The role of chemical transmitters in neuron-glia interaction and pain in sensory ganglion

Matsuka, Yoshizo; Afroz, Shaista; Dalanon, Junhel; Iwasa, Takuma; Waskitho, Arief; Oshima, Masamitsu

doi:10.1016/j.neubiorev.2019.11.019

Cited by 20 publications

(19 citation statements)

References 115 publications

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“…The lack of a blood barrier around the DRG paired with further increases in vascular permeability after injury could contribute to increased delivery of these circulating mediators to DRG neurons and satellite glia, thus altering neuronal excitability or priming for activation by other pathways. In fact, after nerve injury, coincident exposure of cytokines, chemical modulators, and other neuronal mechanisms are thought to contribute to the persistence of pain (Matsuka et al, 2020).…”

Section: A Synopsis Of the Neuropathology Of Axotomymentioning

confidence: 99%

“…In addition to neuron-glia interactions, increased glia-glia coupling is likewise associated with chemotherapyinduced neuropathic pain (Warwick and Hanani, 2013). An emerging hypothesis proposes that changes in neural excitation activate surrounding glia and cause them to release cytokines and other signaling molecules that contribute to pain (Matsuka et al, 2020). These studies show heterogeneity in the pattern of coupling that includes a subset of Aβ LTMRs and TrpV1positive nociceptors, yet it remains unclear whether this coupling involves injured neurons, uninjured neurons, or a mixture of both.…”

Section: Injury-induced Intra-ganglionic Plasticitymentioning

confidence: 99%

“…The ability to fire action potentials in the presence of GABA is therefore dependent upon the physiology and relative abundance of GABA receptors and various chloride channels, and these may differ across distinct types of neurons after injury. Interestingly, satellite glial cells could also be implicated in these mechanisms, as they are reported to have the ability to store GABA (Matsuka et al, 2020). Cell-specific changes in these chloride channels have not been thoroughly explored in the context of neuropathic pain.…”

Section: Possible Mechanisms Unexplored In the Context Of Nerve Injurymentioning

confidence: 99%

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Revisiting PNS Plasticity: How Uninjured Sensory Afferents Promote Neuropathic Pain

Tran

Crawford

2020

Front. Cell. Neurosci.

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Despite the widespread study of how injured nerves contribute to chronic pain, there are still major gaps in our understanding of pain mechanisms. This is particularly true of pain resulting from nerve injury, or neuropathic pain, wherein tactile or thermal stimuli cause painful responses that are particularly difficult to treat with existing therapies. Curiously, this stimulus-driven pain relies upon intact, uninjured sensory neurons that transmit the signals that are ultimately sensed as painful. Studies that interrogate uninjured neurons in search of cell-specific mechanisms have shown that nerve injury alters intact, uninjured neurons resulting in an activity that drives stimulus-evoked pain. This review of neuropathic pain mechanisms summarizes cell-type-specific pathology of uninjured sensory neurons and the sensory ganglia that house their cell bodies. Uninjured neurons have demonstrated a wide range of molecular and neurophysiologic changes, many of which are distinct from those detected in injured neurons. These intriguing findings include expression of pain-associated molecules, neurophysiological changes that underlie increased excitability, and evidence that intercellular signaling within sensory ganglia alters uninjured neurons. In addition to well-supported findings, this review also discusses potential mechanisms that remain poorly understood in the context of nerve injury. This review highlights key questions that will advance our understanding of the plasticity of sensory neuron subpopulations and clarify the role of uninjured neurons in developing anti-pain therapies.

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Section: A Synopsis Of the Neuropathology Of Axotomymentioning

confidence: 99%

Section: Injury-induced Intra-ganglionic Plasticitymentioning

confidence: 99%

Section: Possible Mechanisms Unexplored In the Context Of Nerve Injurymentioning

confidence: 99%

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Revisiting PNS Plasticity: How Uninjured Sensory Afferents Promote Neuropathic Pain

Tran

Crawford

2020

Front. Cell. Neurosci.

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“…Injection of CGRP stimulates the activation of spinal cord microglia in a model of temporomandibular joint disorder, as evidenced by increased OX-42 immunostaining [ 8 ]. Indeed, several findings support the role of SGC and Schwann cells in regulating responses to pain in the trigeminal ganglion (TG) and DRG [ 4 ]. In our previous research, we observed that when CGRP was injected into the TG, it resulted in thermal hyperalgesia in first 6 h, and this was accompanied by an increase in the gene expression of proinflammatory cytokine IL-1β and IL-6 and anti-inflammatory cytokine IL-1RA, as well as an increase in the expression of glial fibrillary acidic protein (GFAP), a marker of glial activation [ 13 ].…”

Section: Introductionmentioning

confidence: 96%

“…Immune activation and the subsequent release of immune mediators in the peripheral nervous system (PNS) contribute to pain [ 1 , 2 ]. The release of cytokines and inflammatory mediators from the peripheral glial cells (satellite glial cells (SGC) or Schwann cells) or blood derived immune cells (mast cells, macrophages, and lymphocytes) in response to some trauma or noxious stimuli to the PNS, has been shown by various researchers to be responsible for causing peripheral and central sensitization, thereby contributing to the development of allodynia and hyperalgesia, two hallmarks of neuropathic pain (NP) [ 1 , 2 , 3 , 4 ]. Different kinds of sciatic nerve injury lead to the activation of nuclear factor kappa B (NF-κB) in dorsal root ganglion (DRG) neurons and in some Schwann cells surrounding unmyelinated fibers in a chronic constriction injury model (CCI) [ 5 ].…”

Section: Introductionmentioning

confidence: 99%

Role of CGRP in Neuroimmune Interaction via NF-κB Signaling Genes in Glial Cells of Trigeminal Ganglia

Afroz

Arakaki

Iwasa

et al. 2020

IJMS

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Activation of the trigeminal system causes the release of various neuropeptides, cytokines, and other immune mediators. Calcitonin gene-related peptide (CGRP), which is a potent algogenic mediator, is expressed in the peripheral sensory neurons of trigeminal ganglion (TG). It affects the inflammatory responses and pain sensitivity by modulating the activity of glial cells. The primary aim of this study was to use array analysis to investigate the effect of CGRP on the glial cells of TG in regulating nuclear factor kappa B (NF-κB) signaling genes and to further check if CGRP in the TG can affect neuron-glia activation in the spinal trigeminal nucleus caudalis. The glial cells of TG were stimulated with CGRP or Minocycline (Min) + CGRP. The effect on various genes involved in NF-κB signaling pathway was analyzed compared to no treatment control condition using a PCR array analysis. CGRP, Min + CGRP or saline was directly injected inside the TG and the effect on gene expression of Egr1, Myd88 and Akt1 and protein expression of cleaved Caspase3 (cleav Casp3) in the TG, and c-Fos and glial fibrillary acidic protein (GFAP) in the spinal section containing trigeminal nucleus caudalis was analyzed. Results showed that CGRP stimulation resulted in the modulation of several genes involved in the interleukin 1 signaling pathway and some genes of the tumor necrosis factor pathway. Minocycline pre-treatment resulted in the modulation of several genes in the glial cells, including anti-inflammatory genes, and neuronal activation markers. A mild increase in cleav Casp3 expression in TG and c-Fos and GFAP in the spinal trigeminal nucleus of CGRP injected animals was observed. These data provide evidence that glial cells can participate in neuroimmune interaction due to CGRP in the TG via NF-κB signaling pathway.

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Sensory root demyelination: Transforming touch into pain

Ding

2021

Glia

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The role of chemical transmitters in neuron-glia interaction and pain in sensory ganglion

Cited by 20 publications

References 115 publications

Revisiting PNS Plasticity: How Uninjured Sensory Afferents Promote Neuropathic Pain

Revisiting PNS Plasticity: How Uninjured Sensory Afferents Promote Neuropathic Pain

Role of CGRP in Neuroimmune Interaction via NF-κB Signaling Genes in Glial Cells of Trigeminal Ganglia

Sensory root demyelination: Transforming touch into pain

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