphering the mechanisms of bidirectional microglial-neuronal communication provides novel insights in understanding microglial function in both the healthy and diseased brain.
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Wong, Wai T., Minhua Wang, and Wei Li. "Regulation of microglia by ionotropic glutamatergic and GABAergic neurotransmission." Neuron Glia Biology 7, no. 1 (February 2011): 41–46. http://dx.doi.org/10.1017/s1740925x11000123.

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Recent studies have indicated that constitutive functions of microglia in the healthy adult central nervous system (CNS) involve immune surveillance, synapse maintenance and trophic support. These functions have been related to the ramified structure of ‘resting’ microglia and the prominent motility in their processes that provide extensive coverage of the entire extracellular milleu. In this review, we examine how external signals, and in particular, ionotropic neurotransmission, regulate features of microglial morphology and process motility. Current findings indicate that microglial physiology in the healthy CNS is constitutively and reciprocally regulated by endogenous ionotropic glutamatergic and GABAergic neurotransmission. These influences do not act directly on microglial cells but indirectly via the activity-dependent release of ATP, likely through a mechanism involving pannexin channels. Microglia in the ‘resting’ state are not only dynamically active, but also constantly engaged in ongoing communication with neuronal and macroglial components of the CNS in a functionally relevant way.
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Peggion, Caterina, Roberto Stella, Paolo Lorenzon, Enzo Spisni, Alessandro Bertoli, and Maria Lina Massimino. "Microglia in Prion Diseases: Angels or Demons?" International Journal of Molecular Sciences 21, no. 20 (October 20, 2020): 7765. http://dx.doi.org/10.3390/ijms21207765.

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Prion diseases are rare transmissible neurodegenerative disorders caused by the accumulation of a misfolded isoform (PrPSc) of the cellular prion protein (PrPC) in the central nervous system (CNS). Neuropathological hallmarks of prion diseases are neuronal loss, astrogliosis, and enhanced microglial proliferation and activation. As immune cells of the CNS, microglia participate both in the maintenance of the normal brain physiology and in driving the neuroinflammatory response to acute or chronic (e.g., neurodegenerative disorders) insults. Microglia involvement in prion diseases, however, is far from being clearly understood. During this review, we summarize and discuss controversial findings, both in patient and animal models, suggesting a neuroprotective role of microglia in prion disease pathogenesis and progression, or—conversely—a microglia-mediated exacerbation of neurotoxicity in later stages of disease. We also will consider the active participation of PrPC in microglial functions, by discussing previous reports, but also by presenting unpublished results that support a role for PrPC in cytokine secretion by activated primary microglia.
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Abdul, Yasir, Sarah Jamil, Lianying He, Weiguo Li, and Adviye Ergul. "Endothelin-1 (ET-1) promotes a proinflammatory microglia phenotype in diabetic conditions." Canadian Journal of Physiology and Pharmacology 98, no. 9 (September 2020): 596–603. http://dx.doi.org/10.1139/cjpp-2019-0679.

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Diabetes increases the risk and severity of cognitive impairment, especially after ischemic stroke. It is also known that the activation of the endothelin (ET) system is associated with cognitive impairment and microglia around the periinfarct area produce ET-1. However, little is known about the effect of ET-1 on microglial polarization, especially under diabetic conditions. We hypothesized that (i) ET-1 activates microglia to the proinflammatory M-1-like phenotype and (ii) hypoxia/ lipopolysaccharide (LPS) activates the microglial ET system and promotes microglial activation towards the M-1 phenotype in diabetic conditions. Microglial cells (C8B4) cultured under normal-glucose (25 mmol/L) conditions and diabetes-mimicking high-glucose (50 mmol/L) conditions for 48 h were stimulated with ET-1, cobalt chloride (200 μmol/L), or LPS (100 ng/mL) for 24 h. PPET-1, ET receptor subtypes, and M1/M2 marker gene mRNA expression were measured by RT-PCR. Secreted ET-1 was measured by ELISA. A high dose of ET-1 (1 μmol/L) increases the mRNA levels of ET receptors and activates the microglia towards the M1 phenotype. Hypoxia or LPS activates the ET system in microglial cells and shifts the microglia towards the M1 phenotype in diabetic conditions. These in vitro observations warrant further investigation into the role of ET-1-mediated activation of proinflammatory microglia in post-stroke cognitive impairment in diabetes.
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Eder, Claudia. "Ion channels in microglia (brain macrophages)." American Journal of Physiology-Cell Physiology 275, no. 2 (August 1, 1998): C327—C342. http://dx.doi.org/10.1152/ajpcell.1998.275.2.c327.

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Microglia are immunocompetent cells in the brain that have many similarities with macrophages of peripheral tissues. In normal adult brain, microglial cells are in a resting state, but they become activated during inflammation of the central nervous system, after neuronal injury, and in several neurological diseases. Patch-clamp studies of microglial cells in cell culture and in tissue slices demonstrate that microglia express a wide variety of ion channels. Six different types of K+ channels have been identified in microglia, namely, inward rectifier, delayed rectifier, HERG-like, G protein-activated, as well as voltage-dependent and voltage-independent Ca2+-activated K+ channels. Moreover, microglia express H+ channels, Na+ channels, voltage-gated Ca2+ channels, Ca2+-release activated Ca2+ channels, and voltage-dependent and voltage-independent Cl− channels. With respect to their kinetic and pharmacological properties, most microglial ion channels closely resemble ion channels characterized in other macrophage preparations. Expression patterns of ion channels in microglia depend on the functional state of the cells. Microglial ion channels can be modulated by exposure to lipopolysaccharide or various cytokines, by activation of protein kinase C or G proteins, by factors released from astrocytes, by changes in the concentration of internal free Ca2+, and by variations of the internal or external pH. There is evidence suggesting that ion channels in microglia are involved in maintaining the membrane potential and are also involved in proliferation, ramification, and the respiratory burst. Further possible functional roles of microglial ion channels are discussed.
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Zhang, Xiang, Yiming Wang, Hongquan Dong, Ying Xu, and Shu Zhang. "Induction of Microglial Activation by Mediators Released from Mast Cells." Cellular Physiology and Biochemistry 38, no. 4 (2016): 1520–31. http://dx.doi.org/10.1159/000443093.

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Background/Aims: Microglia are the resident immune cells in the brain and play a pivotal role in immune surveillance in the central nervous system (CNS). Brain mast cells are activated in CNS disorders and induce the release of several mediators. Thus, brain mast cells, rather than microglia, are the “first responders” due to injury. However, the functional aspects of mast cell-microglia interactions remain uninvestigated. Methods: Conditioned medium from activated HMC-1 cells induces microglial activation similar to co-culture of microglia with HMC-1 cells. Primary cultured microglia were examined by flow cytometry analysis and confocal microscopy. TNF- alpha and IL-6 were measured with commercial ELISA kits. Cell signalling was analysed by Western blotting. Results: In the present study, we found that the conditioned medium from activated HMC-1 cells stimulated microglial activation and the subsequent production of the pro-inflammatory factors TNF-α and IL-6. Co-culture of microglia and HMC-1 cells with corticotropin-releasing hormone (CRH) for 24, 48 and 72 hours increased TNF-α and IL-6 production. Antagonists of histamine receptor 1 (H1R), H4R, proteinase-activated receptor 2 (PAR2) or Toll-like receptor 4 (TLR4) reduced HMC-1-induced pro-inflammatory factor production and MAPK and PI3K/AKT pathway activation. Conclusions: These results imply that activated mast cells trigger microglial activation. Interactions between mast cells and microglia could constitute a new and unique therapeutic target for CNS inflammation-related diseases.
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Lopez-Lopez, Andrea, Begoña Villar-Cheda, Aloia Quijano, Pablo Garrido-Gil, María Garcia-Garrote, Carmen Díaz-Ruiz, Ana Muñoz, and José L. Labandeira-Garcia. "NADPH-Oxidase, Rho-Kinase and Autophagy Mediate the (Pro)renin-Induced Pro-Inflammatory Microglial Response and Enhancement of Dopaminergic Neuron Death." Antioxidants 10, no. 9 (August 25, 2021): 1340. http://dx.doi.org/10.3390/antiox10091340.

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Dysregulation of the tissue renin–angiotensin system (RAS) is involved in tissue oxidative and inflammatory responses. Among RAS components, renin, its precursor (pro)renin and its specific receptor (PRR) have been less investigated, particularly in the brain. We previously showed the presence of PRR in neurons and glial cells in the nigrostriatal system of rodents and primates, including humans. Now, we used rat and mouse models and cultures of BV2 and primary microglial cells to study the role of PRR in microglial pro-inflammatory responses. PRR was upregulated in the nigral region, particularly in microglia during the neuroinflammatory response. In the presence of the angiotensin type-1 receptor blocker losartan, to exclude angiotensin-related effects, treatment of microglial cells with (pro)renin induces the expression of microglial pro-inflammatory markers, which is mediated by upregulation of NADPH-oxidase and Rho-kinase activities, downregulation of autophagy and upregulation of inflammasome activity. Conditioned medium from (pro)renin-treated microglia increased dopaminergic cell death relative to medium from non-treated microglia. However, these effects were blocked by pre-treatment of microglia with the Rho-kinase inhibitor fasudil. Activation of microglial PRR enhances the microglial pro-inflammatory response and deleterious effects of microglia on dopaminergic cells, and microglial NADPH-oxidase, Rho-Kinase and autophagy are involved in this process.
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He, Mingfeng, Hongquan Dong, Yahui Huang, Shunmei Lu, Shu Zhang, Yanning Qian, and Wenjie Jin. "Astrocyte-Derived CCL2 is Associated with M1 Activation and Recruitment of Cultured Microglial Cells." Cellular Physiology and Biochemistry 38, no. 3 (2016): 859–70. http://dx.doi.org/10.1159/000443040.

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Background/Aims: Microglia are an essential player in central nervous system inflammation. Recent studies have demonstrated that the astrocytic chemokine, CCL2, is associated with microglial activation in vivo. However, CCL2-induced microglial activation has not yet been studied in vitro. The purpose of the current study was to understand the role of astrocyte-derived CCL2 in microglial activation and to elucidate the underlying mechanism(s). Methods: Primary astrocytes were pre-treated with CCL2 siRNA and stimulated with TNF-α. The culture medium (CM) was collected and added to cultures of microglia, which were incubated with and without CCR2 inhibitor. Microglial cells were analyzed by quantitative RT-PCR to determine whether they polarized to the M1 or M2 state. Microglial migratory ability was assessed by transwell migration assay. Results: TNF-α stimulated the release of CCL2 from astrocytes, even if the culture media containing TNF-α was replaced with fresh media after 3 h. CM from TNF-α-stimulated astrocytes successfully induced microglial activation, which was ascertained by increased activation of M1 and enhanced migration ability. In contrast, CM from astrocytes pretreated with CCL2 siRNA showed no effect on microglial activation, compared to controls. Additionally, microglia pre-treated with RS102895, a CCR2 inhibitor, were resistant to activation by CM from TNF-α-stimulated astrocytes. Conclusion: This study demonstrates that the CCL2/CCR2 pathway of astrocyte-induced microglial activation is associated with M1 polarization and enhanced migration ability, indicating that this pathway could be a useful target to ameliorate inflammation in the central nervous system.
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Lai, Aaron Y., and Kathryn G. Todd. "Microglia in cerebral ischemia: molecular actions and interactionsThis paper is one of a selection of papers published in this Special Issue, entitled Young Investigator's Forum." Canadian Journal of Physiology and Pharmacology 84, no. 1 (January 2006): 49–59. http://dx.doi.org/10.1139/y05-143.

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The precise role of microglia in stroke and cerebral ischemia has been the subject of debate for a number of years. Microglia are capable of synthesizing numerous soluble and membrane-bound biomolecules, some known to be neuroprotective, some neurotoxic, whereas others have less definitive bioactivities. The molecular mechanisms through which microglia activate these molecules have thus become an important area of ischemia research. Here we provide a survey review that summarizes the key actions of microglial factors in cerebral ischemia including complement proteins, chemokines, pro-inflammatory cytokines, neurotrophic factors, hormones, and proteinases, as well several important messenger molecules that play a part in how these factors respond to extracellular signals during ischemic injuries. We also provide some new perspectives on how microglial intracellular signaling may contribute to the seemingly contradictory roles of several microglial effector molecules.
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Dissertations / Theses on the topic "Microglie – Physiologie"

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Hristovska, Ines. "Dynamique microgliale en conditions physiologiques : un mécanisme contrôlé par les états de vigilance et l’activité neuronale." Thesis, Lyon, 2019. https://n2t.net/ark:/47881/m60c4v3q.

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Les microglies, cellules immunitaires résidentes du système nerveux central (SNC), étaient traditionnellement décrites comme ayant un rôle uniquement lors de blessures ou de maladies du SNC. De manière frappante, dans le cerveau sain, les microglies effectuent une surveillance active du parenchyme en étendant et en rétractant leurs prolongements ramifiés. Ce mouvement est connu sous le nom de motilité microgliale et peut être dirigé vers les synapses. La régulation de ces mouvements et le but des contacts microglie-épines dendritiques restent inconnus. Nous avons examiné l'influence de l'activité neuronale sur la motilité et la morphologie microgliale ainsi que sur les interactions microglies-épines pendant l’éveil et le sommeil. Nous avons observé que les propriétés morpho-dynamiques des microglies sont modulées par les états de vigilance. Les prolongements microgliaux sont attirés par les synapses actives, particulièrement lors de l’éveil, alors que le sommeil régule négativement la proximité des prolongements microgliaux ainsi que les contacts dépendant de l’activité qui lient les prolongements microgliaux aux épines. Le contact des épines avec les prolongements microgliaux entraîne une augmentation de l’activité des épines, principalement observée pendant le sommeil lent. Pour conclure, ces résultats montrent un contrôle complexe de la morpho-dynamique microgliale par l’activité et les états de vigilance. Appréhender les mécanismes régulant la dynamique microgliale et les interactions microglie-épines dendritiques pendant les états de vigilance permettra de mieux comprendre comment les cellules microgliales sont impliquées dans la régulation de l'homéostasie synaptique, l'apprentissage et de la mémoire, des fonctions associées au sommeil. La compréhension des interactions microglies-neurones dans des conditions physiologiques est cruciale pour élucider le fonctionnement synaptique et ses altérations lorsque la microglie est impliquée dans ses fonctions immunes, une caractéristique commune à la plupart des pathologies cérébrales
Microglia, the resident immune cells of the central nervous system (CNS), were traditionally believed to be set into action only by injury or diseases. Strikingly, in the healthy brain, microglia actively carry out parenchyma patrolling by extending and retracting their ramified processes. These movements are referred to as microglial motility and may be to some extent directed toward synapses. However, motility regulation and the purpose of microglia-spine contacts remain elusive. We thus examined the influence of neuronal activity on microglial motility, morphology and microglia-spine interactions during sleep and wakefulness. We found that microglial motility and morphology are modulated by vigilance states. Microglial processes were found to be attracted by active synapses particularly during wake, whereas sleep downregulates microglial proximity and activity-dependent contact with spines. Microglial contact resulted in increased spine activity which was mainly observed during sleep. Understanding the mechanisms regulating microglial dynamics and microglia-spine interactions across the vigilance states will provide further insights into how microglial cells may be involved in sleep- associated functions such as synaptic homeostasis, learning and memory. Grasping these cellular interactions in physiological conditions is crucial to understand synaptic functioning and alterations when microglia are engaged into their immune functions, a hallmark of most brain pathologies
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Richard, Karine. "Étude de l'activation microgliale via les récepteurs TLR dans le contexte de la maladie d'Alzheimer." Thesis, Université Laval, 2010. http://www.theses.ulaval.ca/2010/26955/26955.pdf.

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Simard, Alain. "Le rôle des cellules microgliales and les maladies neurodégénératives = : The role of microglia in neurodegenerative disease." Doctoral thesis, Université Laval, 2006. http://hdl.handle.net/20.500.11794/18341.

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Macouillard-Poulletier, de Gannes Florence. "Caractérisation fonctionnelle de cellules microgliales immortalisées lors de situations de stress thermique et apoptotique." Bordeaux 2, 1998. http://www.theses.fr/1998BOR28602.

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Houalla, Tarek. "Isolation of microglia from goldfish brain." Thesis, McGill University, 2001. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=31238.

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This study aims at providing a new technique for the isolation and culture of goldfish microglial cells. So far no protocol has been designed for the growth of these cells in vitro, despite the growing interest in the remarkable capacity of goldfish central nervous system (CNS) for regenerating severed axons. This newly developed technique has little or no similarity to those used in the isolation of mammalian microglia, and is distinguished by its simple setup and its fast yield for microglial cells. In addition, a virtually pure population of microglia was generated when plated on untreated plastic dishes, eliminating further need for purification. This technique may thus provide a starting point for future characterization of the microglial cells in vitro, which may eventually help toward building a better understanding of the function and biology of these cells. A preliminary morphological characterization of the cells has also been conducted, in addition to groundwork experiments on the phagocytic activity of these cells in vitro, using myelin to stimulate phagocytosis. These assays were oriented toward providing a comparison to the mammalian cultures of microglia, and so far, displayed several similarities in morphologies and phagocytosis.
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Marcaggi, Païkan. "Capture de NH4+ dans les cellules gliales de rétine d'abeille par un transporteur membranaire spécifique." Bordeaux 2, 1999. http://www.theses.fr/1999BOR28698.

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Girolami, Elizabeth. "Regulation of microglial phagocytosis in the regenerating CNS of the goldfish." Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=80276.

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Teleost retinal ganglion cells can regenerate severed axons following injury, something their mammalian counterparts cannot do. In the teleost, successful regeneration has been attributed in part to microglial cell activities including the phagocytosis of myelin. Although the regulation of microglial phagocytosis has been studied in mammals, in the teleost it is largely unexamined. The present study was designed to identify mediators of microglial phagocytosis released by injured goldfish optic nerve during the course of regeneration. We found that microglial phagocytosis was significantly enhanced in the presence of a 7 day regenerating nerve or medium conditioned by the nerve (CM). When either nerve or CM was incubated with microglia along with an antibody against tumour necrosis factor alpha (TNFalpha), this effect was neutralized. The L929 cell cytotoxicity assay further demonstrated TNFalpha activity in the CM. However, Western blot analysis did not confirm this result. Therefore, further work is necessary to clearly establish the presence of TNFalpha.
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Larke, Vollmer Lauren. "Microglial acid-sensing T Cell Death Associated Gene-8 (TDAG8) Receptor in CO2-Evoked Behavior and Physiology: Relevance to Panic." University of Cincinnati / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1397235858.

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Cao, Tuoxin. "Hydrogen Peroxide and Pharmacological Agent Modulation of TRPV2 Channel Gating." VCU Scholars Compass, 2017. http://scholarscompass.vcu.edu/etd/4848.

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Transient receptor potential vanilloid 2 channel (TRPV2) is a Ca2+-permeable ion channel that is highly expressed in leukocytes but is also present in skeletal and cardiac muscle and endocrine cells. The TRPV2 function is implicated in a number of physiological processes, including bacterial phagocytosis, pro-inflammatory cytokine production, cardiac hypertrophy, and cancer development. TRPV2 knockout mice exhibit a high incidence of perinatal mortality, arguing that the channel plays essential roles in physiology. Despite the importance of TRPV2 for normal homeostasis, the mechanisms that control TRPV2 gating in response to pharmacological agonists, heating, membrane stretch, bioactive lipids and reactive oxygen species (ROS) remain poorly understood. Here we demonstrate that TRPV2 is functionally expressed in microglia (i.e., ‘brain macrophages’) and the microglia-like BV-2 cell line, and demonstrate that the gating of an endogenous TRPV2-like conductance is positively modulated by the bacterial toxin lipopolysaccharide (LPS), which is known to cause pro-inflammatory (M1) activation and increase ROS production by NADPH oxidase. To determine how TRPV2 gating is modulated by ROS, we recorded single channel activity in inside-out patches excised from HEK-293 cells expressing GFP-rTRPV2. Unitary currents elicited by the TRPV2 agonist 2-aminophenyl borinate (2-APB) or cannabidiol (CBD) are linear in monovalent recording solutions and give rise to an estimated unitary conductance of ~100pS, which is similar to TRPV1 but significantly smaller than TRPV3. Intriguingly, we find that although TRPV2 is insensitive to ROS (in the form of exogenously applied H2O2) alone, apparent open probability is synergistically enhanced when H2O2 is applied together with CBD. We identify two intracellular Cys residues that are necessary for TRPV2 responses to H2O2 sensitivity and find that these residues are located close to one another, albeit in different subunits, in the TRPV2 structure, suggesting that ROS promote the formation of an inter-subunit disulfide bond that alters sensitivity to pharmacological agonists. We hypothesize that ROS-dependent modulation of TRPV2 activity may be an important contributor to pro-inflammatory activation of microglia underline central nervous system diseases and that TRPV2 antagonism could be a useful therapeutic strategy in the treatment of neuroinflammation.
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Bolton, Hall Amanda Nicholle. "HISTOLOGICAL AND BEHAVIORAL CONSEQUENCES OF REPEATED MILD TRAUMATIC BRAIN INJURY IN MICE." UKnowledge, 2016. http://uknowledge.uky.edu/physiology_etds/26.

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The majority of the estimated three million traumatic brain injuries that occur each year are classified as “mild” and do not require surgical intervention. However, debilitating symptoms such as difficulties focusing on tasks, anxiety, depression, and visual deficits can persist chronically after a mild traumatic brain injury (TBI) even if an individual appears “fine”. These symptoms have been observed to worsen or be prolonged when an individual has suffered multiple mild TBIs. To test the hypothesis that increasing the amount of time between head injuries can reduce the histopathological and behavioral consequences of repeated mild TBI, a mouse model of closed head injury (CHI) was developed. A pneumatically controlled device with a silicone tip was used to deliver a diffuse, midline impact directly onto the mouse skull. A 2.0mm intended depth of injury caused a brief period of apnea and increased righting reflex response with minimal astrogliosis and axonal injury bilaterally in the entorhinal cortex, optic tract, and cerebellum. When five CHIs were repeated at 24h inter-injury intervals, astrogliosis was exacerbated acutely in the hippocampus and entorhinal cortex compared to a single mild TBI. Additionally, in the entorhinal cortex, hemorrhagic lesions developed along with increased neurodegeneration and microgliosis. Axonal injury was observed bilaterally in the white matter tracts of the cerebellum and brainstem. When the inter-injury interval was extended to 48h, the extent of inflammation and cell death was similar to that caused by a single CHI suggesting that, in our mouse model, extending the inter-injury interval from 24h to 48h reduced the acute effects of repeated head injuries. The behavioral consequences of repeated CHI at 24h or 48h inter-injury intervals were evaluated in a ten week longitudinal study followed by histological analyses. Five CHI repeated at 24h inter-injury intervals produced motor and cognitive deficits that persisted throughout the ten week study period. Based upon histological analyses, the acute inflammation, axonal injury, and cell death observed acutely in the entorhinal cortex had resolved by ten weeks after injury. However, axonal degeneration and gliosis were present in the optic tract, optic nerve, and corticospinal tract. Extending the inter-injury interval to 48h did not significantly reduce motor and cognitive deficits, nor did it protect against chronic microgliosis and neurodegeneration in the visual pathway. Together these data suggested that some white matter areas may be more susceptible to our model of repeated mild TBI causing persistent neuropathology and behavioral deficits which were not substantially reduced with a 48h inter-injury interval. In many forms of TBI, microgliosis persists chronically and is believed to contribute to the cascade of neurodegeneration. To test the hypothesis that post-traumatic microgliosis contributes to mild TBI-related neuropathology, mice deficient in the growth factor progranulin (Grn-/-) received repeated CHI and were compared to wildtype, C57BL/6 mice. Penetrating head injury was previously reported to amplify the acute microglial response in Grn-/- mice. In our studies, repeated CHI induced an increased microglial response in Grn-/- mice compared to C57BL/6 mice at 48h, 7d, and 7mo after injury. However, no differences were observed between Grn-/- and WT mice with respect to their behavioral responses or amount of axonal injury or ongoing neurodegeneration at 7 months despite the robust differences in microgliosis. Dietary administration of ibuprofen initiated after the first injury reduced microglial activation within the optic tract of WT mice 7d after repeated mild TBI. However, a two week ibuprofen treatment regimen failed to affect the extent of behavioral dysfunction over 7mo or decrease chronic neurodegeneration, axon loss, or microgliosis in brain-injured Grn-.- mice when compared to standard diet. Together these studies underscore that mild TBIs, when repeated, can result in long lasting behavioral deficits accompanied by neurodegeneration within vulnerable brain regions. Our studies on the time interval between repeated head injuries suggest that a 48h inter-injury interval is within the window of mouse brain vulnerability to chronic motor and cognitive dysfunction and white matter injury. Data from our microglia modulation studies suggest that a chronically heightened microglial response following repeated mild TBI in progranulin deficient mice does not worsen chronic behavioral dysfunction or neurodegeneration. In addition, a two week ibuprofen treatment is not effective in reducing the microglial response, chronic behavioral dysfunction, or chronic neurodegeneration in progranulin deficient mice. Our data suggests that microglia are not a favorable target for the treatment of TBI.
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Books on the topic "Microglie – Physiologie"

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Marie-Ève, Tremblay, and Amanda Sierra. Microglia in health and disease. New York: Springer, 2014.

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Jagasia, Ravi. Role of voltage-gated Kv channels in microglial physiology. Ottawa: National Library of Canada, 2002.

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Noda, Mami, and Alexei Verkhratsky. Physiology of Microglia. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199794591.003.0019.

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This is a digitally enhanced text. Readers can also see the coverage of this topic area in the second edition of Neuroglia. The second edition of Neuroglia was first published digitally in Oxford Scholarship Online and the bibliographic details provided, if cited, will direct people to that version of the text. Readers can also see the coverage of this topic area in the ...
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Giffard, Erica R. Microglia: Physiology, Regulation and Health Implications. Nova Science Publishers, Incorporated, 2015.

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5

M, Berry, and Logan Ann, eds. CNS injuries: Cellular responses and pharmacological strategies. Boca Raton: CRC Press, 1999.

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Berry, Martin, and Ann Logan. CNS Injuries: Cellular Responses and Pharmacological Strategies (Pharmacology & Toxicology (Crc Pr)). CRC, 1998.

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Book chapters on the topic "Microglie – Physiologie"

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Garaschuk, Olga, and Alexei Verkhratsky. "Physiology of Microglia." In Microglia, 27–40. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9658-2_3.

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Watters, Jyoti J., and Jennifer M. Pocock. "Microglial Physiology." In Microglia in Health and Disease, 47–79. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1429-6_3.

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Tay, Tuan Leng, Micaël Carrier, and Marie-Ève Tremblay. "Physiology of Microglia." In Neuroglia in Neurodegenerative Diseases, 129–48. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-9913-8_6.

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Butovsky, Oleg, Charlotte Madore, and Howard Weiner. "Microglial Biology and Physiology." In Neuroimmune Pharmacology, 167–99. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-44022-4_13.

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Verkhratsky, Alexei, and Mami Noda. "General Physiology and Pathophysiology of Microglia." In Neuroinflammation and Neurodegeneration, 47–60. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1071-7_3.

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Streit, Wolfgang J. "Physiology and Pathophysiology of Microglial Cell Function." In Microglia in the Regenerating and Degenerating Central Nervous System, 1–14. New York, NY: Springer New York, 2002. http://dx.doi.org/10.1007/978-1-4757-4139-1_1.

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Patro, Ishan, Aarti Nagayach, Shrstha Sinha, and Nisha Patro. "General Physiology and Pathophysiology of Microglia During Neuroinflammation." In Inflammation: the Common Link in Brain Pathologies, 17–42. Singapore: Springer Singapore, 2016. http://dx.doi.org/10.1007/978-981-10-1711-7_2.

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"Microglia." In Glial Physiology and Pathophysiology, 343–80. Chichester, UK: John Wiley & Sons, Ltd, 2013. http://dx.doi.org/10.1002/9781118402061.ch7.

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De Koninck, Yves. "Modulation of Chloride Homeostasis by Microglia." In Physiology and Pathology of Chloride Transporters and Channels in the Nervous System, 471–88. Elsevier, 2010. http://dx.doi.org/10.1016/b978-0-12-374373-2.00023-6.

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Conference papers on the topic "Microglie – Physiologie"

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Lindhout, Ivan, and Andis Klegeris. "Neurotrophins as intercellular signaling molecules of the brain regulate select immune functions of microglia." In Cell-to-Cell Metabolic Cross-Talk in Physiology and Pathology. Basel, Switzerland: MDPI, 2020. http://dx.doi.org/10.3390/cells2020-08927.

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