Biology and Pathology of Perineuronal Satellite Cells in Sensory Ganglia

Pannese, Ennio

doi:10.1007/978-3-319-60140-3_1

Cited by 12 publications

(8 citation statements)

References 322 publications

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“…Afferent firing or excitatory transmitters such as calcitonin gene-related peptide (CGRP; Li, Vause, & Durham, 2008) or ATP (Borsani et al, 2010) raise intracellular Ca 2+ ([Ca 2+ ] in ) in sensory neurons, which in turn induces NOS activation and NO production. Sensory neurons are enveloped by satellite glial cells (SGCs) with a gap of only 20 nm between these cells types (Hanani, 2005(Hanani, , 2015Pannese, 2018). Therefore, NO that is produced in the neurons can reach SGCs easily by diffusion and induces cGMP synthesis in them (Morris, Southam, Braid, & Garthwaite, 1992;Thippeswamy & Morris, 2002).…”

Section: Introductionmentioning

confidence: 99%

Nitric oxide as a messenger between neurons and satellite glial cells in dorsal root ganglia

Belzer

Hanani

2019

Glia

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Abnormal neuronal activity in sensory ganglia contributes to chronic pain. There is evidence that signals can spread between cells in these ganglia, which may contribute to this activity. Satellite glial cells (SGCs) in sensory ganglia undergo activation following peripheral injury and participate in cellular communication via gap junctions and chemical signaling. Nitric oxide (NO) is released from neurons in dorsal root ganglia (DRG) and induces cyclic GMP (cGMP) production in SCGs, but its role in SGC activation and neuronal excitability has not been explored. It was previously reported that induction of intestinal inflammation with dinitrobenzoate sulfonate (DNBS) increased gap junctional communications among SGCs, which contributed to neuronal excitability and pain. Here we show that DNBS induced SGC activation in mouse DRG, as assayed by glial fibrillary acidic protein upregulation. DNBS also upregulated cGMP level in SGCs, consistent with NO production. In vitro studies on intact ganglia from DNBS‐treated mice showed that blocking NO synthesis inhibited both SGCs activation and cGMP upregulation, indicating an ongoing NO production. Application of NO donor in vitro induced SGC activation, augmented gap junctional communications, and raised neuronal excitability, as assessed by electrical recordings. The cGMP analog 8‐Br‐cGMP mimicked these actions, confirming the role of the NO‐cGMP pathway in intraganglionic communications. NO also augmented Ca2+ waves propagation in DRG cultures. It is proposed that NO synthesis in DRG neurons increases after peripheral inflammation and that NO induces SGC activation, which in turn contributes to neuronal hyperexcitability. Thus, NO plays a major role in neuron–SGC communication.

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Section: Introductionmentioning

confidence: 99%

Nitric oxide as a messenger between neurons and satellite glial cells in dorsal root ganglia

Belzer

Hanani

2019

Glia

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“…Since the discovery of SGCs of the spinal ganglia many decades ago (Pannese, 1956;Pannese, 1964), the precise function of these specialized glial cells has been actively investigated with promising progress. As to the current, we understand that SGCs can respond to neuronal signals during pain states.…”

Section: Discussionmentioning

confidence: 99%

Satellite Glial Cells Bridge Sensory Neuron Crosstalk in Visceral Pain and Cross-Organ Sensitization

Qiao

2024

J Pharmacol Exp Ther

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Following colonic inflammation, the uninjured bladder afferent neurons are also activated.The mechanisms and pathways underlying this sensory neuron cross-activation (from injured neurons to uninjured neurons) are not fully understood. Colonic and bladder afferent neurons reside in the same spinal segments and are separated by satellite glial cells (SGCs) and extracellular matrix in dorsal root ganglia (DRG). SGCs communicate with sensory neurons in a bidirectional fashion. In this review, I summarize the differentially regulated genes/proteins in the injured and uninjured DRG neurons and explore the role of SGCs in regulation of sensory neuron crosstalk in visceral cross-organ sensitization. I also highlight the paracrine pathways in mediating neuron-SGC and SGC-neuron coupling with an emphasis on the neurotrophins and purinergic systems. Finally, I discuss the results from recent RNAseq profiling of SGCs to reveal useful molecular markers for characterization, functional study, and therapeutic targets of SGCs.Keywords: satellite glial cells; dorsal root ganglia; crosstalk; colon; bladder; pain Significant Statements: Satellite glial cells (SGCs) are the largest glial subtypes in sensory ganglia and play a critical role in mediating sensory neuron crosstalk, an underlying mechanism in colon-bladder cross-sensitization. Identification of novel and unique molecular markers of SGCs can advance the discovery of therapeutics targets in treatment of chronic pain including visceral pain comorbidity.

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“…The available evidence suggests that peripheral nerve injury leads to a sensitization of sensory neurons in DRG and evokes SGCs activation. These reactions result in the release of ATP from neurons, leading to the synthesis and release of glial mediators (pro-inflammatory cytokines and chemokines) from SGCs, modulation of glutamate transporters and ion channels as well as an increased neuron–SGC–SGC–neuron coupling which in turn lead to neuronal hyperexcitability and pain [ 18 , 19 , 22 , 47 , 48 , 49 ]. These data are in line with our results, where functional and structural peripheral nerve alterations induced by PTX chronic administration were correlated with the SGC activation and with the occurrence of mechanical allodynia.…”

Section: Discussionmentioning

confidence: 99%

Paclitaxel, but Not Cisplatin, Affects Satellite Glial Cells in Dorsal Root Ganglia of Rats with Chemotherapy-Induced Peripheral Neurotoxicity

Pozzi

Ballarini

Rodriguez-Menendez

et al. 2023

Toxics

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Chemotherapy-induced peripheral neurotoxicity is one of the most common dose-limiting toxicities of several widely used anticancer drugs such as platinum derivatives (cisplatin) and taxanes (paclitaxel). Several molecular mechanisms related to the onset of neurotoxicity have already been proposed, most of them having the sensory neurons of the dorsal root ganglia (DRG) and the peripheral nerve fibers as principal targets. In this study we explore chemotherapy-induced peripheral neurotoxicity beyond the neuronocentric view, investigating the changes induced by paclitaxel (PTX) and cisplatin (CDDP) on satellite glial cells (SGC) in the DRG and their crosstalk. Rats were chronically treated with PTX (10 mg/Kg, 1qwx4) or CDDP (2 mg/Kg 2qwx4) or respective vehicles. Morpho-functional analyses were performed to verify the features of drug-induced peripheral neurotoxicity. Qualitative and quantitative immunohistochemistry, 3D immunofluorescence, immunoblotting, and transmission electron microscopy analyses were also performed to detect alterations in SGCs and their interconnections. We demonstrated that PTX, but not CDDP, produces a strong activation of SGCs in the DRG, by altering their interconnections and their physical contact with sensory neurons. SGCs may act as principal actors in PTX-induced peripheral neurotoxicity, paving the way for the identification of new druggable targets for the treatment and prevention of chemotherapy-induced peripheral neurotoxicity.

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Biology and Pathology of Perineuronal Satellite Cells in Sensory Ganglia

Cited by 12 publications

References 322 publications

Nitric oxide as a messenger between neurons and satellite glial cells in dorsal root ganglia

Nitric oxide as a messenger between neurons and satellite glial cells in dorsal root ganglia

Satellite Glial Cells Bridge Sensory Neuron Crosstalk in Visceral Pain and Cross-Organ Sensitization

Paclitaxel, but Not Cisplatin, Affects Satellite Glial Cells in Dorsal Root Ganglia of Rats with Chemotherapy-Induced Peripheral Neurotoxicity

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