Relevant bibliographies by topics / Satellite glia

Academic literature on the topic 'Satellite glia'

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Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Satellite glia"

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Garrett, Filip G., and Paul L. Durham. "Differential expression of connexins in trigeminal ganglion neurons and satellite glial cells in response to chronic or acute joint inflammation." Neuron Glia Biology 4, no. 4 (November 2008): 295–306. http://dx.doi.org/10.1017/s1740925x09990093.

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Trigeminal nerve activation in response to inflammatory stimuli has been shown to increase neuron–glia communication via gap junctions in trigeminal ganglion. The goal of this study was to identify changes in the expression of gap junction proteins, connexins (Cxs), in trigeminal ganglia in response to acute or chronic joint inflammation. Although mRNA for Cxs 26, 36, 40 and 43 was detected under basal conditions, protein expression of only Cxs 26, 36 and 40 increased following capsaicin or complete Freund's adjuvant (CFA) injection into the temporomandibular joint (TMJ). While Cx26 plaque formation between neurons and satellite glia was transiently increased following capsaicin injections, Cx26 plaque formation between neurons and satellite glia was sustained in response to CFA. Interestingly, levels of Cx36 and Cx40 were only elevated in neurons following capsaicin or CFA injections, but the temporal response was similar to that observed for Cx26. In contrast, Cx43 expression was not increased in neurons or satellite glial cells in response to CFA or capsaicin. Thus, trigeminal ganglion neurons and satellite glia can differentially regulate Cx expression in response to the type and duration of inflammatory stimuli, which likely facilitates increased neuron–glia communication during acute and chronic inflammation and pain in the TMJ.
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Krawczyk, Aleksandra Ewa, and Jadwiga Jaworska-Adamu. "The immunoreactivity of satellite glia of the spinal ganglia of rats treated with monosodium glutamate." Acta Veterinaria Brno 85, no. 4 (2016): 337–41. http://dx.doi.org/10.2754/avb201685040337.

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Satellite glia of the peripheral nervous system ganglia provide metabolic protection to the neurons. The aim of this study was to determine the effects of monosodium glutamate administered parenterally to rats on the expression of glial fibrillary acidic protein, S-100β protein and Ki-67 antigen in the satellite glial cells. Adult, 60-day-old male rats received monosodium glutamate at two doses of 2 g/kg b.w. (group 1) and 4 g/kg b.w. (group 2) subcutaneously for 3 consecutive days. Animals in the control group (group C) were treated with corresponding doses of 0.9% sodium chloride. Immediately after euthanasia, spinal ganglia of the lumbar region were dissected. Immunohistochemical peroxidase anti-peroxidase reactions were performed on the sections containing the examined material using antibodies against glial fibrillary acidic protein, S-100β and Ki-67. Next, morphological and morphometric analyses of immunopositive and immunonegative glia were conducted. The data were presented as the mean number of cells with standard deviation. Significant differences were analysed using ANOVA (P < 0.05). In all 63-day-old rats, immunopositivity for the examined proteins glia was observed. Increased number of cells expressing glial fibrillary acidic protein was demonstrated in group 2, whereas the number of S-100β-positive glia grew in the groups with the increasing doses of monosodium glutamate. The results indicate the early stage reactivity of glia in response to increased levels of glutamate in the extracellular space. These changes may be of a neuroprotective nature under the conditions of excitotoxicity induced by the action of this excitatory neurotransmitter.
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Lee, Ji Hwan, and Woojin Kim. "The Role of Satellite Glial Cells, Astrocytes, and Microglia in Oxaliplatin-Induced Neuropathic Pain." Biomedicines 8, no. 9 (September 2, 2020): 324. http://dx.doi.org/10.3390/biomedicines8090324.

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Oxaliplatin is a third-generation platinum-based chemotherapeutic drug. Although its efficacy against colorectal cancer is well known, peripheral neuropathy that develops during and after infusion of the agents could decrease the quality of life of the patients. Various pathways have been reported to be the cause of the oxaliplatin-induced paresthesia and dysesthesia; however, its mechanism of action has not been fully understood yet. In recent years, researchers have investigated the function of glia in pain, and demonstrated that glia in the peripheral and central nervous system could play a critical role in the development and maintenance of neuropathic pain. These results suggest that targeting the glia may be an effective therapeutic option. In the past ten years, 20 more papers focused on the role of glia in oxaliplatin-induced thermal and mechanical hypersensitivity. However, to date no review has been written to summarize and discuss their results. Thus, in this study, by reviewing 23 studies that conducted in vivo experiments in rodents, the change of satellite glial cells, astrocytes, and microglia activation in the dorsal root ganglia, spinal cord, and the brain of oxaliplatin-induced neuropathic pain animals is discussed.
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Magni, Giulia, and Stefania Ceruti. "The Purinergic System and Glial Cells: Emerging Costars in Nociception." BioMed Research International 2014 (2014): 1–13. http://dx.doi.org/10.1155/2014/495789.

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It is now well established that glial cells not only provide mechanical and trophic support to neurons but can directly contribute to neurotransmission, for example, by release and uptake of neurotransmitters and by secreting pro- and anti-inflammatory mediators. This has greatly changed our attitude towards acute and chronic disorders, paving the way for new therapeutic approaches targeting activated glial cells to indirectly modulate and/or restore neuronal functions. A deeper understanding of the molecular mechanisms and signaling pathways involved in neuron-to-glia and glia-to-glia communication that can be pharmacologically targeted is therefore a mandatory step toward the success of this new healing strategy. This holds true also in the field of pain transmission, where the key involvement of astrocytes and microglia in the central nervous system and satellite glial cells in peripheral ganglia has been clearly demonstrated, and literally hundreds of signaling molecules have been identified. Here, we shall focus on one emerging signaling system involved in the cross talk between neurons and glial cells, the purinergic system, consisting of extracellular nucleotides and nucleosides and their membrane receptors. Specifically, we shall summarize existing evidence of novel “druggable” glial purinergic targets, which could help in the development of innovative analgesic approaches to chronic pain states.
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Durham, Paul L., and F. G. Garrett. "Development of functional units within trigeminal ganglia correlates with increased expression of proteins involved in neuron–glia interactions." Neuron Glia Biology 6, no. 3 (August 2010): 171–81. http://dx.doi.org/10.1017/s1740925x10000232.

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Cell bodies of trigeminal nerves, which are located in the trigeminal ganglion, are completely surrounded by satellite glial cells and together form a functional unit that regulates neuronal excitability. The goals of this study were to investigate the cellular organization of the rat trigeminal ganglia during postnatal development and correlate those findings with expression of proteins implicated in neuron–glia interactions. During postnatal development there was an increase in the volume of the neuronal cell body, which correlated with a steady increase in the number of glial cells associated with an individual neuron from an average of 2.16 at birth to 7.35 on day 56 in young adults. Interestingly, while the levels of the inwardly rectifying K+ channel Kir4.1 were barely detectable during the first week, its expression in satellite glial cells increased by day 9 and correlated with initial formation of functional units. Similarly, expression of the vesicle docking protein SNAP-25 and neuropeptide calcitonin gene-related peptide was readily detected beginning on day 9 and remained elevated throughout postnatal development. Based on our findings, we propose that the expression of proteins involved in facilitating neuron–glia interactions temporally correlates with the formation of mature functional units during postnatal development of trigeminal ganglion.
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Gazerani, Parisa. "Contribution of Central and Peripheral Glial Cells in the Development and Persistence of Itch: Therapeutic Implication of Glial Modulation." Neuroglia 4, no. 1 (January 17, 2023): 15–27. http://dx.doi.org/10.3390/neuroglia4010002.

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Chronic itch (CI) is an unpleasant skin sensation accompanied by an intense scratching desire that lasts 6 weeks or longer. Despite the high prevalence and negative impact on affected individuals and a huge healthcare burden, CI mechanisms are only partially understood, and consequently, treatment of CI remains sub-optimal. The complexity of CI treatment also stems from the comorbid existence of persistent itch with other somatic and psychological disorders. Etiologies of CI are multiple and diverse, although CI is often a result of dermatologically related conditions such as atopic dermatitis and psoriasis. Unfolding the pathophysiology of CI can provide possibilities for better therapy. Itch signaling is complex and neurons and non-neuronal cells play a role. This review focuses on recent findings on the role of glial cells in itch. Central glia (astrocytes and microglia) and peripheral glia (satellite glial cells and Schwann cells) are found to contribute to the development or persistence of itch. Hence, glial modulation has been proposed as a potential option in CI treatment. In experimental models of itch, the blockade of signal transducer and the activator of transcription (STAT) 3-mediated reactive astrogliosis have been shown to suppress chronic itch. Administration of a microglial inhibitor, minocycline, has also been demonstrated to suppress itch-related microglial activation and itch. In sensory ganglia, gap-junction blockers have successfully blocked itch, and hence, gap-junction-mediated coupling, with a potential role of satellite glial cells have been proposed. This review presents examples of glial involvement in itch and opportunities and challenges of glial modulation for targeting itch.
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Ye, Yi, Elizabeth Salvo, Marcela Romero-Reyes, Simon Akerman, Emi Shimizu, Yoshifumi Kobayashi, Benoit Michot, and Jennifer Gibbs. "Glia and Orofacial Pain: Progress and Future Directions." International Journal of Molecular Sciences 22, no. 10 (May 19, 2021): 5345. http://dx.doi.org/10.3390/ijms22105345.

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Orofacial pain is a universal predicament, afflicting millions of individuals worldwide. Research on the molecular mechanisms of orofacial pain has predominately focused on the role of neurons underlying nociception. However, aside from neural mechanisms, non-neuronal cells, such as Schwann cells and satellite ganglion cells in the peripheral nervous system, and microglia and astrocytes in the central nervous system, are important players in both peripheral and central processing of pain in the orofacial region. This review highlights recent molecular and cellular findings of the glia involvement and glia–neuron interactions in four common orofacial pain conditions such as headache, dental pulp injury, temporomandibular joint dysfunction/inflammation, and head and neck cancer. We will discuss the remaining questions and future directions on glial involvement in these four orofacial pain conditions.
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Robering, Jan W., Lisa Gebhardt, Katharina Wolf, Helen Kühn, Andreas E. Kremer, and Michael J. M. Fischer. "Lysophosphatidic acid activates satellite glia cells and Schwann cells." Glia 67, no. 5 (January 13, 2019): 999–1012. http://dx.doi.org/10.1002/glia.23585.

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Afroz, Shaista, Rieko Arakaki, Takuma Iwasa, Masamitsu Oshima, Maki Hosoki, Miho Inoue, Otto Baba, Yoshihiro Okayama, and Yoshizo Matsuka. "CGRP Induces Differential Regulation of Cytokines from Satellite Glial Cells in Trigeminal Ganglia and Orofacial Nociception." International Journal of Molecular Sciences 20, no. 3 (February 7, 2019): 711. http://dx.doi.org/10.3390/ijms20030711.

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Neuron-glia interactions contribute to pain initiation and sustainment. Intra-ganglionic (IG) secretion of calcitonin gene-related peptide (CGRP) in the trigeminal ganglion (TG) modulates pain transmission through neuron-glia signaling, contributing to various orofacial pain conditions. The present study aimed to investigate the role of satellite glial cells (SGC) in TG in causing cytokine-related orofacial nociception in response to IG administration of CGRP. For that purpose, CGRP alone (10 μL of 10−5 M), Minocycline (5 μL containing 10 μg) followed by CGRP with one hour gap (Min + CGRP) were administered directly inside the TG in independent experiments. Rats were evaluated for thermal hyperalgesia at 6 and 24 h post-injection using an operant orofacial pain assessment device (OPAD) at three temperatures (37, 45 and 10 °C). Quantitative real-time PCR was performed to evaluate the mRNA expression of IL-1β, IL-6, TNF-α, IL-1 receptor antagonist (IL-1RA), sodium channel 1.7 (NaV 1.7, for assessment of neuronal activation) and glial fibrillary acidic protein (GFAP, a marker of glial activation). The cytokines released in culture media from purified glial cells were evaluated using antibody cytokine array. IG CGRP caused heat hyperalgesia between 6–24 h (paired-t test, p < 0.05). Between 1 to 6 h the mRNA and protein expressions of GFAP was increased in parallel with an increase in the mRNA expression of pro-inflammatory cytokines IL-1β and anti-inflammatory cytokine IL-1RA and NaV1.7 (one-way ANOVA followed by Dunnett’s post hoc test, p < 0.05). To investigate whether glial inhibition is useful to prevent nociception symptoms, Minocycline (glial inhibitor) was administered IG 1 h before CGRP injection. Minocycline reversed CGRP-induced thermal nociception, glial activity, and down-regulated IL-1β and IL-6 cytokines significantly at 6 h (t-test, p < 0.05). Purified glial cells in culture showed an increase in release of 20 cytokines after stimulation with CGRP. Our findings demonstrate that SGCs in the sensory ganglia contribute to the occurrence of pain via cytokine expression and that glial inhibition can effectively control the development of nociception.
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Mapps, Aurelia A., Michael B. Thomsen, Erica Boehm, Haiqing Zhao, Samer Hattar, and Rejji Kuruvilla. "Diversity of satellite glia in sympathetic and sensory ganglia." Cell Reports 38, no. 5 (February 2022): 110328. http://dx.doi.org/10.1016/j.celrep.2022.110328.

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Dissertations / Theses on the topic "Satellite glia"

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Rabah, Yasmine. "Satellite glial cell-proprioceptor interactions in dorsal root ganglia Characterization of transgenic mouse lines for selectively targeting glial cells in dorsal root ganglia Satellite glial cells modulate proprioceptive neuron function." Thesis, Sorbonne Paris Cité, 2018. http://www.theses.fr/2018USPCB208.

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Les neurones propriocepteurs sont nécessaires au contrôle du mouvement et à la locomotion. Ils connectent les fuseaux musculaires et les tendons aux motoneurones de la moelle épinière pour informer le système nerveux central de l’état d’élongation et de contraction des muscles. Leurs corps cellulaires sont localisés dans les ganglions rachidiens dorsaux (GRD), où ils sont intimement entourés de cellules gliales GFAP-positives appelées cellules satellites gliales (CSG). Comme les astrocytes du système nerveux central, les CSG expriment à leur surface des récepteurs couplés aux protéines Gq (Gq RCPG) qui peuvent être activés par les neurotransmetteurs libérés par les corps cellulaires de neurones sensoriels du GRD. Les corps cellulaires des neurones sensoriels expriment aussi un certain nombre de récepteurs et transmetteurs. Ces caractéristiques, ainsi que la proximité physique entre les CSG et les neurones sensoriels a permis d’émettre l’hypothèse que les deux types cellulaires sont capables de communiquer. De récentes données de la littérature suggèrent que les CSG et les neurones sensoriels responsables de la détection de la douleur sont capables de dialoguer. Cependant, à notre connaissance, aucune donnée n’a permis jusqu’à présent de démontrer une interaction entre les CSG et les neurones propriocepteurs. Dans cette étude, nous avons émis l’hypothèse que l’activation des Gq RCPG des CSG permet la modulation de l’activité des propriocepteurs. Pour tester cette hypothèse, nous avons utilisé des approches techniques complémentaires (imagerie calcique bi-photonique, immunohistochimie, biochimie et analyses comportementales) combinées à un outil chemogénétique puissant basé sur la technologie DREADD afin d’activer sélectivement la voie de signalisation Gq RCPG dans les CSG. Nous avons démontré dans une préparation de GRD intacte que les CSG sont capables de moduler l’activité des propriocepteurs via une signalisation purinergique. Pour tester la pertinence de cette communication, nous avons réalisé des expériences de comportement sensorimoteur et mis en évidence que l’activation des cellules gliales GFAP-positives induit des déficits sensorimoteurs. Déterminer si la modulation des propriocepteurs par les CSG affecte la transmission sensorimotrice a de profondes implications pour la compréhension du système sensorimoteur et de ses dérèglements
Proprioceptive neurons (one’s own neurons) are necessary for controlling motor control and locomotion. They arise from muscle spindles and tendons and synapse onto ventral horn motoneurons to deliver information about the length and contraction of muscles. Proprioceptor somata reside within the dorsal root ganglia (DRG) and are tightly enwrapped in a thin sheath of GFAP-expressing glial cells, called satellite glial cells (SGCs). Interestingly, SGCs express a number of Gq protein- coupled receptors (Gq GPCRs), which can be activated by neurotransmitters released by sensory neuron somata. Sensory neuron somata also express a number of receptors and transmitters. Both the expression of receptors and the close contact between SGCs and sensory neurons led to the hypothesis that these two cell types communicate. There is emerging evidence that SGCs and nociceptive sensory neuron (pain-sensing neurons) somata can communicate. Furthermore, to date, there is no study conducted on SGC-proprioceptor interaction. We hypothesized that SGC Gq GPCR signaling induces the release of neuroactive molecules from SGCs, leading to the modulation of proprioceptor activity. The main goal of this project has been to test this hypothesis using complementary technical approaches (2-photon Ca2+ imaging, immunohistochemistry, biochemistry and behavior) combined with a powerful chemogenetic DREADD-based tool to activate SGC Gq GPCR activity. We have demonstrated ex vivo that SGCs modulate proprioceptive neuron activity through a purinergic pathway. In order to test the physiological relevance of this discovery in vivo, we performed sensorimotor behavioral experiments and have shown that activating GFAP-expressing glial cells induces sensorimotor deficits. Determining whether SGC-induced proprioceptor activity has profound implications in the understanding of sensorimotor functions in health and diseases
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Bustamante, Diaz Hedie A. "The role of potassium buffering and apoptosis of trigeminal satellite glial cells in the induction and maintenance of orofacial neuropathic pain in rats." Diss., Virginia Tech, 2011. http://hdl.handle.net/10919/77103.

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Satellite glial cells (SGC) are laminar cells that wrap completely around the sensory neuron and are responsible for buffering extracellular K+ after neuronal excitation. A decrease in the potassium buffering capacity of SGC has been associated with neuropathic pain (NP) behavior and apoptosis. This dissertation investigated the role of the potassium buffering capacity and apoptosis of trigeminal satellite glial cells (SGC) in the maintenance and development of orofacial NP in rats using in vivo and in vitro methodologies. In vivo endpoints were evaluated after performing chronic constriction injury (CCI) of the infraorbital nerve (IoN). NP signs and behavior were evaluated at 5, 10, 20 40 and 80 hours after injury. We evaluated the potassium buffering capacity of SGC by measuring the intracellular potassium concentration and protein levels and gene expression of the Kir4.1 and the SK3 potassium channels and gap junction protein connexin 43 (Cx43). We evaluated apoptosis endpoints including protein levels and gene expression of apoptotic related proteins bcl-2, caspase 9, caspase 3 and p53. Results indicate that NP signs developed as early as 5 hours after injury. After PNI, SGC responded by increasing their intracellular potassium concentration and by increasing protein levels of Kir4.1, SK3 and Cx43. Nonetheless, this increase in protein levels was not accompanied by an increase in gene expression. Apoptosis results revealed that SGC decreased protein levels and gene expression of anti-apoptotic protein Bcl-2. Using in vitro methodologies, we developed primary trigeminal SGC cultures and evaluated how a decrease in the intracellular potassium concentration modulates apoptosis induced by the mitochondrial and death receptor pathways. SGC depleted of potassium after hypoosmotic shock showed a significant increase in early apoptosis after incubation with mitochondrial pathway apoptotic inducer staurosporine when compared to SGC with normal intracellular concentration. This research has revealed that SGC respond early to PNI by increasing their potassium buffering capacity. We also determined that the mitochondrial apoptotic pathway might be involved in the trigeminal SGC response to PNI. From our in vitro experiments we have revealed that potassium is an important modulator of apoptosis induced by the mitochondrial pathway in cultured trigeminal SGC.
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Smith, Sarah K. "Effects of Peripheral Nerve Injury on the Cells of the Dorsal Root Ganglion: a Role for Primary Cilia." Thesis, University of North Texas, 2012. https://digital.library.unt.edu/ark:/67531/metadc177258/.

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Primary cilia are ubiquitous sensory organelles found on most cell types including cells of the dorsal root ganglia (DRG). The DRG are groups of peripheral neurons that relay sensory information from the periphery to the CNS. Other cell types in the DRG include a type of glial cell, the satellite glial cells (SGCs). The SGCs surround the DRG neurons and, with the neurons, form functional sensory units. Currently are no reports describing the numbers of DRG cells that have cilia. We found that 26% of the SGCs had primary cilia. The incidence of cilia on neurons varied with neuron size, a property that roughly correlates with physiological characteristics. We found that 29% of the small, 16% of the medium and 5% of the large neurons had primary cilia. Primary cilia have been shown to have a role in cell proliferation in a variety of cell types. In some of the cells the cilia mediate the proliferative effects of Sonic hedgehog (Shh). In the CNS, Shh signaling through primary cilia affects proliferation during development as well as following injury, but no studies have looked at this function in the PNS. The SGCs and neurons of the DRG undergo complex changes following peripheral nerve injury such as axotomy. One marked change seen after axotomy is SGC proliferation and at later stages, neuronal death. We found that following axotomy there is a significant increase in the percentage of SGCs with primary cilia. We also found a significant increase in the percentage of medium-sized neurons with primary cilia. In other experiments we tested the idea that Shh plays a role in SGC proliferation. When Shh signaling was blocked following axotomy we found decreased proliferation of SGCs. This is the first report of a change in the percentage of cells with cilia following injury in the PNS, and the first report of a role for Shh in SGC proliferation following axotomy.
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Lemes, Júlia Borges Paes. "Participação dos receptores P2X7 presentes em células da glia do gânglio da raiz dorsal na nocicepção." Universidade Federal de Uberlândia, 2017. https://repositorio.ufu.br/handle/123456789/19722.

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Nos gânglios sensitivos, os corpos celulares dos neurônios encontram-se circundados por células gliais denominadas células satélites. Estudos recentes apontam para uma possível comunicação entre neurônios e células satélites através da liberação de ATP e ativação de receptores P2X7 presentes nas células gliais. Além disto, células satélites adjacentes podem estar conectadas através de junções comunicantes (“gap junctions”). Até o presente, a comunicação entre células satélites e neurônios tem sido implicada na cronificação da dor e em processos inflamatórios. Nesse estudo buscamos avaliar o papel da comunicação entre neurônios e células satélites através da ativação dos receptores P2X7 assim como das junções comunicantes em modelos de dor aguda. Em culturas primárias de gânglios da raiz dorsal, verificamos que a administração de capsaicina leva a um aumento de cálcio em neurônios e em seguida em células satélites sendo que a resposta das células satélites foi bloqueada por A740003, um antagonista seletivo para receptores P2X7, indicando que os nociceptores quando ativados liberam ATP que, por sua vez, ativa receptores P2X7 nas células gliais. Para avaliar o papel desta comunicação celular in vivo, o antagonista P2X7 ou o bloqueador de junções comunicantes, carbenoxolona, foram administrados por via intraganglionar (L5) e foram avaliados os efeitos das injeções intraplantares de capsaicina, mentol e formalina em ratos. Tanto o A740003 quanto a carbenoxolona reduziram a nocicepção induzida por capsaicina e mentol. No teste da formalina, ambas as substâncias afetaram apenas a segunda fase do teste, considerada a fase inflamatória. Capsaicina ativa seletivamente receptores TRPV1 e mentol ativa receptores TRPM8, e possivelmente receptores TRPA1, que são expressos majoritariamente em neurônios nociceptivos associados a fibras C. Além disto, estudos de outros autores indicam a primeira fase do teste da formalina envolve principalmente a ativação de fibras do tipo Aδ enquanto que a segunda fase envolve a ativação de fibras Aδ e C. Considerando estes dados juntamente como os presentes resultados, podemos sugerir que a comunicação entre células satélites e neurônios ocorre também na dor aguda, mas apenas quando esta depende da ativação de fibras C. Deste modo, a comunicação entre neurônios e células satélites, via liberação de ATP e ativação de receptores P2X7, assim como uma comunicação entre células satélites adjacentes através de junções comunicantes parecem estar envolvidos em um processamento rápido do sinal doloroso no gânglio da raiz dorsal.
In sensory ganglia, the cellular bodies of neurons are surrounded by glial cells called satellite cells. Recent studies point to a possible communication between neurons and satellite cells through the release of ATP and activation of P2X7 receptors present in glial cells. In addition, adjacent satellite cells may be connected through gap junctions. Still today, the communication between satellite cells and neurons has been implicated in chronic pain and in inflammatory processes. In this study we sought to evaluate the role of communication between neurons and satellite cells through the activation of the P2X7 receptors as well as of the communicating junctions in acute pain models. In primary cultures of dorsal root ganglia, we found that the administration of capsaicin leads to an increase of calcium in neurons and then in satellite cells. The response of satellite cells was blocked by A740003, a selective antagonist for P2X7 receptors, indicating that nociceptors when activated release ATP, which in turn activates P2X7 receptors in the glial cells. To assess the role of this in vivo cellular communication, the P2X7 antagonist or the gap junction blocker, carbenoxolone, were administered by intraganglionar injection (L5) and the effects of intraplantar injections of capsaicin, menthol or formalin in rats were evaluated. Both A740003 and carbenoxolone reduced nociception induced by capsaicin and menthol. In the formalin test, both substances affected only the second phase of the test, considered the inflammatory phase. Capsaicin selectively activates TRPV1 receptors while menthol activates TRPM8 receptors, and possibly TRPA1 receptors, which are expressed mainly in nociceptive neurons associated with C fibers. In addition, studies by other authors indicate that the first phase of the formalin test involves primarily the activation of Aδ fibers whereas the second phase involves the activation of Aδ and C fibers. Considering these data together with the present results, we can suggest that the communication between satellite cells and neurons also occurs in acute pain, but only, when it depends on the activation of C fibers. Thus, communication between neurons and satellite cells, via release of ATP and activation of P2X7 receptors, as well as communication between adjacent satellite cells through gap junctions seems to be involved in a rapid processing of the pain signal in the dorsal root ganglion.
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Walker, Ryan G. "Plasticity of adult sympathetic neurons following injury." Miami University / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=miami1250091703.

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Tongtako, Witchaya [Verfasser]. "In situ and in vitro characterization of canine and murine satellite glial cells and canine neurons from dorsal root ganglia / Witchaya Tongtako." Hannover : Bibliothek der Tierärztlichen Hochschule Hannover, 2017. http://d-nb.info/1150445408/34.

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[Verfasser], Witchaya Tongtako. "In situ and in vitro characterization of canine and murine satellite glial cells and canine neurons from dorsal root ganglia / Witchaya Tongtako." Hannover : Bibliothek der Tierärztlichen Hochschule Hannover, 2017. http://nbn-resolving.de/urn:nbn:de:gbv:95-111008.

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Voronova, Anastassia. "The Transcriptional Regulation of Stem Cell Differentiation Programs by Hedgehog Signalling." Thèse, Université d'Ottawa / University of Ottawa, 2012. http://hdl.handle.net/10393/23223.

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The Hedgehog (Hh) signalling pathway is one of the key signalling pathways orchestrating intricate organogenesis, including the development of neural tube, heart and skeletal muscle. Yet, insufficient mechanistic understanding of its diverse roles is available. Here, we show the molecular mechanisms regulating the neurogenic, cardiogenic and myogenic properties of Hh signalling, via effector protein Gli2, in embryonic and adult stem cells. In Chapter 2, we show that Gli2 induces neurogenesis, whereas a dominant-negative form of Gli2 delays neurogenesis in P19 embryonal carcinoma (EC) cells, a mouse embryonic stem (ES) cell model. Furthermore, we demonstrate that Gli2 associates with Ascl1/Mash1 gene elements in differentiating P19 cells and activates the Ascl1/Mash1 promoter in vitro. Thus, Gli2 mediates neurogenesis in P19 cells at least in part by directly regulating Ascl1/Mash1 expression. In Chapter 3, we demonstrate that Gli2 and MEF2C bind each other’s regulatory elements and regulate each other’s expression while enhancing cardiomyogenesis in P19 cells. Furthermore, dominant-negative Gli2 and MEF2C proteins downregulate each other’s expression while imparing cardiomyogenesis. Lastly, we show that Gli2 and MEF2C form a protein complex, which synergistically activates cardiac muscle related promoters. In Chapter 4, we illustrate that Gli2 associates with MyoD gene elements while enhancing skeletal myogenesis in P19 cells and activates the MyoD promoter in vitro. Furthermore, inhibition of Hh signalling in muscle satellite cells and in proliferating myoblasts leads to reduction in MyoD and MEF2C expression. Finally, we demonstrate that endogenous Hh signalling is important for MyoD transcriptional activity and that Gli2, MEF2C and MyoD form a protein complex capable of inducing skeletal muscle-specific gene expression. Thus, Gli2, MEF2C and MyoD participate in a regulatory loop and form a protein complex capable of inducing skeletal muscle-specific gene expression. Our results provide a link between the regulation of tissue-restricted factors like Mash1, MEF2C and MyoD, and a general signal-regulated Gli2 transcription factor. We therefore provide novel mechanistic insights into the neurogenic, cardiogenic and myogenic properties of Gli2 in vitro, and offer novel plausible explanations for its in vivo functions. These results may also be important for the development of stem cell therapy strategies.
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9

Silva, Ricardo Eustáquio da. "Avaliação estrutural e quantitativa dos efeitos do envelhecimento sobre o gânglio trigeminal de ratos Wistar." Universidade de São Paulo, 2010. http://www.teses.usp.br/teses/disponiveis/10/10132/tde-04022011-111947/.

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O envelhecimento é uma falha progressiva nos processos fisiológicos celulares, produzindo alterações morfológicas nas células e nos tecidos. No sistema nervoso, produz uma redução no número de neurônios, nas fibras nervosas, principalmente nas arborizações dendríticas e nas espinhas sinápticas, e nas células da glia que, de acordo com sua localização e tipo celular, podem diminuir, permanecer constantes ou mesmo aumentar numericamente. Na presente pesquisa, avaliou-se os efeitos do envelhecimento sobre o gânglio trigeminal (GT) de ratos Wistar em animais jovens (2 meses de vida), adultos (12 meses de vida) e idosos (24 meses de vida). Os GT foram submetidos às técnicas histológicas da hematoxilina e eosina e Picro-sírius, onde avaliou-se, respectivamente, a densidade das células satélites glias (CGS) e o componente colágeno ganglionar. Através da técnica histoquímica da NADH-d, avaliou-se a área do perfil do GT, a área do perfil dos corpos celulares dos neurônios ganglionares e a densidade neuronal. Uma avaliação qualitativa foi também realizada relativamente à imunorreatividade dos neurônios ganglionares à substância P (SP) e ao peptídeo intestinal vasoativo (VIP). A densidade das CGS foi maior nos animais jovens do que nos animais adultos e idosos. Verificou-se, qualitativamente, que à medida que o animal envelhece há uma diminuição das fibras colágenas do tipo III, passando a predominar, nos animais idosos, as fibras do tipo I. A área do perfil celular dos corpos neuronais foi maior nos animais adultos sendo que em todos os grupos predominaram neurônios de tamanho médio, com a área do perfil celular entre 490 e 1100 μm2. A densidade neuronal apresentou-se maior nos animais jovens, e sem variações estatísticas entre os animais adultos e idosos. Em todos os grupos estudados, os neurônios pequenos foram os que apresentaram maior imunorreatividade à SP e ao VIP.
Aging is a progressive failure in cellular physiological processes. It determines morphological changes in cells of different tissues. In the nervous system, a reduction in neuron number and in neuron fibers, mainly in dendritic tree and synaptic, are described. With aging the glial cells may increase or decrease in number or also remain constant. In the present work the effects of aging were evaluated on the trigeminal ganglion (TG) comparing young (2 months age), adult (12 months age) and old rats (24 months age). Histological sections of TG were stained with hematoxilin-eosin technique to determine the density of satellite glial cells and Picro-sirius under polarized light to evaluate the Types I and III of collagen fibers. The NADH-diaphorase technique allowed determining the perycarion area. The immunoreactivity of ganglionar neurons to Substance P (SP) and vasoactive intestinal peptide (VIP) were also qualitatively evaluated. The glial cells density was higher in young and adult animals than in old animals. The type I collagen fibers predominates in ganglia of old animals whereas in the young animals is characteristic the presence of the type III collagen fibers. Although the perycarion area was higher in adult animals the medium-sized neurons predominated in all groups. Their areas ranged from 490 to 1100 μm2. It was also observed that the neuron density was higher in young animals. In the adult and old animals the neuron density was similar. In all groups the immunoreactivity both to SP an VIP was detected mainly in neurons of small perycarion.
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10

Bagnato, Beatrice. "Sulla precisazione matematica delle scoperte astronomiche nel corso dei secoli: gli esempi dei satelliti di Giove e dei pianeti Urano e Nettuno." Master's thesis, Alma Mater Studiorum - Università di Bologna, 2015. http://amslaurea.unibo.it/8409/.

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Dai Sumeri a Galileo lo studio dei cinque pianeti conosciuti era stato effettuato ad occhio nudo e aveva consentito di comprendere le modalità del loro moto. Con Galileo gli strumenti tecnologici sono posti a servizio della scienza, per migliorare le prestazioni dei sensi umani. La ricerca subisce così una netta accelerazione che porta, nell'arco di soli tre secoli, alla scoperta dei satelliti di Giove e dei pianeti Urano e Nettuno. Quest'ultima è considerata il trionfo della matematica perché effettuata esclusivamente con lunghi e complessi calcoli.
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Books on the topic "Satellite glia"

1

Salstein, David A. Diagnostic studies with GLA fields. [Cambridge, MA]: Atmospheric and Environmental Research, Inc., 1997.

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2

Wen, Joseph Yao Min. Neuronal-glial signaling involved in explant induced satellite cell proliferation in the adult trigeminal ganglia. Ottawa: National Library of Canada, 1993.

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3

1937-, Levi Giulio, and International Society for Neurochemistry. Meeting, eds. Differentiation and functions of glial cells: Proceedings of a satellite meeting of the International Society for Neurochemistry held in Rome, Italy, April 19-21, 1989. New York: Wiley-Liss, 1990.

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Book chapters on the topic "Satellite glia"

1

Hanani, Menachem. "Satellite Glial Cells and Chronic Pain." In Encyclopedia of Pain, 3436–43. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-28753-4_3874.

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Hanani, Menachem, and David C. Spray. "Satellite Glial Cells as a Target for Chronic Pain Therapy." In Pathological Potential of Neuroglia, 473–92. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-0974-2_20.

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Valentini, Ada. "Competenze lessicali in italiano L2: gli eventi di moto in testi narrativi." In Competenza lessicale e apprendimento dell’Italiano L2, 83–96. Florence: Firenze University Press, 2021. http://dx.doi.org/10.36253/978-88-5518-403-8.07.

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This paper deals with a case of lexical cross-linguistic influence from a source language, known as conceptual transfer. In particular, narratives in Italian L2 produced by different L1 learners are examined. The theoretical framework adopted is lexical typology as developed by L. Talmy, according to which languages fall into two types as to how they encode motion events: The so-called verb-framed languages would tend to lexicalize the semantic component of the Path (eg the movement from inside to outside or vice versa) in the verb (eg It. uscire "to go out"); the satellite-framed languages preferentially encode the Path component outside the verb (eg in Eng. in the satellite out, as in "The boy ran out"). The preferences adopted in each L1 are supposed to influence production in L2. The presentation of the data in Italian L2 allows us to observe the subtle role that the L1s play in this lexical domain and to recommend giving attention to typological differences between L2 and L1 in the classroom.
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Chattopadhyay, Munmun. "The Emerging Role of Satellite and Schwann Cells of the Peripheral Neuroglial System in Nerve Repair." In The Biology of Glial Cells: Recent Advances, 593–607. Singapore: Springer Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-8313-8_21.

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"Satellite Glia Cells, SCG." In Encyclopedia of Pain, 3436. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-28753-4_102048.

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"Satellite Glial Cells." In Encyclopedia of Pain, 3436. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-28753-4_102049.

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Conference papers on the topic "Satellite glia"

1

Nakajima, Teruyuki, Y. Awaya, Motoaki Kishino, T. Ohishi, G. Saitou, Akihiro Uchiyama, Takashi Nakajima, Masakatsu Nakajima, and T. Uesugi. "Current status of the ADEOS-II/GLI Mission." In Satellite Remote Sensing III, edited by Hiroyuki Fujisada, Guido Calamai, and Martin N. Sweeting. SPIE, 1997. http://dx.doi.org/10.1117/12.265431.

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Mandge, Darshan, Archit Bhatnagar, and Rohit Manchanda. "Computational model for intercellular communication between DRG neurons via satellite glial cells using ATP." In 2017 8th International IEEE/EMBS Conference on Neural Engineering (NER). IEEE, 2017. http://dx.doi.org/10.1109/ner.2017.8008434.

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Murakami, Hiroshi, Mitsuhiro Toratani, and Hajime Fukushima. "Satellite ocean color observation with 250 m spatial resolution using ADEOS-II GLI." In Asia-Pacific Remote Sensing Symposium, edited by Robert J. Frouin, Vijay K. Agarwal, Hiroshi Kawamura, Shailesh Nayak, and Delu Pan. SPIE, 2006. http://dx.doi.org/10.1117/12.693469.

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Huang, B., I. Zdora, N. de Buhr, W. Baumgärtner, and E. Leitzen. "Characterization of murine satellite glial cells of the dorsal root ganglia – a unique cell population with potential regenerative capacities." In 64. Jahrestagung der Fachgruppe Pathologie der Deutschen Veterinärmedizinischen Gesellschaft. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1729412.

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Kuji, Makoto. "Retrieval of cloud top and bottom heights using advanced Earth observing satellite / global imager (ADEOS-II / GLI) data." In RADIATION PROCESSES IN THE ATMOSPHERE AND OCEAN (IRS2012): Proceedings of the International Radiation Symposium (IRC/IAMAS). AIP, 2013. http://dx.doi.org/10.1063/1.4804775.

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Mandge, Darshan, Pooja Rajesh Shukla, Archit Bhatnagar, and Rohit Manchanda. "Computational Model for Cross-Depolarization in DRG Neurons via Satellite Glial Cells using [K]o: Role of Kir4.1 Channels and Extracellular Leakage." In 2019 41st Annual International Conference of the IEEE Engineering in Medicine & Biology Society (EMBC). IEEE, 2019. http://dx.doi.org/10.1109/embc.2019.8857153.

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