scholarly journals Puriner 2 Receptor Mediating the Communication between Neurons Cell Body and Satellite Glial Cells in Primary Sensory Ganglion

2016 ◽  
Vol 05 (01) ◽  
pp. 1-8
Author(s):  
唯 谢
Keyword(s):  
Glial Cells ◽  
Cell Body ◽  
Sensory Ganglion ◽  
Satellite Glial Cells

Cisplatin-induced activation and functional modulation of satellite glial cells lead to cytokine-mediated modulation of sensory neuron excitability

2021 ◽  
Vol 341 ◽  
pp. 113695
Author(s):  
Markus Leo ◽  
Linda-Isabell Schmitt ◽  
Andrea Kutritz ◽  
Christoph Kleinschnitz ◽  
Tim Hagenacker
Keyword(s):  
Sensory Neuron ◽  
Glial Cells ◽  
Satellite Glial Cells ◽  
Neuron Excitability ◽  
Functional Modulation

P2Y 14 receptor is functionally expressed in satellite glial cells and mediates interleukin‐1β and chemokine CCL2 secretion

2019 ◽  
Vol 234 (11) ◽  
pp. 21199-21210 ◽  
Author(s):  
Jiu Lin ◽  
Fei Liu ◽  
Yan‐yan Zhang ◽  
Ning Song ◽  
Meng‐ke Liu ◽  
...  
Keyword(s):  
Glial Cells ◽  
Interleukin 1Β ◽  
Satellite Glial Cells

scholarly journals Satellite glial cells in sensory ganglia express functional transient receptor potential ankyrin 1 that is sensitized in neuropathic and inflammatory pain

2020 ◽  
Vol 16 ◽  
pp. 174480692092542 ◽  
Author(s):  
Seung Min Shin ◽  
Brandon Itson-Zoske ◽  
Yongsong Cai ◽  
Chensheng Qiu ◽  
Bin Pan ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Nerve Injury ◽  
Glial Cells ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Allyl Isothiocyanate ◽  
Sensory Ganglia ◽  
Satellite Glial Cells ◽  
Intracellular Ca ◽  
Transient Receptor

Transient receptor potential ankyrin 1 (TRPA1) is well documented as an important molecule in pain hypersensitivity following inflammation and nerve injury and in many other cellular biological processes. Here, we show that TRPA1 is expressed not only by sensory neurons of the dorsal root ganglia (DRG) but also in their adjacent satellite glial cells (SGCs), as well as nonmyelinating Schwann cells. TRPA1 immunoreactivity is also detected in various cutaneous structures of sensory neuronal terminals, including small and large caliber cutaneous sensory fibers and endings. The SGC-expressed TRPA1 is functional. Like DRG neurons, dissociated SGCs exhibit a robust response to the TRPA1-selective agonist allyl isothiocyanate (AITC) by an increase of intracellular Ca2+ concentration ([Ca2+]i). These responses are abolished by the TRPA1 antagonist HC030031 and are absent in SGCs and neurons from global TRPA1 null mice. SGCs and neurons harvested from DRG proximal to painful tissue inflammation induced by plantar injection of complete Freund’s adjuvant show greater AITC-evoked elevation of [Ca2+]i and slower recovery compared to sham controls. Similar TRPA1 sensitization occurs in both SGCs and neurons during neuropathic pain induced by spared nerve injury. Together, these results show that functional TRPA1 is expressed by sensory ganglia SGCs, and TRPA1 function in SGCs is enhanced after both peripheral inflammation and nerve injury, and suggest that TRPA1 in SGCs may contribute to inflammatory and neuropathic pain.

Morphological and electrophysiological changes in mouse dorsal root ganglia after partial colonic obstruction

2005 ◽  
Vol 289 (4) ◽  
pp. G670-G678 ◽  
Author(s):  
Tian-Ying Huang ◽  
Menachem Hanani
Keyword(s):  
Glial Cells ◽  
Dorsal Root Ganglia ◽  
Dorsal Root ◽  
Neuronal Excitability ◽  
Colonic Obstruction ◽  
Resting Potential ◽  
Dye Coupling ◽  
Drg Neurons ◽  
Satellite Glial Cells ◽  
Colon Wall

There is evidence that sensitization of neurons in dorsal root ganglia (DRG) may contribute to pain induced by intestinal injury. We hypothesized that obstruction-induced pain is related to changes in DRG neurons and satellite glial cells (SGCs). In this study, partial colonic obstruction was induced by ligation. The neurons projecting to the colon were traced by an injection of 1,1′-dioctadecyl-3,3,3′,3′-tetramethylindocarbocyanine perchlorate into the colon wall. The electrophysiological properties of DRG neurons were determined using intracellular electrodes. Dye coupling was examined with an intracellular injection of Lucifer yellow (LY). Morphological changes in the colon and DRG were examined. Pain was assessed with von Frey hairs. Partial colonic obstruction caused the following changes. First, coupling between SGCs enveloping different neurons increased 18-fold when LY was injected into SGCs near neurons projecting to the colon. Second, neurons were not coupled to other neurons or SGCs. Third, the firing threshold of neurons projecting to the colon decreased by more than 40% ( P < 0.01), and the resting potential was more positive by 4–6 mV ( P < 0.05). Finally, the number of neurons displaying spontaneous spikes increased eightfold, and the number of neurons with subthreshold voltage oscillations increased over threefold. These changes are consistent with augmented neuronal excitability. The pain threshold to abdominal stimulation decreased by 70.2%. Inflammatory responses were found in the colon wall. We conclude that obstruction increased neuronal excitability, which is likely to be a major factor in the pain behavior observed. The augmented dye coupling between glial cells may contribute to the neuronal hyperexcitability.

Purinergic signaling between neurons and satellite glial cells of mouse dorsal root ganglia modulates neuronal excitability in vivo

Pain ◽  
2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Zhiyong Chen ◽  
Qian Huang ◽  
Xiaodan Song ◽  
Neil C. Ford ◽  
Chi Zhang ◽  
...  
Keyword(s):  
Glial Cells ◽  
Dorsal Root Ganglia ◽  
Dorsal Root ◽  
Neuronal Excitability ◽  
Purinergic Signaling ◽  
Satellite Glial Cells

scholarly journals Hemokinin-1 Gene Expression Is Upregulated in Trigeminal Ganglia in an Inflammatory Orofacial Pain Model: Potential Role in Peripheral Sensitization

2020 ◽  
Vol 21 (8) ◽  
pp. 2938
Author(s):  
Timea Aczél ◽  
Angéla Kecskés ◽  
József Kun ◽  
Kálmán Szenthe ◽  
Ferenc Bánáti ◽  
...  
Keyword(s):  
Gene Expression ◽  
Glial Cells ◽  
Orofacial Pain ◽  
Model Potential ◽  
Trigeminal System ◽  
Trigeminal Ganglia ◽  
Peripheral Sensitization ◽  
Satellite Glial Cells ◽  
Pain Model ◽  
Nociceptive Neurons

A large percentage of primary sensory neurons in the trigeminal ganglia (TG) contain neuropeptides such as tachykinins or calcitonin gene-related peptide. Neuropeptides released from the central terminals of primary afferents sensitize the secondary nociceptive neurons in the trigeminal nucleus caudalis (TNC), but also activate glial cells contributing to neuroinflammation and consequent sensitization in chronic orofacial pain and migraine. In the present study, we investigated the newest member of the tachykinin family, hemokinin-1 (HK-1) encoded by the Tac4 gene in the trigeminal system. HK-1 had been shown to participate in inflammation and hyperalgesia in various models, but its role has not been investigated in orofacial pain or headache. In the complete Freund’s adjuvant (CFA)-induced inflammatory orofacial pain model, we showed that Tac4 expression increased in the TG in response to inflammation. Duration-dependent Tac4 upregulation was associated with the extent of the facial allodynia. Tac4 was detected in both TG neurons and satellite glial cells (SGC) by the ultrasensitive RNAscope in situ hybridization. We also compared gene expression changes of selected neuronal and glial sensitization and neuroinflammation markers between wild-type and Tac4-deficient (Tac4-/-) mice. Expression of the SGC/astrocyte marker in the TG and TNC was significantly lower in intact and saline/CFA-treated Tac4-/- mice. The procedural stress-related increase of the SGC/astrocyte marker was also strongly attenuated in Tac4-/- mice. Analysis of TG samples with a mouse neuroinflammation panel of 770 genes revealed that regulation of microglia and cytotoxic cell-related genes were significantly different in saline-treated Tac4-/- mice compared to their wild-types. It is concluded that HK-1 may participate in neuron-glia interactions both under physiological and inflammatory conditions and mediate pain in the trigeminal system.

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