Satellite glia activation in dorsal root ganglion contributes to mechanical allodynia after selective motor fiber injury in adult rats

Yuan, Qiuju; Liu, Xiao Dong; Xian, Yan‐Fang; Yao, Min; Xie, Zhaoxiong; Huang, Pengyun; Wu, Wutian; Lin, Zhi‐Xiu

doi:10.1016/j.biopha.2020.110187

Cited by 23 publications

(28 citation statements)

References 41 publications

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“… 52 Similarly, GFAP expression is upregulated in activated, injured murine and rat SGCs of sensory ganglia, while it is often below detectable level in a non‐activated state. 16 , 35 , 53 , 54 , 55 In contrast to mSGCs, the majority of cSGCs within this study expressed GFAP, which is in accordance with previously published data. 23 It can be hypothesized that adult cSGCs possess a phenotype, which more closely resembles that of CNS glial cells, especially astrocytes.…”

Section: Discussionsupporting

confidence: 93%

“…For instance, murine and rat SGCs begin to proliferate, become hypertrophic and upregulate the expression of glial fibrillary acidic protein (GFAP) in pathologic conditions. 14 , 15 , 16 , 17 A recent study investigating transcriptional changes in SGCs following peripheral nerve injury demonstrates that SGCs are also engaged in ‘injury‐induced immune‐related processes in the DRG’. 18 Furthermore, human trigeminal SGCs express a variety of Toll‐like receptors (TLR) and produce cytokines after stimulation with eligible TLR ligands.…”

Section: Introductionmentioning

confidence: 99%

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Phenotypical peculiarities and species‐specific differences of canine and murine satellite glial cells of spinal ganglia

Huang

Zdora

Buhr

et al. 2021

J Cellular Molecular Medi

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Satellite glial cells (SGCs) of the sensory ganglia are a glial cell population of the peripheral nervous system (PNS) with diverse and remarkable features. Within the past two decades, SGCs have received increasing attention in a wide field of research. In addition to studying their morphological and functional qualities, their role in pathologic states and the development of neuropathic pain has been investigated. 1 The sensory ganglia, including the trigeminal ganglion as well as the spinal ganglia (SG), also known as dorsal root ganglia (DRG), are part of the PNS and transmit sensory signals fromthe periphery towards the central nervous system (CNS).

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Phenotypical peculiarities and species‐specific differences of canine and murine satellite glial cells of spinal ganglia

Huang

Zdora

Buhr

et al. 2021

J Cellular Molecular Medi

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“…Satellite glial cells that surround the cell bodies of dorsal root ganglia (DRG) neurons represent an additional source of primary inflammatory mediators (2,78,142,(207)(208)(209). IL-1β may also be derived from macrophages that invade DRG after injury (141) as well as from sensory neuron resident macrophages (210).…”

Section: Nerve Injury Wallerian Degeneration Inflammation and Generation Of Primary Mediatorsmentioning

confidence: 99%

Mediators of Neuropathic Pain; Focus on Spinal Microglia, CSF-1, BDNF, CCL21, TNF-α, Wnt Ligands, and Interleukin 1β

2021

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Intractable neuropathic pain is a frequent consequence of nerve injury or disease. When peripheral nerves are injured, damaged axons undergo Wallerian degeneration. Schwann cells, mast cells, fibroblasts, keratinocytes and epithelial cells are activated leading to the generation of an “inflammatory soup” containing cytokines, chemokines and growth factors. These primary mediators sensitize sensory nerve endings, attract macrophages, neutrophils and lymphocytes, alter gene expression, promote post-translational modification of proteins, and alter ion channel function in primary afferent neurons. This leads to increased excitability and spontaneous activity and the generation of secondary mediators including colony stimulating factor 1 (CSF-1), chemokine C-C motif ligand 21 (CCL-21), Wnt3a, and Wnt5a. Release of these mediators from primary afferent neurons alters the properties of spinal microglial cells causing them to release tertiary mediators, in many situations via ATP-dependent mechanisms. Tertiary mediators such as BDNF, tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β), and other Wnt ligands facilitate the generation and transmission of nociceptive information by increasing excitatory glutamatergic transmission and attenuating inhibitory GABA and glycinergic transmission in the spinal dorsal horn. This review focusses on activation of microglia by secondary mediators, release of tertiary mediators from microglia and a description of their actions in the spinal dorsal horn. Attention is drawn to the substantial differences in the precise roles of various mediators in males compared to females. At least 25 different mediators have been identified but the similarity of their actions at sensory nerve endings, in the dorsal root ganglia and in the spinal cord means there is considerable redundancy in the available mechanisms. Despite this, behavioral studies show that interruption of the actions of any single mediator can relieve signs of pain in experimental animals. We draw attention this paradox. It is difficult to explain how inactivation of one mediator can relieve pain when so many parallel pathways are available.

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“…Oxaliplatin is known to have poor permeability across the blood-brain barrier (BBB) thus primarily affecting the DRG [41]. In normal conditions, the activities of SGCs are not significantly increased and only a small number of DRG neurons (4-9%) are known to share a common glial envelop [42], whereas when peripheral nerve damage-induced neuropathic pain occurs, the percentage of activated SGCs surrounding DRG neurons and coupling with other SGCs significantly increased [43,44]. In this review, three studies observed the change of SGCs activities in the DRG after oxaliplatin administration [22][23][24].…”

Section: Discussionmentioning

confidence: 99%

The Role of Satellite Glial Cells, Astrocytes, and Microglia in Oxaliplatin-Induced Neuropathic Pain

Lee

Kim

2020

Biomedicines

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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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Satellite glia activation in dorsal root ganglion contributes to mechanical allodynia after selective motor fiber injury in adult rats

Cited by 23 publications

References 41 publications

Phenotypical peculiarities and species‐specific differences of canine and murine satellite glial cells of spinal ganglia

Phenotypical peculiarities and species‐specific differences of canine and murine satellite glial cells of spinal ganglia

Mediators of Neuropathic Pain; Focus on Spinal Microglia, CSF-1, BDNF, CCL21, TNF-α, Wnt Ligands, and Interleukin 1β

The Role of Satellite Glial Cells, Astrocytes, and Microglia in Oxaliplatin-Induced Neuropathic Pain

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