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Journal articles on the topic 'Satellite glial cells'

Author: Grafiati

Published: 4 June 2021

Last updated: 7 February 2022

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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.

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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.

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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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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.

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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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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.

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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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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.

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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.

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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.

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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.

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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.

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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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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.

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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.

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11

Cairns, Brian E., Lars Arendt-Nielsen, and Paola Sacerdote. "Perspectives in Pain Research 2014: Neuroinflammation and glial cell activation: The cause of transition from acute to chronic pain?" Scandinavian Journal of Pain 6, no. 1 (January 1, 2015): 3–6. http://dx.doi.org/10.1016/j.sjpain.2014.10.002.

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AbstractBackgroundIt is unknown why an acute pain condition under various circumstances can transition into a chronic pain condition.There has been a shift towards neuroinflammation and hence glial cell activations specifically in the dorsal root ganglion and spinal cord as a mechanism possibly driving the transition to chronic pain. This has led to a focus on non-neuronal cells in the peripheral and central nervous system. Besides infiltrating macrophages, Schwann cells and satellite glial cells release cytokines and therefore important mechanisms in the maintenance of pain. Activated Schwann cells, satellite glial cells, microglia, and astrocytes may contribute to pain sensitivity by releasing cytokines leading to altered neuronal function in the direction of sensitisation.Aims of this perspective paper1) Highlight the complex but important recent achievement in the area of neuroinflammation and pain at spinal cord level and in the dorsal root ganglion.2) Encourage further research which hopefully may provide better understanding of new key elements driving the transition from acute to chronic pain.Recent results in the area of neuroinflammation and painFollowing a sciatic nerve injury, local macrophages, and Schwann cells trigger an immune response immediately followed by recruitment of blood-derived immune cells. Schwann cells, active resident, and infiltrating macrophages release proinflammatory cytokines. Proinflammatory cytokines contribute to axonal damage and also stimulate spontaneous nociceptor activity. This results in activation of satellite glial cells leading to an immune response in the dorsal root ganglia driven by macrophages, lymphocytes and satellite cells. The anterograde signalling progresses centrally to activate spinal microglia with possible up regulation of glial-derived proinflammatory/pronociceptive mediators.An important aspect is extrasegmental spreading sensitisation where bilateral elevations in TNF-α, IL-6, and IL-10 are found in dorsal root ganglion in neuropathic models. Similarly in inflammatory pain models, bilateral up regulation occurs for TNF-α, IL-1 β, and p38 MAPK. Bilateral alterations in cytokine levels in the DRG and spinal cord may underlie the spread of pain to the uninjured side.An important aspect is how the opioids may interact with immune cells as opioid receptors are expressed by peripheral immune cells and thus can induce immune signaling changes. Furthermore, opioids may stimulate microglia cells to produce proinflammatory cytokines such as IL-1.ConclusionsThe present perspective paper indicates that neuroinflammation and the associated release of pro-inflammatory cytokines in dorsal root ganglion and at the spinal cord contribute to the transition from acute to chronic pain. Neuroinflammatory changes have not only been identified in the spinal cord and brainstem, but more recently, in the sensory ganglia and in the nerves as well. The glial cell activation may be responsible for contralateral spreading and possible widespread sensitisation.ImplicationsCommunication between glia and neurons is proposed to be a critical component of neuroinflammatory changes that may lead to chronic pain. Sensory ganglia neurons are surrounded by satellite glial cells but how communication between the cells contributes to altered pain sensitivity is still unknown. Better understanding may lead to new possibilities for (1) preventing development of chronic pain and (2) better pain management.

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12

Rudel, C., and H. Rohrer. "Analysis of glia cell differentiation in the developing chick peripheral nervous system: sensory and sympathetic satellite cells express different cell surface antigens." Development 115, no. 2 (June 1, 1992): 519–26. http://dx.doi.org/10.1242/dev.115.2.519.

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To identify and analyse precursor cells of neuronal and glial cell lineages during the early development of the chick peripheral nervous system, monoclonal antibodies were raised against a population of undifferentiated cells of E6 dorsal root ganglia (DRG). Non-neuronal cells of E6 DRG express surface antigens that are recognized by four monoclonal antibodies, G1, G2, GLI 1 and GLI 2. The proportion of non-neuronal cells in DRG that express the GLI 1 antigen is very high during ganglion formation (80% at E4) and decreases during later development (15% at E14). GLI 2 antigen is expressed only on a minority of the cells at E6 and increases with development. The G1 and G2 antigens are expressed on about 60–80% of the cells between E6 and E14. All cells that express the established glia marker O4 are also positive for the new antigens. In addition, it was demonstrated that GLI 1-positive cells from early DRG, which are devoid of O4 antigen, could be induced in vitro to express the O4 antigen. Thus, the antigen-positive cells are considered as glial cells or glial precursor cells. Surprisingly, the antigen expression by satellite cells of peripheral ganglia is dependent on the type of ganglion: antigens G1, G2 and GLI 1 were not detectable on glial cells of lumbosacral sympathetic ganglia and GLI 2 was expressed only by a small subpopulation. These results demonstrate an early immunological difference between satellite cells of sensory DRG and sympathetic ganglia.(ABSTRACT TRUNCATED AT 250 WORDS)

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13

George, Dale, Paige Ahrens, and Stephen Lambert. "Satellite glial cells represent a population of developmentally arrested Schwann cells." Glia 66, no. 7 (March 9, 2018): 1496–506. http://dx.doi.org/10.1002/glia.23320.

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14

Rusu, Mugurel, Valentina Mănoiu, Nicolae Mirancea, and Gheorghe Nini. "Quiescent satellite glial cells of the adult trigeminal ganglion." Open Medicine 9, no. 3 (June 1, 2014): 500–504. http://dx.doi.org/10.2478/s11536-013-0285-z.

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AbstractSensory ganglia comprise functional units built up by neurons and satellite glial cells (SGCs). In animal species there was proven the presence of neuronoglial progenitor cells in adult samples. Such neural crest-derived progenitors were found in immunohistochemistry (IHC). These findings were not previously documented in transmission electron microscopy (TEM). It was thus aimed to assess in TEM if cells of the human adult trigeminal ganglion indeed have ultrastructural features to qualify for a progenitor, or quiescent phenotype. Trigeminal ganglia were obtained from fifteen adult donor cadavers. In TEM, cells with heterochromatic nuclei, a pancytoplasmic content of free ribosomes, few perinuclear mitochondria, poor developed endoplasmic reticulum, lack of Golgi complexes and membrane trafficking specializations, were found included in the neuronal envelopes built-up by SGCs. The ultrastructural pattern was strongly suggestive for these cells being quiescent progenitors. However, further experiments should correlate the morphologic and immune phenotypes of such cells.

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15

Enes, Joana, Marián Haburčák, Surbhi Sona, Nega Gerard, Alexander C. Mitchell, Wenqi Fu, and Susan J. Birren. "Satellite glial cells modulate cholinergic transmission between sympathetic neurons." PLOS ONE 15, no. 2 (February 4, 2020): e0218643. http://dx.doi.org/10.1371/journal.pone.0218643.

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16

Fan, Wenguo, Xiao Zhu, Yifan He, Mengzhu Zhu, Zhi Wu, Fang Huang, and Hongwen He. "The role of satellite glial cells in orofacial pain." Journal of Neuroscience Research 97, no. 4 (November 19, 2018): 393–401. http://dx.doi.org/10.1002/jnr.24341.

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17

Koike, Taro, Taketoshi Wakabayashi, Tetsuji Mori, Yukie Hirahara, and Hisao Yamada. "Sox2 promotes survival of satellite glial cells in vitro." Biochemical and Biophysical Research Communications 464, no. 1 (August 2015): 269–74. http://dx.doi.org/10.1016/j.bbrc.2015.06.141.

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18

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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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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Belzer, Vitali, Nathanael Shraer, and Menachem Hanani. "Phenotypic changes in satellite glial cells in cultured trigeminal ganglia." Neuron Glia Biology 6, no. 4 (November 2010): 237–43. http://dx.doi.org/10.1017/s1740925x1100007x.

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Satellite glial cells (SGCs) are specialized cells that form a tight sheath around neurons in sensory ganglia. In recent years, there is increasing interest in SGCs and they have been studied in both intact ganglia and in tissue culture. Here we studied phenotypic changes in SGCs in cultured trigeminal ganglia from adult mice, containing both neurons and SGCs, using phase optics, immunohistochemistry and time-lapse photography. Cultures were followed for up to 14 days. After isolation virtually every sensory neuron is ensheathed by SGCs, as in the intact ganglia. After one day in culture, SGCs begin to migrate away from their parent neurons, but in most cases the neurons still retain an intact glial cover. At later times in culture, there is a massive migration of SGCs away from the neurons and they undergo clear morphological changes, and at 7 days they become spindle-shaped. At one day in culture SGCs express the glial marker glutamine synthetase, and also the purinergic receptor P2X7. From day 2 in culture the glutamine synthetase expression is greatly diminished, whereas that of P2X7 is largely unchanged. We conclude that SGCs retain most of their characteristics for about 24 h after culturing, but undergo major phenotypic changes at later times.

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21

Wakamatsu, Y., T. M. Maynard, and J. A. Weston. "Fate determination of neural crest cells by NOTCH-mediated lateral inhibition and asymmetrical cell division during gangliogenesis." Development 127, no. 13 (July 1, 2000): 2811–21. http://dx.doi.org/10.1242/dev.127.13.2811.

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Avian trunk neural crest cells give rise to a variety of cell types including neurons and satellite glial cells in peripheral ganglia. It is widely assumed that crest cell fate is regulated by environmental cues from surrounding embryonic tissues. However, it is not clear how such environmental cues could cause both neurons and glial cells to differentiate from crest-derived precursors in the same ganglionic locations. To elucidate this issue, we have examined expression and function of components of the NOTCH signaling pathway in early crest cells and in avian dorsal root ganglia. We have found that Delta1, which encodes a NOTCH ligand, is expressed in early crest-derived neuronal cells, and that NOTCH1 activation in crest cells prevents neuronal differentiation and permits glial differentiation in vitro. We also found that NUMB, a NOTCH antagonist, is asymmetrically segregated when some undifferentiated crest-derived cells in nascent dorsal root ganglia undergo mitosis. We conclude that neuron-glia fate determination of crest cells is regulated, at least in part, by NOTCH-mediated lateral inhibition among crest-derived cells, and by asymmetric cell division.

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SVENNINGSEN, ÅSA FEX, DAVID R. COLMAN, and LILIANA PEDRAZA. "Satellite cells of dorsal root ganglia are multipotential glial precursors." Neuron Glia Biology 1, no. 1 (February 2004): 85–93. http://dx.doi.org/10.1017/s1740925x04000110.

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The evolutionary origin of myelinating cells in the vertebrate nervous system remains a mystery. A clear delineation of the developmental potentialities of neuronal support cells in the CNS and PNS might aid in formulating a hypothesis about the origins of myelinating cells. Although a glial-precursor cell in the CNS can differentiate into oligodendrocytes (OLs), Schwann cells (SCs) and astrocytes, a homologous multipotential cell has not yet been found in the PNS. Here, we identify a cell type of embryonic dorsal root ganglia (DRG) of the PNS – the satellite cell – that develops into OLs, SCs and astrocytes. Interestingly, satellite-cell-derived OL precursors were found in cultures prepared from embryonic day 17 (E17) to postnatal day 8 (P8) ganglia, but not from adult DRGs, revealing a narrow developmental window for multipotentiality. We suggest that compromising the organization of the ganglia triggers a differentiation pathway in a subpopulation of satellite cells, inducing them to become myelinating cells with either a CNS or PNS phenotype. Our data provide an additional, novel piece in the myelinating-cell-precursor puzzle, and lead to the concept that cells in the CNS and PNS that function to ensheath neuronal cell bodies and axons can differentiate into OLs, SCs and astrocytes. In sum, it appears that glial fate might be determined over and above the CNS/PNS dichotomy. Last, we suggest that primordial ensheathing cells form the original cell population in which the myelination program first evolved.

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Jager, Sara Buskbjerg, Lone Tjener Pallesen, and Christian Bjerggaard Vaegter. "Isolation of satellite glial cells for high-quality RNA purification." Journal of Neuroscience Methods 297 (March 2018): 1–8. http://dx.doi.org/10.1016/j.jneumeth.2018.01.001.

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Jasmin, Luc, Jean-Philippe Vit, Aditi Bhargava, and Peter T. Ohara. "Can satellite glial cells be therapeutic targets for pain control?" Neuron Glia Biology 6, no. 1 (February 2010): 63–71. http://dx.doi.org/10.1017/s1740925x10000098.

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Satellite glial cells (SGCs) undergo phenotypic changes and divide the following injury into a peripheral nerve. Nerve injury, also elicits an immune response and several antigen-presenting cells are found in close proximity to SGCs. Silencing SCG-specific molecules involved in intercellular transport (Connexin 43) or glutamate recycling (glutamine synthase) can dramatically alter nociceptive responses of normal and nerve-injured rats. Transducing SGCs with glutamic acid decarboxylase can produce analgesia in models of trigeminal pain. Taken together these data suggest that SGCs may play a role in the genesis or maintenance of pain and open a range of new possibilities for curing neuropathic pain.

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25

Hanani, Menachem. "Satellite glial cells: more than just ‘rings around the neuron’." Neuron Glia Biology 6, no. 1 (February 2010): 1–2. http://dx.doi.org/10.1017/s1740925x10000104.

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Souza, G. R., J. Talbot, C. M. Lotufo, F. Q. Cunha, T. M. Cunha, and S. H. Ferreira. "Fractalkine mediates inflammatory pain through activation of satellite glial cells." Proceedings of the National Academy of Sciences 110, no. 27 (June 17, 2013): 11193–98. http://dx.doi.org/10.1073/pnas.1307445110.

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27

Hanani, Menachem. "Satellite glial cells in sensory ganglia: from form to function." Brain Research Reviews 48, no. 3 (June 2005): 457–76. http://dx.doi.org/10.1016/j.brainresrev.2004.09.001.

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28

Costa, Filipa Alexandra Leite, and Fani Lourença Moreira Neto. "Satellite glial cells in sensory ganglia: its role in pain." Brazilian Journal of Anesthesiology (English Edition) 65, no. 1 (January 2015): 73–81. http://dx.doi.org/10.1016/j.bjane.2013.07.013.

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29

Kolosov, Mikhail, and Anatoly Uzdensky. "Crayfish mechanoreceptor neuron prevents photoinduced apoptosis of satellite glial cells." Brain Research Bulletin 69, no. 5 (May 2006): 495–500. http://dx.doi.org/10.1016/j.brainresbull.2006.02.018.

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30

Gorelikov, Petr L. "Peculiarities of energy production in glial cells of sympathetic ganglia." I.P. Pavlov Russian Medical Biological Herald 27, no. 1 (April 2, 2019): 5–9. http://dx.doi.org/10.23888/pavlovj20192715-9.

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Aim. To determine the energy profile of satellite gliocytes in the cranial cervical sympathe-tic ganglia (CCSG) in normal functioning of nicotinic cholinergic synapses (nChS) and in their pharmaceutical deprivation. Materials and Methods. Deprivation of CCSG in rabbits was implemented by using cholinolytic dimecolinum. The activity of H- and M-isoforms of lactate de-hydrogenase (LDH) was determined in gliocytes offrozen sections by integral cytophotomentry using Brumberg and Pevzner method. Results. In satellite gliocytes a considerably higher activity of M-isoforms of LDH in comparison with that of H-isoforms was found which evidences predomination of anaerobic mechanisms of energy metabolism over aerobic ones in the studied cells. The relationship between the levels of activity of (Н/М) isoforms of LDH in gliocytes with experimental deprivation of nChR exhibited a complete inversion as compared to glial cells of CCSG with normal functioning of synapses. Conclusion. Satellite gliocytes of cranial cervical sympathetic ganglion, like any other somatic cells, possess initially programmed aerobic system of energy production which transforms into anaerobic system under influence of impulses arriving through nicotine-sensitive cholinergic synapses.

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31

Kurtz, A., A. Zimmer, F. Schnutgen, G. Bruning, F. Spener, and T. Muller. "The expression pattern of a novel gene encoding brain-fatty acid binding protein correlates with neuronal and glial cell development." Development 120, no. 9 (September 1, 1994): 2637–49. http://dx.doi.org/10.1242/dev.120.9.2637.

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Fatty acid binding proteins (FABPs) are a multigene family of small intracellular proteins that bind hydrophobic ligands. In this report we describe the cloning and expression pattern of a novel member of this gene family that is specifically expressed in the developing and adult nervous system and thus was designated brain (B)-FABP. B-FABP is closely related to heart (H)-FABP with 67% amino acid identity. B-FABP expression was first detected at mouse embryonic day 10 in neuroepithelial cells and its pattern correlates with early neuronal differentiation. Upon further development, B-FABP was confined to radial glial cells and immature astrocytes. B-FABP mRNA and protein were found in glial cells of the peripheral nervous system such as satellite cells of spinal and cranial ganglia and ensheathing cells of the olfactory nerve layer from as early as embryonic day 11 until adulthood. In the adult mouse brain, B-FABP was found in the glia limitans, in radial glial cells of the hippocampal dentate gyrus and Bergman glial cells. These findings suggest a function of B-FABP during neurogenesis or neuronal migration in the developing nervous system. The partially overlapping expression pattern with that of cellular retinoid binding proteins suggests that B-FABP is involved in the metabolism of a so far unknown hydrophobic ligand with potential morphogenic activity during CNS development.

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Ohara, Peter T., Jean-Philippe Vit, Aditi Bhargava, and Luc Jasmin. "Evidence for a Role of Connexin 43 in Trigeminal Pain Using RNA Interference In Vivo." Journal of Neurophysiology 100, no. 6 (December 2008): 3064–73. http://dx.doi.org/10.1152/jn.90722.2008.

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The importance of glial cells in the generation and maintenance of neuropathic pain is becoming widely accepted. We examined the role of glial-specific gap junctions in nociception in the rat trigeminal ganglion in nerve-injured and -uninjured states. The connexin 43 (Cx43) gap-junction subunit was found to be confined to the satellite glial cells (SGCs) that tightly envelop primary sensory neurons in the trigeminal ganglion and we therefore used Cx43 RNA interference (RNAi) to alter gap-junction function in SGCs. Using behavioral evaluation, together with immunocytochemical and Western blot monitoring, we show that Cx43 increased in the trigeminal ganglion in rats with a chronic constriction injury (CCI) of the infraorbital nerve. Reducing Cx43 expression using RNAi in CCI rats reduced painlike behavior, whereas in non-CCI rats, reducing Cx43 expression increased painlike behavior. The degree of painlike behavior in CCI rats and intact, Cx43-silenced rats was similar. Our results support previous suggestions that increases in glial gap junctions after nerve injury increases nociceptive behavior but paradoxically the reduction of gap junctions in normal ganglia also increases nociceptive behavior, possibly a reflection of the multiple functions performed by glia.

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Wagner, Lysann, Rebekah A. Warwick, Thomas Pannicke, Andreas Reichenbach, Antje Grosche, and Menachem Hanani. "Glutamate release from satellite glial cells of the murine trigeminal ganglion." Neuroscience Letters 578 (August 2014): 143–47. http://dx.doi.org/10.1016/j.neulet.2014.06.047.

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Weick, M., P. S. Cherkas, W. Härtig, T. Pannicke, O. Uckermann, A. Bringmann, M. Tal, A. Reichenbach, and M. Hanani. "P2 receptors in satellite glial cells in trigeminal ganglia of mice." Neuroscience 120, no. 4 (September 2003): 969–77. http://dx.doi.org/10.1016/s0306-4522(03)00388-9.

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Feldman-Goriachnik, Rachel, Bing Wu, and Menachem Hanani. "Cholinergic responses of satellite glial cells in the superior cervical ganglia." Neuroscience Letters 671 (April 2018): 19–24. http://dx.doi.org/10.1016/j.neulet.2018.01.051.

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Kolosov, M. S., D. E. Bragin, A. S. Kohany, and A. B. Uzdensky. "Photodynamic injury of isolated neuron and satellite glial cells: morphological study." IEEE Journal of Selected Topics in Quantum Electronics 9, no. 2 (March 2003): 337–42. http://dx.doi.org/10.1109/jstqe.2003.812510.

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Vaegter, ChristianBjerggaard. "Neurotrophins and their receptors in satellite glial cells following nerve injury." Neural Regeneration Research 9, no. 23 (2014): 2038. http://dx.doi.org/10.4103/1673-5374.147924.

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Warwick, R. A., and M. Hanani. "The contribution of satellite glial cells to chemotherapy-induced neuropathic pain." European Journal of Pain 17, no. 4 (October 12, 2012): 571–80. http://dx.doi.org/10.1002/j.1532-2149.2012.00219.x.

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Zhang, Haijun, Xiaofeng Mei, Pu Zhang, Chao Ma, Fletcher A. White, David F. Donnelly, and Robert H. Lamotte. "Altered functional properties of satellite glial cells in compressed spinal ganglia." Glia 57, no. 15 (November 15, 2009): 1588–99. http://dx.doi.org/10.1002/glia.20872.

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Huang, Li-Yen M., Yanping Gu, and Yong Chen. "Communication between neuronal somata and satellite glial cells in sensory ganglia." Glia 61, no. 10 (August 5, 2013): 1571–81. http://dx.doi.org/10.1002/glia.22541.

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41

Huang, Tian-Ying, Pavel S. Cherkas, David W. Rosenthal, and Menachem Hanani. "Dye coupling among satellite glial cells in mammalian dorsal root ganglia." Brain Research 1036, no. 1-2 (March 2005): 42–49. http://dx.doi.org/10.1016/j.brainres.2004.12.021.

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Hanani, Menachem, Vitaly Belzer, and Pavel S. Cherkas. "Functional characteristics of satellite glial cells in the mouse nodose ganglion." Autonomic Neuroscience 135, no. 1-2 (September 2007): 60–61. http://dx.doi.org/10.1016/j.autneu.2007.06.091.

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Feldman-Goriachnik, Rachel, and Menachem Hanani. "How do neurons in sensory ganglia communicate with satellite glial cells?" Brain Research 1760 (June 2021): 147384. http://dx.doi.org/10.1016/j.brainres.2021.147384.

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Hibino, Hiroshi, Yoshiyuki Horio, Akikazu Fujita, Atsushi Inanobe, Katsumi Doi, Takahiro Gotow, Yasuo Uchiyama, Takeshi Kubo, and Yoshihisa Kurachi. "Expression of an inwardly rectifying K+ channel, Kir4.1, in satellite cells of rat cochlear ganglia." American Journal of Physiology-Cell Physiology 277, no. 4 (October 1, 1999): C638—C644. http://dx.doi.org/10.1152/ajpcell.1999.277.4.c638.

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Satellite cells are glial cells wrapped around somata of sensory and autonomic ganglion neurons. Neither their functional roles nor electrical properties have been fully clarified so far. Using immunohistochemistry, we found that inwardly rectifying K+ channel subunit Kir4.1 (also called Kir1.2 or KAB-2) was expressed prominently in the satellite cells of cochlear ganglia. The Kir4.1 immunoreactivity was localized specifically at the myelin sheaths of satellite cells wrapping the somata of the ganglion neurons. Developmental expression of Kir4.1 in satellite cells paralleled development of the action potential in the auditory nerve. These results suggest that this channel in satellite cells may be responsible for the regulation of K+ extruded from the ganglion neurons during excitation.

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Suadicani, Sylvia O., Pavel S. Cherkas, Jonathan Zuckerman, David N. Smith, David C. Spray, and Menachem Hanani. "Bidirectional calcium signaling between satellite glial cells and neurons in cultured mouse trigeminal ganglia." Neuron Glia Biology 6, no. 1 (November 6, 2009): 43–51. http://dx.doi.org/10.1017/s1740925x09990408.

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Astrocytes communicate with neurons, endothelial and other glial cells through transmission of intercellular calcium signals. Satellite glial cells (SGCs) in sensory ganglia share several properties with astrocytes, but whether this type of communication occurs between SGCs and sensory neurons has not been explored. In the present work we used cultured neurons and SGCs from mouse trigeminal ganglia to address this question. Focal electrical or mechanical stimulation of single neurons in trigeminal ganglion cultures increased intracellular calcium concentration in these cells and triggered calcium elevations in adjacent glial cells. Similar to neurons, SGCs responded to mechanical stimulation with increase in cytosolic calcium that spread to the adjacent neuron and neighboring glial cells. Calcium signaling from SGCs to neurons and among SGCs was diminished in the presence of the broad-spectrum P2 receptor antagonist suramin (50 μM) or in the presence of the gap junction blocker carbenoxolone (100 μM), whereas signaling from neurons to SGCs was reduced by suramin, but not by carbenoxolone. Following induction of submandibular inflammation by Complete Freund's Adjuvant injection, the amplitude of signaling among SGCs and from SGCs to neuron was increased, whereas the amplitude from neuron to SGCs was reduced. These results indicate for the first time the presence of bidirectional calcium signaling between neurons and SGCs in sensory ganglia cultures, which is mediated by the activation of purinergic P2 receptors, and to some extent by gap junctions. Furthermore, the results indicate that not only sensory neurons, but also SGCs release ATP. This form of intercellular calcium signaling likely plays key roles in the modulation of neuronal activity within sensory ganglia in normal and pathological states.

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Lee, Jun, Kinuyo Ohara, Masamichi Shinoda, Yoshinori Hayashi, Asako Kubo, Shiori Sugawara, Sayaka Asano, et al. "Involvement of Satellite Cell Activation via Nitric Oxide Signaling in Ectopic Orofacial Hypersensitivity." International Journal of Molecular Sciences 21, no. 4 (February 13, 2020): 1252. http://dx.doi.org/10.3390/ijms21041252.

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The mechanical head-withdrawal threshold (MHWT) was significantly reduced following inferior alveolar nerve transection (IANX) in rats. Nitrate and nitrite synthesis was dramatically increased in the trigeminal ganglion (TG) at 6 h after the IANX. The relative number of neuronal nitric oxide synthase (nNOS)-immunoreactive (IR) cells was significantly higher in IANX rats compared to sham-operated and N-propyl-L-arginine (NPLA)-treated IANX rats. On day 3 after NPLA administration, the MHWT recovered considerably in IANX rats. Following L-arginine injection into the TG, the MHWT was significantly reduced within 15 min, and the mean number of TG cells encircled by glial fibrillary acidic protein (GFAP)-IR cells was substantially higher. The relative number of nNOS-IR cells encircled by GFAP-IR cells was significantly increased in IANX rats. In contrast, after NPLA injection into the TG, the relative number of GFAP-IR cells was considerably reduced in IANX rats. Fluorocitrate administration into the TG significantly reduced the number of GFAP-IR cells and prevented the MHWT reduction in IANX rats. The present findings suggest that following IANX, satellite glial cells are activated via nitric oxide (NO) signaling from TG neurons. The spreading satellite glial cell activation within the TG results in mechanical hypersensitivity of face regions not directly associated with the trigeminal nerve injury.

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Gong, Kerui, and Qing Lin. "Minocycline Inhibits the Enhanced Antidromic Stimulation-induced Sensitization of C-Fibers Following Intradermal Capsaicin Injection." Open Pain Journal 12, no. 1 (June 30, 2019): 11–18. http://dx.doi.org/10.2174/1876386301912010011.

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Background: Our previous studies indicated that retrograde signaling initiating from the spinal cord was mediated by the plasticity of Dorsal Root Ganglion (DRG) neurons. Both retrograde signaling and neuronal plasticity contributed to neurogenic inflammation, which were modulated by the activity of Satellite Glial Cells (SGCs). Thus, we want to know whether retrograde signaling is involved in the hypersensitivity of nociceptive afferents, and whether this process is affected by the plasticity of DRG neurons and glia. Objective: The study aims to examine if retrograde signaling can induce hypersensitivity of primary afferent nociceptors and if hypersensitivity involves glial modulation. Methods: Antidromic Electrical Stimulation (ES) of dorsal roots was used to mimic retrograde signaling activity. C- primary nociceptive afferent activity was recorded for testing the effect of antidromic ES. In a separate group, intradermal capsaicin injection to the ipsilateral hindpaw was used to prime DRG nociceptive neurons. For the third group, a glial inhibitor, minocycline, was pre-administered to test glial modulation in this process. Results: Antidromic ES sensitized the responses of C-fibers to nociceptive mechanical stimuli. For rats subjected to intradermal capsaicin injection, C fibers experienced more drastic sensitization induced by antidromic ES, shown as a greater response and longer duration, implying that sensitization correlates with the activation of DRG neurons. Minocycline pretreatment significantly blocked the priming effect of capsaicin on C-fiber sensitization induced by antidromic ES, indicating the involvement of SGCs in DRG neuronal sensitization. Conclusion: Retrograde signaling may be one of the important mechanisms in neurogenic inflammation-mediated nociception, and this process is subjected to satellite glial modulation.

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Gregory, William A., David H. Hall, and Michael V. L. Bennett. "Satellite glial cells penetrate neurosecretory cells to perinuclear position in the goldfish preoptic area." Developmental Brain Research 44, no. 1 (November 1988): 1–8. http://dx.doi.org/10.1016/0165-3806(88)90113-7.

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Niederkinkhaus, Vanessa, Romy Marx, Gerd Hoffmann, and Irmgard D. Dietzel. "Thyroid Hormone (T3)-Induced Up-Regulation of Voltage-Activated Sodium Current in Cultured Postnatal Hippocampal Neurons Requires Secretion of Soluble Factors from Glial Cells." Molecular Endocrinology 23, no. 9 (September 1, 2009): 1494–504. http://dx.doi.org/10.1210/me.2009-0132.

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Abstract We have previously shown that treatment with the thyroid hormone T3 increases the voltage-gated Na+current density (Nav-D) in hippocampal neurons from postnatal rats, leading to accelerated action potential upstrokes and increased firing frequencies. Here we show that the Na+ current regulation depends on the presence of glial cells, which secrete a heat-instable soluble factor upon stimulation with T3. The effect of conditioned medium from T3-treated glial cells was mimicked by basic fibroblast growth factor (bFGF), known to be released from cerebellar glial cells after T3 treatment. Neutralization assays of astrocyte-conditioned media with anti-bFGF antibody inhibited the regulation of the Nav-D by T3. This suggests that the up-regulation of the neuronal sodium current density by T3 is not a direct effect but involves bFGF release and satellite cells. Thus glial cells can modulate neuronal excitability via secretion of paracrinely acting factors.

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Magni, Giulia, Marta Boccazzi, Antonella Bodini, Maria P. Abbracchio, Arn MJM van den Maagdenberg, and Stefania Ceruti. "Basal astrocyte and microglia activation in the central nervous system of Familial Hemiplegic Migraine Type I mice." Cephalalgia 39, no. 14 (July 1, 2019): 1809–17. http://dx.doi.org/10.1177/0333102419861710.

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Background Gain-of-function missense mutations in the α1A subunit of neuronal CaV2.1 channels, which define Familial Hemiplegic Migraine Type 1 (FHM1), result in enhanced cortical glutamatergic transmission and a higher susceptibility to cortical spreading depolarization. It is now well established that neurons signal to surrounding glial cells, namely astrocytes and microglia, in the central nervous system, which in turn become activated and in pathological conditions can sustain neuroinflammation. We and others previously demonstrated an increased activation of pro-algogenic pathways, paralleled by augmented macrophage infiltration, in both isolated trigeminal ganglia and mixed trigeminal ganglion neuron-satellite glial cell cultures of FHM1 mutant mice. Hence, we hypothesize that astrocyte and microglia activation may occur in parallel in the central nervous system. Methods We have evaluated signs of reactive glia in brains from naïve FHM1 mutant mice in comparison with wild type animals by immunohistochemistry and Western blotting. Results Here we show for the first time signs of reactive astrogliosis and microglia activation in the naïve FHM1 mutant mouse brain. Conclusions Our data reinforce the involvement of glial cells in migraine, and suggest that modulating such activation may represent an innovative approach to reduce pathology.

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