Activation of Satellite Glial Cells in Rat Trigeminal Ganglion after Upper Molar Extraction

Gunjigake, Kaori; Goto, Tetsuya; Nakao, Kayoko; Kobayashi, Shigeru; Yamaguchi, Kazunori

doi:10.1267/ahc.09017

Cited by 33 publications

(31 citation statements)

References 30 publications

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“…We also found no evidence of SGC stress as indicated by ATF3 immunoreactivity, a member of the ATF/cAMP family of transcription factors that is upregulated by nerve injury and other stress responses (Tsujino et al, 2000). This corresponds with other studies that have not reported ATF3 in SGCs after tooth extraction (Gunjigake et al, 2009) or CCI of the ION in mice (Xu et al, 2008). However, ATF3 has been reported in SGCs 7 days following paclitaxel induced nerve injury (Peters et al, 2007).…”

Section: Discussionsupporting

confidence: 92%

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Satellite glial cell proliferation in the trigeminal ganglia after chronic constriction injury of the infraorbital nerve

Donegan

Kernisant

Cua

et al. 2013

Glia

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We have examined satellite glial cell (SGC) proliferation in trigeminal ganglia following chronic constriction injury of the infraorbital nerve. Using BrdU labeling combined with immunohistochemistry for SGC specific proteins we positively confirmed proliferating cells to be SGCs. Proliferation peaks at approximately 4 days after injury and dividing SGCs are preferentially located around neurons that are immunopositive for ATF-3, a marker of nerve injury. After nerve injury there is an increase GFAP expression in SGCs associated with both ATF-3 immunopositive and immunonegative neurons throughout the ganglia. SGCs also express the non-glial proteins, CD45 and CD163, which label resident macrophages and circulating leukocytes, respectively. In addition to SGCs, we found some Schwann cells, endothelial cells, resident macrophages, and circulating leukocytes were BrdU immunopositive.

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Section: Discussionsupporting

confidence: 92%

“…4A1). The time of GFAP expression in SGCs seems to vary depending on the injury model (Gunjigake et al, 2009; Mika et al, 2010; Peters et al, 2007; Xie et al, 2009). As previously reported, GFAP immunoreactivity was not seen in contralateral (control) ganglia but was visible in the trigeminal ganglia ipsilateral to the injured nerve.…”

Section: Resultsmentioning

confidence: 99%

Satellite glial cell proliferation in the trigeminal ganglia after chronic constriction injury of the infraorbital nerve

Donegan

Kernisant

Cua

et al. 2013

Glia

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“…Beyond evidence of altered neuron/SGC communication in response to reduced neuronal p75NTR expression, the SGC/SGC communication axis is also likely altered by the increased incidence of gap junction Cx43 expression in SGCs, normally observed at lower levels in the absence of nerve injury . This implies increased SGC coupling may occur and also parallels changes observed following nerve injury (Gunjigake et al, 2009).…”

Section: Induction Of a Reactive State In Perineuronal Sgcsmentioning

confidence: 55%

Induction of a reactive state in perineuronal satellite glial cells akin to that produced by nerve injury is linked to the level of p75NTR expression in adult sensory neurons

Nadeau

Wilson-Gerwing

Verge

2014

Glia

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Satellite glial cells (SGCs) surrounding primary sensory neurons are similar to astrocytes of the central nervous system in that they buffer the extracellular environment via potassium and calcium channels and express the intermediate filament glial fibrillary acidic protein (GFAP). Peripheral nerve injury induces a reactive state in SGCs that includes SGC proliferation, increased SGC/SGC coupling via gap junctions, decreased inward rectifying potassium channel 4.1 (Kir 4.1) expression and increased expression of GFAP and the common neurotrophin receptor, p75NTR. In contrast, neuronal p75NTR expression, normally detected in ∼80% of adult rat sensory neurons, decreases in response to peripheral axotomy. Given the differential regulation of p75NTR expression in neurons versus SGCs with injury, we hypothesized that reduced signaling via neuronal p75NTR contributes to the induction of a reactive state in SGCs. We found that reducing neuronal p75NTR protein expression in uninjured sensory neurons by intrathecal subarachnoid infusion of p75NTR-selective anti-sense oligodeoxynucleotides for one week was sufficient to induce a "reactive-like" state in the perineuronal SGCs akin to that normally observed following peripheral nerve injury. This reactive state included significantly increased SGC p75NTR, GFAP and gap junction protein connexin-43 protein expression, increased numbers of SGCs surrounding individual sensory neurons and decreased SGC Kir 4.1 channel expression. Collectively, this supports the tenet that reductions in target-derived trophic support leading to, or as a consequence of, reduced neuronal p75NTR expression plays a critical role in switching the SGC to a reactive state.

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“…Like other glial cells, the satellite glial cells are known to respond to nerve injury by up-regulating GFAP [61]. We identified Schwann cells in rhesus DRG tissue explants by the expression of p75NTR and CNPase [29,30,62].…”

Section: Discussionmentioning

confidence: 99%

The Lyme disease spirochete Borrelia burgdorferi induces inflammation and apoptosis in cells from dorsal root ganglia

Ramesh

Santana-Gould

Inglis

et al. 2013

J Neuroinflammation

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BackgroundLyme neuroborreliosis (LNB), caused by the spirochete Borrelia burgdorferi, affects both the peripheral and the central nervous systems. Radiculitis or nerve root inflammation, which can cause pain, sensory loss, and weakness, is the most common manifestation of peripheral LNB in humans. We previously reported that rhesus monkeys infected with B. burgdorferi develop radiculitis as well as inflammation in the dorsal root ganglia (DRG), with elevated levels of neuronal and satellite glial cell apoptosis in the DRG. We hypothesized that B. burgdorferi induces inflammatory mediators in glial and neuronal cells and that this inflammatory milieu precipitates glial and neuronal apoptosis.MethodsTo model peripheral neuropathy in LNB we incubated normal rhesus DRG tissue explants with live B. burgdorferi ex vivo and identified immune mediators, producer cells, and verified the presence of B. burgdorferi in tissue sections by immunofluorescence staining and confocal microscopy. We also set up primary cultures of DRG cells from normal adult rhesus macaques and incubated the cultures with live B. burgdorferi. Culture supernatants were subjected to multiplex ELISA to detect immune mediators, while the cells were evaluated for apoptosis by the in situ TUNEL assay. A role for inflammation in mediating apoptosis was assessed by evaluating the above phenomena in the presence and absence of various concentrations of the anti-inflammatory drug dexamethasone. As Schwann cells ensheath the dorsal roots of the DRG, we evaluated the potential of live B. burgdorferi to induce inflammatory mediators in human Schwann cell (HSC) cultures.ResultsRhesus DRG tissue explants exposed to live B. burgdorferi showed localization of CCL2 and IL-6 in sensory neurons, satellite glial cells and Schwann cells while IL-8 was seen in satellite glial cells and Schwann cells. Live B. burgdorferi induced elevated levels of IL-6, IL-8 and CCL2 in HSC and DRG cultures and apoptosis of sensory neurons. Dexamethasone reduced the levels of immune mediators and neuronal apoptosis in a dose dependent manner.ConclusionIn this model, B. burgdorferi induced an inflammatory response and neuronal apoptosis of DRG. These pathophysiological processes could contribute to peripheral neuropathy in LNB.

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Activation of Satellite Glial Cells in Rat Trigeminal Ganglion after Upper Molar Extraction

Cited by 33 publications

References 30 publications

Satellite glial cell proliferation in the trigeminal ganglia after chronic constriction injury of the infraorbital nerve

Satellite glial cell proliferation in the trigeminal ganglia after chronic constriction injury of the infraorbital nerve

Induction of a reactive state in perineuronal satellite glial cells akin to that produced by nerve injury is linked to the level of p75NTR expression in adult sensory neurons

The Lyme disease spirochete Borrelia burgdorferi induces inflammation and apoptosis in cells from dorsal root ganglia

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