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Journal articles on the topic 'Satellite glia'

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Author: Grafiati

Published: 10 December 2022

Last updated: 28 January 2023

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1

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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2

Krawczyk, Aleksandra Ewa, and Jadwiga Jaworska-Adamu. "The immunoreactivity of satellite glia of the spinal ganglia of rats treated with monosodium glutamate." Acta Veterinaria Brno 85, no. 4 (2016): 337–41. http://dx.doi.org/10.2754/avb201685040337.

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Satellite glia of the peripheral nervous system ganglia provide metabolic protection to the neurons. The aim of this study was to determine the effects of monosodium glutamate administered parenterally to rats on the expression of glial fibrillary acidic protein, S-100β protein and Ki-67 antigen in the satellite glial cells. Adult, 60-day-old male rats received monosodium glutamate at two doses of 2 g/kg b.w. (group 1) and 4 g/kg b.w. (group 2) subcutaneously for 3 consecutive days. Animals in the control group (group C) were treated with corresponding doses of 0.9% sodium chloride. Immediately after euthanasia, spinal ganglia of the lumbar region were dissected. Immunohistochemical peroxidase anti-peroxidase reactions were performed on the sections containing the examined material using antibodies against glial fibrillary acidic protein, S-100β and Ki-67. Next, morphological and morphometric analyses of immunopositive and immunonegative glia were conducted. The data were presented as the mean number of cells with standard deviation. Significant differences were analysed using ANOVA (P < 0.05). In all 63-day-old rats, immunopositivity for the examined proteins glia was observed. Increased number of cells expressing glial fibrillary acidic protein was demonstrated in group 2, whereas the number of S-100β-positive glia grew in the groups with the increasing doses of monosodium glutamate. The results indicate the early stage reactivity of glia in response to increased levels of glutamate in the extracellular space. These changes may be of a neuroprotective nature under the conditions of excitotoxicity induced by the action of this excitatory neurotransmitter.

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Lee, Ji Hwan, and Woojin Kim. "The Role of Satellite Glial Cells, Astrocytes, and Microglia in Oxaliplatin-Induced Neuropathic Pain." Biomedicines 8, no. 9 (September 2, 2020): 324. http://dx.doi.org/10.3390/biomedicines8090324.

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

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4

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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5

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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6

Gazerani, Parisa. "Contribution of Central and Peripheral Glial Cells in the Development and Persistence of Itch: Therapeutic Implication of Glial Modulation." Neuroglia 4, no. 1 (January 17, 2023): 15–27. http://dx.doi.org/10.3390/neuroglia4010002.

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Chronic itch (CI) is an unpleasant skin sensation accompanied by an intense scratching desire that lasts 6 weeks or longer. Despite the high prevalence and negative impact on affected individuals and a huge healthcare burden, CI mechanisms are only partially understood, and consequently, treatment of CI remains sub-optimal. The complexity of CI treatment also stems from the comorbid existence of persistent itch with other somatic and psychological disorders. Etiologies of CI are multiple and diverse, although CI is often a result of dermatologically related conditions such as atopic dermatitis and psoriasis. Unfolding the pathophysiology of CI can provide possibilities for better therapy. Itch signaling is complex and neurons and non-neuronal cells play a role. This review focuses on recent findings on the role of glial cells in itch. Central glia (astrocytes and microglia) and peripheral glia (satellite glial cells and Schwann cells) are found to contribute to the development or persistence of itch. Hence, glial modulation has been proposed as a potential option in CI treatment. In experimental models of itch, the blockade of signal transducer and the activator of transcription (STAT) 3-mediated reactive astrogliosis have been shown to suppress chronic itch. Administration of a microglial inhibitor, minocycline, has also been demonstrated to suppress itch-related microglial activation and itch. In sensory ganglia, gap-junction blockers have successfully blocked itch, and hence, gap-junction-mediated coupling, with a potential role of satellite glial cells have been proposed. This review presents examples of glial involvement in itch and opportunities and challenges of glial modulation for targeting itch.

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7

Ye, Yi, Elizabeth Salvo, Marcela Romero-Reyes, Simon Akerman, Emi Shimizu, Yoshifumi Kobayashi, Benoit Michot, and Jennifer Gibbs. "Glia and Orofacial Pain: Progress and Future Directions." International Journal of Molecular Sciences 22, no. 10 (May 19, 2021): 5345. http://dx.doi.org/10.3390/ijms22105345.

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Orofacial pain is a universal predicament, afflicting millions of individuals worldwide. Research on the molecular mechanisms of orofacial pain has predominately focused on the role of neurons underlying nociception. However, aside from neural mechanisms, non-neuronal cells, such as Schwann cells and satellite ganglion cells in the peripheral nervous system, and microglia and astrocytes in the central nervous system, are important players in both peripheral and central processing of pain in the orofacial region. This review highlights recent molecular and cellular findings of the glia involvement and glia–neuron interactions in four common orofacial pain conditions such as headache, dental pulp injury, temporomandibular joint dysfunction/inflammation, and head and neck cancer. We will discuss the remaining questions and future directions on glial involvement in these four orofacial pain conditions.

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8

Robering, Jan W., Lisa Gebhardt, Katharina Wolf, Helen Kühn, Andreas E. Kremer, and Michael J. M. Fischer. "Lysophosphatidic acid activates satellite glia cells and Schwann cells." Glia 67, no. 5 (January 13, 2019): 999–1012. http://dx.doi.org/10.1002/glia.23585.

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9

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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10

Mapps, Aurelia A., Michael B. Thomsen, Erica Boehm, Haiqing Zhao, Samer Hattar, and Rejji Kuruvilla. "Diversity of satellite glia in sympathetic and sensory ganglia." Cell Reports 38, no. 5 (February 2022): 110328. http://dx.doi.org/10.1016/j.celrep.2022.110328.

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11

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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12

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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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

Spray, David C., Rodolfo Iglesias, Nathanael Shraer, Sylvia O. Suadicani, Vitali Belzer, Regina Hanstein, and Menachem Hanani. "Gap junction mediated signaling between satellite glia and neurons in trigeminal ganglia." Glia 67, no. 5 (February 4, 2019): 791–801. http://dx.doi.org/10.1002/glia.23554.

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15

Bradman, Matthew J. G., Daleep K. Arora, Richard Morris, and Thimmasettappa Thippeswamy. "How do the satellite glia cells of the dorsal root ganglia respond to stressed neurons? – nitric oxide saga from embryonic development to axonal injury in adulthood." Neuron Glia Biology 6, no. 1 (February 2010): 11–17. http://dx.doi.org/10.1017/s1740925x09990494.

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Dorsal root ganglia (DRG) respond to peripheral nerve injury by up-regulating nitric oxide (NO) production by neurons and glia in addition to local fibroblasts, endothelium and macrophages. We hypothesise that NO produced from these cells has specific roles. We have shown that when neuronal NO synthase (nNOS) is blocked in axotomised DRG, neurons undergo degenerative changes (Thippeswamy et al., 2001, 2007a). Further, we demonstrated that increased neuronal NO production, in response to axotomy/growth factor-deprivation in vitro, signals glial cells to produce trophic factors to support neuronal survival (Thippeswamy et al., 2005a). Recently, we found that treating satellite glia–neuron co-cultures with nNOS inhibitor, 7-nitroindazole (7NI), decreases the number of nestin+ cells that show neuron-like morphology. Cultured/axotomised DRG also upregulate inducible NOS (iNOS) in non-neuronal cells. Therefore, it is plausible that degenerative changes following nNOS inhibition are also due to iNOS-mediated excessive NO production by non-neuronal cells, which indeed is cytotoxic. NG-nitro-l-arginine methylester (L-NAME), the pan NOS inhibitor did not significantly change nNOS+ neuron number in axotomised DRG compared to 7NI suggesting that iNOS-mediated NO contributes to the degenerative process. In this paper, these findings from our and others' past work on NO-mediated neuron–glia signalling in axotomised DRG are discussed.

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16

Jager, Sara E., Lone T. Pallesen, Mette Richner, Peter Harley, Zoe Hore, Stephen McMahon, Franziska Denk, and Christian B. Vægter. "Changes in the transcriptional fingerprint of satellite glial cells following peripheral nerve injury." Glia 68, no. 7 (February 11, 2020): 1375–95. http://dx.doi.org/10.1002/glia.23785.

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17

White, P. M., and D. J. Anderson. "In vivo transplantation of mammalian neural crest cells into chick hosts reveals a new autonomic sublineage restriction." Development 126, no. 19 (October 1, 1999): 4351–63. http://dx.doi.org/10.1242/dev.126.19.4351.

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The study of mammalian neural crest development has been limited by the lack of an accessible system for in vivo transplantation of these cells. We have developed a novel transplantation system to study lineage restriction in the rodent neural crest. Migratory rat neural crest cells (NCCs), transplanted into chicken embryos, can differentiate into sensory, sympathetic, and parasympathetic neurons, as shown by the expression of neuronal subtype-specific and pan-neuronal markers, as well as into Schwann cells and satellite glia. In contrast, an immunopurified population of enteric neural precursors (ENPs) from the fetal gut can also generate neurons in all of these ganglia, but only expresses appropriate neuronal subtype markers in Remak's and associated pelvic parasympathetic ganglia. ENPs also appear restricted in the kinds of glia they can generate in comparison to NCCs. Thus ENPs have parasympathetic and presumably enteric capacities, but not sympathetic or sensory capacities. These results identify a new autonomic lineage restriction in the neural crest, and suggest that this restriction preceeds the choice between neuronal and glial fates.

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18

Agapov, P. A., and I. N. Bogolepova. "Cytoarchitectonics of the Superior Parietal Cortex of an Outstanding Russian Scientist-Physiologist." Journal of Anatomy and Histopathology 10, no. 3 (September 20, 2021): 9–14. http://dx.doi.org/10.18499/2225-7357-2021-10-3-9-14.

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The aim of the study is to identify possible cytoarchitectonic features of the structure of the cortex in the superior parietal region of an outstanding and talented scientist-physiologist.Material and methods. The cortex (area 7) of the superior parietal region of a scientist-physiologist and men of the senile age in the control group (8 hemispheres) was studied on the series of frontal brain slices, 20 μ thick, stained with cresyl purple according to Nissl method. The cortex area thickness, the thickness of the cytoarchitectonics layer III, the area of profile field of pyramidal neurons in layers III and V, the density of neurons surrounded by satellite glia and satellite glia density in layers III and V were measured in the cortex (area 7) of the superior parietal region in the left and right hemispheres of the brain.Results. We have identified several features of the cytoarchitectonics structure of the cortex (area 7) in the brain of the scientist-physiologist that may correlate with his outstanding scientific abilities. The cortex of a scientist-physiologist is characterized by a large thickness of the studied cortex and its cytoarchitectonic layers III and V, and a greater value of the area of the profile field of neurons if compared with the cortex in men of the senile age from the control group. A higher value of the neuron density and satellite glia in the cortex of the superior parietal region of the scientist-physiologist was revealed. There was also a lower severity of age-related changes in the cortex of the scientist-physiologist compared with the control group of men.Conclusion. The structure of the cortex (area 7) of the superior parietal region of the scientistphysiologist is characterized by a greater parameter of the cortical thickness and the thickness of the associative layer III, the size of neurons and the density of satellite glia if compared with those in men of the senile age of the control group. These features distinguish the structure of his cortex from the similar cortex of the control group of men and may be related to the features of the cognitive activity of the outstanding scientist-physiologist.

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19

Elson, Karen, Anthony Simmons, and Peter Speck. "Satellite cell proliferation in murine sensory ganglia in response to scarification of the skin." Glia 45, no. 1 (2003): 105–9. http://dx.doi.org/10.1002/glia.10294.

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20

Callahan, Thomas, Heather M. Young, Richard B. Anderson, Hideki Enomoto, and Colin R. Anderson. "Development of satellite glia in mouse sympathetic ganglia: GDNF and GFRα1 are not essential." Glia 56, no. 13 (October 2008): 1428–37. http://dx.doi.org/10.1002/glia.20709.

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21

Zhang, Li, Rougang Xie, Jiping Yang, Youyi Zhao, Chuchu Qi, Ganlan Bian, Mengmeng Wang, et al. "Chronic pain induces nociceptive neurogenesis in dorsal root ganglia from Sox2‐positive satellite cells." Glia 67, no. 6 (January 16, 2019): 1062–75. http://dx.doi.org/10.1002/glia.23588.

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22

Feldman-Goriachnik, Rachel, Vitali Belzer, and Menachem Hanani. "Systemic inflammation activates satellite glial cells in the mouse nodose ganglion and alters their functions." Glia 63, no. 11 (June 23, 2015): 2121–32. http://dx.doi.org/10.1002/glia.22881.

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23

Belzer, Vitali, and Menachem Hanani. "Nitric oxide as a messenger between neurons and satellite glial cells in dorsal root ganglia." Glia 67, no. 7 (February 23, 2019): 1296–307. http://dx.doi.org/10.1002/glia.23603.

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Hanani, Menachem, and David C. Spray. "Emerging importance of satellite glia in nervous system function and dysfunction." Nature Reviews Neuroscience 21, no. 9 (July 22, 2020): 485–98. http://dx.doi.org/10.1038/s41583-020-0333-z.

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25

Castillo, C., M. Norcini, L. A. Martin Hernandez, G. Correa, T. J. J. Blanck, and E. Recio-Pinto. "Satellite glia cells in dorsal root ganglia express functional NMDA receptors." Neuroscience 240 (June 2013): 135–46. http://dx.doi.org/10.1016/j.neuroscience.2013.02.031.

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Donegan, Macayla, Melanie Kernisant, Criselda Cua, Luc Jasmin, and Peter T. Ohara. "Satellite glial cell proliferation in the trigeminal ganglia after chronic constriction injury of the infraorbital nerve." Glia 61, no. 12 (October 3, 2013): 2000–2008. http://dx.doi.org/10.1002/glia.22571.

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Weperen, Valerie Y. H., Russell J. Littman, Douglas V. Arneson, Jaime Contreras, Xia Yang, and Olujimi A. Ajijola. "Single‐cell transcriptomic profiling of satellite glial cells in stellate ganglia reveals developmental and functional axial dynamics." Glia 69, no. 5 (January 12, 2021): 1281–91. http://dx.doi.org/10.1002/glia.23965.

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Demartini, Chiara, Rosaria Greco, Giulia Magni, Anna Maria Zanaboni, Benedetta Riboldi, Miriam Francavilla, Cristina Nativi, Stefania Ceruti, and Cristina Tassorelli. "Modulation of Glia Activation by TRPA1 Antagonism in Preclinical Models of Migraine." International Journal of Molecular Sciences 23, no. 22 (November 15, 2022): 14085. http://dx.doi.org/10.3390/ijms232214085.

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Preclinical data point to the contribution of transient receptor potential ankyrin 1 (TRPA1) channels to the complex mechanisms underlying migraine pain. TRPA1 channels are expressed in primary sensory neurons, as well as in glial cells, and they can be activated/sensitized by inflammatory mediators. The aim of this study was to investigate the relationship between TRPA1 channels and glial activation in the modulation of trigeminal hyperalgesia in preclinical models of migraine based on acute and chronic nitroglycerin challenges. Rats were treated with ADM_12 (TRPA1 antagonist) and then underwent an orofacial formalin test to assess trigeminal hyperalgesia. mRNA levels of pro- and anti-inflammatory cytokines, calcitonin gene-related peptide (CGRP) and glia cell activation were evaluated in the Medulla oblongata and in the trigeminal ganglia. In the nitroglycerin-treated rats, ADM_12 showed an antihyperalgesic effect in both acute and chronic models, and it counteracted the changes in CGRP and cytokine gene expression. In the acute nitroglycerin model, ADM_12 reduced nitroglycerin-induced increase in microglial and astroglial activation in trigeminal nucleus caudalis area. In the chronic model, we detected a nitroglycerin-induced activation of satellite glial cells in the trigeminal ganglia that was inhibited by ADM_12. These findings show that TRPA1 antagonism reverts experimentally induced hyperalgesia in acute and chronic models of migraine and prevents multiple changes in inflammatory pathways by modulating glial activation.

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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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Magni, Giulia, Davide Merli, Claudia Verderio, Maria P. Abbracchio, and Stefania Ceruti. "P2Y2receptor antagonists as anti-allodynic agents in acute and sub-chronic trigeminal sensitization: Role of satellite glial cells." Glia 63, no. 7 (March 16, 2015): 1256–69. http://dx.doi.org/10.1002/glia.22819.

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Liang, H., H. Hu, D. Shan, J. Lyu, X. Yan, Y. Wang, F. Jian, X. Li, W. Lai, and H. Long. "CGRP Modulates Orofacial Pain through Mediating Neuron-Glia Crosstalk." Journal of Dental Research 100, no. 1 (August 27, 2020): 98–105. http://dx.doi.org/10.1177/0022034520950296.

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Calcitonin gene-related peptide (CGRP) plays a crucial role in the modulation of orofacial pain, and we hypothesized that CGRP mediated a neuron-glia crosstalk in orofacial pain. The objective of this study was to elucidate the mechanisms whereby CGRP mediated trigeminal neuron-glia crosstalk in modulating orofacial pain. Orofacial pain was elicited by ligating closed-coil springs between incisors and molars. Trigeminal neurons and satellite glial cells (SGCs) were cultured for mechanistic exploration. Gene and protein expression were determined through immunostaining, polymerase chain reaction, and Western blot. Orofacial pain was evaluated through the rat grimace scale. Our results revealed that the expressions of CGRP were elevated in both trigeminal neurons and SGCs following the induction of orofacial pain. Intraganglionic administration of CGRP and olcegepant exacerbated and alleviated orofacial pain, respectively. The knockdown of CGRP through viral vector-mediated RNA interference was able to downregulate CGRP expressions in both neurons and SGCs and to alleviate orofacial pain. CGRP upregulated the expression of inducible nitric oxide synthase through the p38 signaling pathway in cultured SGCs. In turn, L-arginine (nitric oxide donor) was able to enhance orofacial pain by upregulating CGRP expressions in vivo. In cultured trigeminal neurons, L-arginine upregulated the expression of CGRP, and this effect was diminished by cilnidipine (N-type calcium channel blocker) while not by mibefradil (L-type calcium channel blocker). In conclusion, CGRP modulated orofacial pain through upregulating the expression of nitric oxide through the p38 signaling pathway in SGCs, and the resulting nitric oxide in turn stimulated CGRP expression through N-type calcium channel in neurons, building a CGRP-mediated positive-feedback neuron-glia crosstalk.

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Schaeffer, V��ronique, Laurence Meyer, Christine Patte-mensah, Anne Eckert, and Ayikoe G. Mensah-nyagan. "Sciatic nerve injury induces apoptosis of dorsal root ganglion satellite glial cells and selectively modifies neurosteroidogenesis in sensory neurons." Glia 58, no. 2 (January 15, 2010): 169–80. http://dx.doi.org/10.1002/glia.20910.

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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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Sterman, Adam, Regina Hanstein, and David C. Spray. "The role of pannexin 1 in chemotherapy-induced peripheral neuropathy (CIPN)." Journal of Clinical Oncology 33, no. 29_suppl (October 10, 2015): 6. http://dx.doi.org/10.1200/jco.2015.33.29_suppl.6.

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6 Background: CIPN is a debilitating side effect and dose limiting toxicity of anticancer drug therapies. CIPN induces pathological changes in dorsal root ganglia (DRG), leading to increased cross-talk between sensory neurons and satellite glial cells (SGCs), specifically ATP mediated SGC-neuron signaling. We therefore investigated CIPN in mice with neuron- or glia-specific deletion of the ATP-releasing channel Pannexin 1 (Panx 1). Methods: To induce CIPN, mice were given two i.p. oxaliplatin (oxa) injections two days apart. Controls received saline (sal). We used C57Bl6 wildtype and transgenic mice with neuron- or glia-specific Panx1 deletion (NFHcre or GFAPcre:Panx1F/F) and littermate controls (Panx1F/F), 7-11 per group. Tactile sensitivity of the hindpaws was assessed prior to and every week after injections for 3 weeks using von Frey filaments. The number of paw withdrawals to 10 stimulations with each filament and pain thresholds (corresponding to filament that elicits 8/10 responses) were recorded. Overall mouse condition was assessed using Open Field Tests. Results: C57Bl6 mice developed transient tactile hypersensitivity after oxa injection, which was most prominent at day 9 and ceased at day 21. Oxa-injected mice had lower tactile thresholds (at 9 days: sal 5.5±0.3g vs. oxa 2.7±0.4g, p < 0.001) and higher response rates to filaments compared to sal-injected controls (p < 0.05), but revealed no changes in any other behavior. Mice with glia-specific Panx1 deletion did not display significant tactile hypersensitivity at any time after oxa (tactile threshold at 9 days: sal 5.5±0.3g vs. oxa 5.8±0.2g), whereas oxa induced tactile hypersensitivity did occur in mice with neuron-specific Panx1 deletion (at 9 days: sal 6±0g vs. oxa 1.3±0g, p < 0.0001) and Panx1F/F littermates (at 9 days: sal 6.0±0g vs. oxa 1.3±0.1g, p < 0.0001). Conclusions: We found that oxaliplatin induces transient CIPN, but no other behavioral changes in wildtype mice. Deletion of the ATP-releasing channel Panx1 in glia, but not in neurons, prevented CIPN development. This points to a new molecule (Panx1) and a new cell type (glia) as potential novel targets for pain therapy.

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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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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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Durham, P. L., and F. G. Garrett. "Emerging Importance of Neuron-Satellite Glia Interactions within Trigeminal Ganglia in Craniofacial Pain." Open Pain Journal 3, no. 1 (January 1, 2010): 3–13. http://dx.doi.org/10.2174/1876386301003010003.

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Hanani, Menachem, and David C. Spray. "Author Correction: Emerging importance of satellite glia in nervous system function and dysfunction." Nature Reviews Neuroscience 21, no. 12 (October 22, 2020): 732. http://dx.doi.org/10.1038/s41583-020-00402-y.

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Takeda, Mamoru, Masayuki Takahashi, and Shigeji Matsumoto. "Contribution of the activation of satellite glia in sensory ganglia to pathological pain." Neuroscience & Biobehavioral Reviews 33, no. 6 (June 2009): 784–92. http://dx.doi.org/10.1016/j.neubiorev.2008.12.005.

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Hall, A. K., and S. C. Landis. "Division and migration of satellite glia in the embryonic rat superior cervical ganglion." Journal of Neurocytology 21, no. 9 (September 1992): 635–47. http://dx.doi.org/10.1007/bf01191725.

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Qiao, Liya Y., and Namrata Tiwari. "Spinal neuron-glia-immune interaction in cross-organ sensitization." American Journal of Physiology-Gastrointestinal and Liver Physiology 319, no. 6 (December 1, 2020): G748—G760. http://dx.doi.org/10.1152/ajpgi.00323.2020.

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Inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS), historically considered as regional gastrointestinal disorders with heightened colonic sensitivity, are increasingly recognized to have concurrent dysfunction of other visceral and somatic organs, such as urinary bladder hyperactivity, leg pain, and skin hypersensitivity. The interorgan sensory cross talk is, at large, termed “cross-organ sensitization.” These organs, anatomically distant from one another, physiologically interlock through projecting their sensory information into dorsal root ganglia (DRG) and then the spinal cord for integrative processing. The fundamental question of how sensitization of colonic afferent neurons conveys nociceptive information to activate primary afferents that innervate distant organs remains ambiguous. In DRG, primary afferent neurons are surrounded by satellite glial cells (SGCs) and macrophage accumulation in response to signals of injury to form a neuron-glia-macrophage triad. Astrocytes and microglia are major resident nonneuronal cells in the spinal cord to interact, physically and chemically, with sensory synapses. Cumulative evidence gathered so far indicate the indispensable roles of paracrine/autocrine interactions among neurons, glial cells, and immune cells in sensory cross-activation. Dichotomizing afferents, sensory convergency in the spinal cord, spinal nerve comingling, and extensive sprouting of central axons of primary afferents each has significant roles in the process of cross-organ sensitization; however, more results are required to explain their functional contributions. DRG that are located outside the blood-brain barrier and reside upstream in the cascade of sensory flow from one organ to the other in cross-organ sensitization could be safer therapeutic targets to produce less central adverse effects.

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Uzdensky, Anatoly, Mikhail Kolosov, Denis Bragin, Olga Dergacheva, Olga Vanzha, and Lidiya Oparina. "Involvement of adenylate cyclase and tyrosine kinase signaling pathways in response of crayfish stretch receptor neuron and satellite glia cell to photodynamic treatment." Glia 49, no. 3 (2004): 339–48. http://dx.doi.org/10.1002/glia.20122.

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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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Song, Dan-dan, Yong Li, Dong Tang, Li-ya Huang, and Yao-zong Yuan. "Neuron-glial communication mediated by TNF-α and glial activation in dorsal root ganglia in visceral inflammatory hypersensitivity." American Journal of Physiology-Gastrointestinal and Liver Physiology 306, no. 9 (May 1, 2014): G788—G795. http://dx.doi.org/10.1152/ajpgi.00318.2013.

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Communication between neurons and glia in the dorsal root ganglia (DRG) and the central nervous system is critical for nociception. Both glial activation and proinflammatory cytokine induction underlie this communication. We investigated whether satellite glial cell (SGC) and tumor necrosis factor-α (TNF-α) activation in DRG participates in a 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced rat model of visceral hyperalgesia. In TNBS-treated rats, TNF-α expression increased in DRG and was colocalized to SGCs enveloping a given neuron. These SGCs were activated as visualized under electron microscopy: they had more elongated processes projecting into the connective tissue space and more gap junctions. When nerves attached to DRG (L6-S1) were stimulated with a series of electrical stimulations, TNF-α were released from DRG in TNBS-treated animals compared with controls. Using a current clamp, we noted that exogenous TNF-α (2.5 ng/ml) increased DRG neuron activity, and visceral pain behavioral responses were reversed by intrathecal administration of anti-TNF-α (10 μg·kg−1·day−1). Based on our findings, TNF-α and SGC activation in neuron-glial communication are critical in inflammatory visceral hyperalgesia.

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Butt, Arthur, and Alexei Verkhratsky. "Neuroglia: Realising their true potential." Brain and Neuroscience Advances 2 (January 2018): 239821281881749. http://dx.doi.org/10.1177/2398212818817495.

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The name neuroglia is generally translated as nerve glue. In the recent past, this has been used to describe passive structural cells. Presently, this view has been challenged and the true dynamic and multifunctional nature of neuroglia is beginning to be appreciated. In the central nervous system, the main kinds of neuroglia are astrocytes (the primary homeostatic cells that ensure synaptic transmission), oligodendrocytes (which form the myelin that ensures rapid electrical transmission) and microglia (the main immune cells). In the peripheral nervous system, neuroglia comprise Schwann cells, satellite glia and enteric glia. These functionally diverse and specialised cells are fundamental to function at the molecular, cellular, tissue and system levels. Without nerve glue, the body cannot function and the future will begin to unlock their importance in higher cognitive functions that set humans apart from other animals and their true potential as therapeutic targets in neurodegenerative and other diseases.

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Villa, Giovanni, Marta Fumagalli, Claudia Verderio, Maria P. Abbracchio, and Stefania Ceruti. "Expression and contribution of satellite glial cells purinoceptors to pain transmission in sensory ganglia: an update." Neuron Glia Biology 6, no. 1 (February 2010): 31–42. http://dx.doi.org/10.1017/s1740925x10000086.

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The role of adenosine-5′-triphosphate (ATP) and of the ligand-gated P2X3receptor in neuronal dorsal root ganglia (DRG) pain transmission is relatively well established. Much less is known about the purinergic system in trigeminal ganglia (TG), which are involved in certain types of untreatable neuropathic and inflammatory pain, as well as in migraine. Emerging data suggest that purinergic metabotropic P2Y receptors on both neurons and satellite glial cells (SGCs) may also participate in both physiological and pathological pain development. Here, we provide an updated literature review on the role of purinergic signaling in sensory ganglia, with special emphasis on P2Y receptors on SGCs. We also provide new original data showing a time-dependent downregulation of P2Y2and P2Y4receptor expression and function in purified SGCs cultures from TG, in comparison with primary mixed neuron–SGCs cultures. These data highlight the importance of the neuron–glia cross-talk in determining the SGCs phenotype. Finally, we show that, in mixed TG cultures, both adenine and guanosine induce intracellular calcium transients in neurons but not in SGCs, suggesting that also these purinergic-related molecules can participate in pain signaling. These findings may have relevant implications for the development of new therapeutic strategies for chronic pain treatment.

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Maniglier, Madlyne, Marie Vidal, Corinne Bachelin, Cyrille Deboux, Jérémy Chazot, Beatriz Garcia-Diaz, and Anne Baron-Van Evercooren. "Satellite glia of the adult dorsal root ganglia harbor stem cells that yield glia under physiological conditions and neurons in response to injury." Stem Cell Reports 17, no. 11 (November 2022): 2467–83. http://dx.doi.org/10.1016/j.stemcr.2022.10.002.

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48

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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Nadeau, Joelle R., Tracy D. Wilson-Gerwing, and Valerie M. K. Verge. "Induction of a reactive state in perineuronal satellite glial cells akin to that produced by nerve injury is linked to the level of p75NTR expression in adult sensory neurons." Glia 62, no. 5 (February 24, 2014): 763–77. http://dx.doi.org/10.1002/glia.22640.

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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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