Academic literature on the topic 'Satellite glial cells'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Satellite glial cells.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Journal articles on the topic "Satellite glial cells"
1
Batista, Daniel R., and Antonio C. Cassola. "Metabotropic Purinergic Receptors in Satellite Glial Cells." Biophysical Journal 98, no. 3 (January 2010): 495a—496a. http://dx.doi.org/10.1016/j.bpj.2009.12.2699.
Full text
2
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.
Full textAbstract:
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.
3
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.
Full textAbstract:
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.
4
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.
Full textAbstract:
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.
5
Ohara, Peter T., Jean-Philippe Vit, Aditi Bhargava, Marcela Romero, Christopher Sundberg, Andrew C. Charles, and Luc Jasmin. "Gliopathic Pain: When Satellite Glial Cells Go Bad." Neuroscientist 15, no. 5 (October 2009): 450–63. http://dx.doi.org/10.1177/1073858409336094.
Full text
6
Liu, Xiaojuan, Travis Goettemoeller, and Temugin Berta. "How Do Satellite Glial Cells Control Chronic Pain?" Journal of Anesthesia and Perioperative Medicine 5, no. 6 (November 26, 2018): 306–15. http://dx.doi.org/10.24015/japm.2018.0114.
Full text
7
Mackay Smith, David John. "Satellite glial cells of the peripheral nervous system." Journal of Dermatology & Cosmetology 5, no. 2 (2021): 38–41. http://dx.doi.org/10.15406/jdc.2021.05.00181.
Full text
8
Hanani, Menachem, and Alexei Verkhratsky. "Satellite Glial Cells and Astrocytes, a Comparative Review." Neurochemical Research 46, no. 10 (February 1, 2021): 2525–37. http://dx.doi.org/10.1007/s11064-021-03255-8.
Full text
9
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.
Full textAbstract:
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.
10
Deshmukh, Vishwajit Ravindra, Pranav Prasoon, and Subrata Basu Ray. "Expression of gap junctions bearing connexin-43 subunits and glial fibrillary acidic protein in the rat dorsal root ganglia following hind paw incision." International Journal of Research in Medical Sciences 5, no. 1 (December 19, 2016): 306. http://dx.doi.org/10.18203/2320-6012.ijrms20164568.
Full textAbstract:
Background: Dorsal root ganglion (DRG) neurons mediate the transmission of sensation from the periphery. DRG neurons are pseudounipolar in nature and enveloped by the satellite glial cells (SC). Satellite glial cells have been reported to influence neuronal excitability via gap junctions. Postoperative pain causes induction of various neurotransmitters such as connexin-43 and glial fibrillary acidic protein (GFAP), in the satellite cells surrounding neuronal cell bodiesObjective: To study the expression of connexin-43 and Glial fibrillary acidic protein after hind paw incision.Methods: Male adult Sprague-Dawley rats (n=12) were used. Rats were randomly divided into two groups. Group I (n=6) and Group II (n=6) for immunohistochemical study with glial fibrillary acidic protein (GFAP) and connexin-43 (Cx-43) respectively. In this study, rats were subjected to noxious stimuli on the right hind paw under general anesthesia. Dorsal root ganglia of both sides (L4 spinal nerves) were isolated after transcardiac fixation with 4% paraformaldehyde. The ganglia from the non-incised side were taken as the control group.Results: Unipolar neurons in the DRG were surrounded by satellite cells. The satellite cells were positive for GFAP, which showed increased expression on the surgical side after noxious stimuli. Cx-43 immunostaining also showed an increased expression in the periphery of neuronal cell bodies of surgical side representing the location of gap junctions and hyperexcitability of neurons.Conclusions: Small to medium sized neurons carry pain sensation from the periphery to the central nervous system. Increased gap junctions were noted in small neurons and satellite cells after surgery. Gap junctions might contribute to increased excitability of small neurons in postoperative pain.
Dissertations / Theses on the topic "Satellite glial cells"
1
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.
Full textAbstract:
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 dérèglementsProprioceptive 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
2
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.
Full textAbstract:
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.Ph. D.
3
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/.
Full textAbstract:
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.
4
Walker, Ryan G. "Plasticity of adult sympathetic neurons following injury." Miami University / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=miami1250091703.
Full text
5
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.
Full text
6
[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.
Full text
7
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/.
Full textAbstract:
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.
8
Desiderá, Amanda de Carvalho. "Análise da expressão de metaloproteinases da matriz em células satélites gliais do gânglio trigeminal de ratos portadores de inflamação da articulação temporomandibular persistente submetidos a laserterapia de baixa intensidade." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/58/58131/tde-29042016-152106/.
Full textAbstract:
A dor é uma das principais sintomatologias capazes de levar indivíduos a buscar tratamento médico-odontológico. Na odontologia estima-se que cerca de 40 a 75% da população seja portadora de dor de origem orofacial e tenha pelo menos um sinal ou sintoma de disfunção temporomandibular (DTM). A DTM corresponde a um quadro patológico de caráter multifatorial que acomete a articulação temporomandibular (ATM) e os músculos mastigatórios, ocasionando dores na região orofacial bom como alterações na realização de movimentos bucais. O principal sinal desta enfermidade é a inflamação articular, a qual gera dor nas estruturas relacionadas. A inflamação, por sua vez, leva a liberação de mediadores tais como, substância P, peptídeo relacionada ao gene da calcitonina (CGRP), além de fator de necrose tumoral a (TNF-α) e interleucina 1β (IL-1β). Estes mediadores sensibilizam as terminações nervosas livres e a informação nociceptiva caminha para a primeira estação sináptica, o gânglio trigeminal. A inflamação quando persistente promove a expressão de metaloproteinases da matriz (MMP), cuja ação modifica a matriz extracelular podendo, então, modular vias neuronais de percepção. Células satélites gliais (CSGs) são células envolvidas no suporte microambiente neuronal e, possivelmente, células que atuariam na modulação de vias de percepção nociceptiva. Conhecendo mais profundamente os mecanismos de modulação da dor, são buscadas terapêuticas não invasivas eficientes para atenuar a sintomatologia dolorosa advinda da DTM. A laserterapia de baixa intensidade (LLLT) mostra-se como um tratamento eficiente, porém seu efeito dose-dependente gera resultados ambíguos. Nesse contexto o presente trabalho teve como objetivos verificar os biomarcadores inflamatórios presentes no fluído sinovial em ratos portadores de inflamação persistente da ATM, tratados ou não com LLLT. Foram utilizados ratos Wistar (200-240g, n=440 - CEUA 2013.1.1111.58.7), os quais receberam administração de CFA (Adjuvante Completo de Freund) ou salina 0,9% (SAL) intraarticular e que foram submetidos (LLLT) ou não a aplicação de laser na região temporomandibular no primeiro dia, 1 hora após a indução da inflamação,, e nos dias 3, 5, 7 e 10 após indução da inflamação. Resultados obtidos neste trabalho mostram que a LLLT reduz as células polimorfonucleares presentes na cápsula articular das ATM, e, também, de espécies reativas de oxigênio (redução da atividade de mieloperoxidase - MPO). Ainda, verificou-se a redução da expressão de MMP-2 e MMP-9 no líquido sinovial de ratos com inflamação persistente induzida pela administração de CFA intraarticular. Citocinas pró-inflamatórias (por exemplo: IL-1α, IL-1β, IL-6, IL-12p70, IFN-ϒ, GM-CSF e TNF-α.) analisadas do líquido sinovial mostraram aumento significativo em sua expressão quando da presença de inflamação, a LLLT reduziu a expressão de dessas citocinas. No entanto, a fotoestimulação em alguns momentos na ausência de inflamação estimulou a expressão das citocinas IL-2, IL-5, IL-12p70, GM-CSF. Além disso, a terapia fotodinâmica aumentou expressão das citocinas anti-inflamatórias IL-4, IL-10 e IL-13 na presença de inflamação. A análise da imunofluorescência para marcação de MMP-2 e MMP-9 co-localizadas para células suporte mostrou que a expressão mais significativa ocorreu em neurônios, e resultados apontam que a LLLT na dose de 60J/cm² não reduziu a expressão dessas gelatinases no gânglio trigeminal.Pain is one of the main symptomatology able to lead individuals to seek medical and dental treatment. In dentistry it is estimated that about 40-75% of the population is a carrier of orofacial pain source and has at least one sign or symptom of temporomandibular disorders (TMD). The TMD corresponds to a pathological condition of multifactorial affecting the temporomandibular joint (TMJ) and masticatory muscles, causing pain in the orofacial region well as changes in the performance of mouth movements. The main sign of this disease is joint inflammation, which generates pain related structures. The inflammation leads to release of mediators such as substance P, calcitonin-related peptide gene (CGRP), and tumor necrosis factor (TNF-α) and interleukin-1β (IL-1β). These mediators sensitize terminal fiber nerves and nociceptive information goes to the first synaptic station, the trigeminal ganglion. The persistent inflammation when promotes the expression of metalloproteinase (MMP), whose operation modifies the extracellular matrix may therefore modulate neuronal pathways perception. Satellite glial cells (CSGs) are involved in neuronal microenvironment support, and possibly cells that act in the modulation of nociceptive pathways perception. Knowing deeper into the mechanisms of pain modulation, are sought noninvasive therapeutic effective to alleviate the painful symptoms arising from the DTM. The low level laser therapy (LLLT) is shown as an effective treatment, but their dose-dependent effect produces ambiguous results. In this context, this study aimed to verify the inflammatory biomarkers present in the synovial fluid in rats with persistent inflammation of the ATM, or not treated with LLLT. Wistar rats (200-240g, n = 440 - CEUA 2013.1.1111.58.7), which received CFA administration (Complete Freund\'s Adjuvant) or 0.9% saline (SAL) intraarticular and underwent (LLLT) or not applying laser temporomandibular region on the first day, 1 hour after inflammation induction, and after days 3, 5, 7 and 10. Our results showed that LLLT reduces polymorphonuclear cells present in the joint capsule of the TMJ, and also of reactive oxygen species (reduction in myeloperoxidase activity - MPO). Still, there was a reduction in expression of MMP-2 and MMP-9 in the synovial fluid of rats with persistent inflammation induced by the intraarticular administration of CFA. Pro-inflammatory cytokines (IL-1α, IL-1β, IL-6, IL-12p70, IFN-ϒ, GM-CSF and TNF-α) analyzed synovial fluid showed a significant increase in its expression induced by TMJ 20 inflammation, and LLLT reduced expression of these cytokines. However, the photostimulation in the absence of inflammation stimulated the expression of cytokines IL-2, IL-5, IL-12p70, GM-CSF. Furthermore, photodynamic therapy increased expression of anti-inflammatory cytokines IL-4, IL-10 and IL-13 in rats with TMJ inflammation. Analysis of immunofluorescence for MMP-2 and MMP-9 co-located to support cells showed that the most significant expression was located in neurons, and results indicate that LLLT at a dose of 60 J/cm² did not reduce the expression of these gelatinases in the ganglion trigeminal.
9
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.
Full textAbstract:
CAPES - Coordenação de Aperfeiçoamento de Pessoal de Nível SuperiorNos 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.
Dissertação (Mestrado)
10
"The impact of reduced neuronal p75NTR expression on sensory neuron phenotype and associated glia." Thesis, 2011. http://hdl.handle.net/10388/ETD-2011-10-185.
Full textAbstract:
The common neurotrophin receptor, p75NTR, has been implicated in diverse responses of sensory neurons including a role in nociception following nerve injury, suggesting that it may serve a similar role in intact sensory neurons and their satellite glial cells (SGCs). To examine the impact of suppressing neuronal p75NTR expression on known molecular modulators/regulators of the nociceptive state namely, the sodium channels NaV1.8 and NaV1.9, the nerve growth factor receptor TrkA, the potassium channel Kir4.1, glial fibrillary acidic protein (GFAP), SGC p75NTR, connexin 43, we intrathecally infused p75NTR anti-sense oligonucleotides (AS OGN), previously shown by Obata et al. (2006) to effectively suppress p75NTR expression in intact neurons. Male, Wistar rats were divided into three groups, receiving either no treatment (non-infused), seven day intrathecal infusion of p75NTR AS OGN or sense control (SC OGN) via an osmotic pump. Serial L4 and L5 DRG sections were processed for immunohistochemistry to detect alterations in NaV1.8, NaV1.9, TrkA, Kir4.1, p75NTR, GFAP and connexin-43 protein expression. Sciatic nerve sections were also processed for immunohistochemistry to detect NaV1.8, NaV1.9, TrkA and GFAP protein expression.
Infusion of p75NTR AS OGNs resulted in a significant decrease in neuronal p75NTR expression, however no significant change was observed in neuronal NaV1.8, NaV1.9 or TrkA expression relative to SC OGN treated or non-infused controls. On the contrary, SGC expression of phenotypic markers normally associated with the reactive state that is induced in these cells in response to peripheral nerve axotomy was dramatically altered. More specifically, in response to p75NTR AS OGN infusion, there was a significant increase in SGC protein expression of the cytoskeletal protein GFAP and p75NTR, along with a significant decrease in expression of the inward rectifying potassium channel Kir4.1. Preliminary data also revealed this induced reactive state in SGCs to be associated with an increase in the number of SGCs surrounding individual neurons as well as increased SGC expression of the gap junction protein, connexin 43.
In conclusion, reductions in neuronal p75NTR expression and potentially reduced neurotrophin signaling lead to alterations in neuron/glial or axon/glial communication that results in induction of a reactive phenotype in the associated SGCs. With our ever increasing understanding of the role of SGCs modulating pain states, elucidation of the pathways leading to adoption of pathological phenotypes can help in the identification of novel therapeutic targets.
Books on the topic "Satellite glial cells"
1
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.
Find full text
2
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.
Find full textBook chapters on the topic "Satellite glial cells"
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.
Full text
2
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.
Full text
3
"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.
Full text
4
"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.
Full textConference papers on the topic "Satellite glial cells"
1
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.
Full text
2
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.
Full text
3
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.
Full text