scholarly journals Disrupted Association of Sensory Neurons With Enveloping Satellite Glial Cells in Fragile X Mouse Model

2022 ◽  
Vol 14 ◽  
Author(s):  
Oshri Avraham ◽  
Pan-Yue Deng ◽  
Dario Maschi ◽  
Vitaly A. Klyachko ◽  
Valeria Cavalli
Keyword(s):  
Sensory Neuron ◽  
Glial Cells ◽  
Fragile X ◽  
Sensory System ◽  
Structural Defects ◽  
Learning Networks ◽  
Sensory Stimuli ◽  
Satellite Glial Cells ◽  
Sensory Deficits ◽  
Peripheral Sensory

Among most prevalent deficits in individuals with Fragile X syndrome (FXS) is hypersensitivity to sensory stimuli and somatosensory alterations. Whether dysfunction in peripheral sensory system contributes to these deficits remains poorly understood. Satellite glial cells (SGCs), which envelop sensory neuron soma, play critical roles in regulating neuronal function and excitability. The potential contributions of SGCs to sensory deficits in FXS remain unexplored. Here we found major structural defects in sensory neuron-SGC association in the dorsal root ganglia (DRG), manifested by aberrant covering of the neuron and gaps between SGCs and the neuron along their contact surface. Single-cell RNAseq analyses demonstrated transcriptional changes in both neurons and SGCs, indicative of defects in neuronal maturation and altered SGC vesicular secretion. We validated these changes using fluorescence microscopy, qPCR, and high-resolution transmission electron microscopy (TEM) in combination with computational analyses using deep learning networks. These results revealed a disrupted neuron-glia association at the structural and functional levels. Given the well-established role for SGCs in regulating sensory neuron function, altered neuron-glia association may contribute to sensory deficits in FXS.

scholarly journals Hyperexcitability of Sensory Neurons in Fragile X Mouse Model

2021 ◽  
Vol 14 ◽  
Author(s):  
Pan-Yue Deng ◽  
Oshri Avraham ◽  
Valeria Cavalli ◽  
Vitaly A. Klyachko
Keyword(s):  
Mouse Model ◽  
Sensory Neuron ◽  
Sensory Neurons ◽  
Fragile X ◽  
Input Resistance ◽  
Resting Membrane Potential ◽  
Hcn Channels ◽  
Satellite Glial Cells ◽  
Peripheral Sensory Neurons ◽  
Peripheral Sensory

Sensory hypersensitivity and somatosensory deficits represent the core symptoms of Fragile X syndrome (FXS). These alterations are believed to arise from changes in cortical sensory processing, while potential deficits in the function of peripheral sensory neurons residing in dorsal root ganglia remain unexplored. We found that peripheral sensory neurons exhibit pronounced hyperexcitability in Fmr1 KO mice, manifested by markedly increased action potential (AP) firing rate and decreased threshold. Unlike excitability changes found in many central neurons, no significant changes were observed in AP rising and falling time, peak potential, amplitude, or duration. Sensory neuron hyperexcitability was caused primarily by increased input resistance, without changes in cell capacitance or resting membrane potential. Analyses of the underlying mechanisms revealed reduced activity of HCN channels and reduced expression of HCN1 and HCN4 in Fmr1 KO compared to WT. A selective HCN channel blocker abolished differences in all measures of sensory neuron excitability between WT and Fmr1 KO neurons. These results reveal a hyperexcitable state of peripheral sensory neurons in Fmr1 KO mice caused by dysfunction of HCN channels. In addition to the intrinsic neuronal dysfunction, the accompanying paper examines deficits in sensory neuron association/communication with their enveloping satellite glial cells, suggesting contributions from both neuronal intrinsic and extrinsic mechanisms to sensory dysfunction in the FXS mouse model.

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

scholarly journals Glial ensheathment of the somatodendritic compartment regulates sensory neuron structure and activity

2019 ◽  
Vol 116 (11) ◽  
pp. 5126-5134 ◽  
Author(s):  
Smita Yadav ◽  
Susan H. Younger ◽  
Linghua Zhang ◽  
Katherine L. Thompson-Peer ◽  
Tun Li ◽  
...  
Keyword(s):  
Sensory Neuron ◽  
Sensory Neurons ◽  
Cell Types ◽  
Environmental Cues ◽  
Sensory Stimuli ◽  
Neuronal Soma ◽  
Selective Elimination ◽  
Light Stimuli ◽  
Peripheral Sensory ◽  
Structure And Activity

Sensory neurons perceive environmental cues and are important of organismal survival. Peripheral sensory neurons interact intimately with glial cells. While the function of axonal ensheathment by glia is well studied, less is known about the functional significance of glial interaction with the somatodendritic compartment of neurons. Herein, we show that three distinct glia cell types differentially wrap around the axonal and somatodendritic surface of the polymodal dendritic arborization (da) neuron of the Drosophila peripheral nervous system for detection of thermal, mechanical, and light stimuli. We find that glial cell-specific loss of the chromatin modifier gene dATRX in the subperineurial glial layer leads to selective elimination of somatodendritic glial ensheathment, thus allowing us to investigate the function of such ensheathment. We find that somatodendritic glial ensheathment regulates the morphology of the dendritic arbor, as well as the activity of the sensory neuron, in response to sensory stimuli. Additionally, glial ensheathment of the neuronal soma influences dendritic regeneration after injury.

scholarly journals Growth and Survival of Satellite Glial Cells in Different Culture Supplementations

2021 ◽  
Author(s):  
Na Wei ◽  
Ya-Ping Liu ◽  
Rui-Rui Wang ◽  
Xiao-Liang Wang ◽  
Yan Yang ◽  
...  
Keyword(s):  
Cell Death ◽  
Glial Cells ◽  
High Purity ◽  
Biological Properties ◽  
Neonatal Rats ◽  
Satellite Glial Cells ◽  
Growth And Survival ◽  
Sensory Transmission ◽  
Peripheral Sensory ◽  
Nutrition Source

Abstract Background: In dorsal root ganglion (DRG), satellite glial cells (SGCs) tightly surrounded neurons and modulated microenvironment and sensory transmission. However, the biological properties of primary SGCs in culture were not fully understood. In the present study, we provided a method to harvest abundant and high-purity SGCs from neonatal rats. Three supplementations containing Dulbecco’s Modified Eagle Medium (DMEM)/F12, DMEM high glucose (HG) and Neurobasal-A (NB) were used to evaluate SGCs growth and survival in culture. Results: CCK-8 proliferation assay showed the increased proliferation in DMEM/F12 and DMEM/HG, but not in NB medium. NB medium caused cell death indicated by Bax, AnnexinV and PI staining. Glutamine was the major nutrition source for SGCs in culture and its exogenous application improved the poor proliferation and severe cell death in NB medium. SGCs markers GS and GFAP were similar in three supplementations and intensively expressed in culture. Differently, GS but not GFAP was remarkable in the intact DRG under normal condition. Conclusions: These results suggested that SGCs growth in culture depended on time and culture supplementation and DMEM/F12 medium was recommended to get high-purity SGCs. Glutamine was the major nutrition and the key molecule to maintain cell growth and survival in culture. Our study shed a new light on understanding the biological property and modulation of glial cells in the peripheral sensory ganglia.

scholarly journals Connexin43 Hemichannels in Satellite Glial Cells, Can They Influence Sensory Neuron Activity?

2017 ◽  
Vol 10 ◽  
Author(s):  
Mauricio A. Retamal ◽  
Manuel A. Riquelme ◽  
Jimmy Stehberg ◽  
Julio Alcayaga
Keyword(s):  
Sensory Neuron ◽  
Glial Cells ◽  
Neuron Activity ◽  
Satellite Glial Cells

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.

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