The effects of sympathetic nerve damage on satellite glial cells in the mouse superior cervical ganglion

Feldman-Goriachnik, Rachel; Hanani, Menachem

doi:10.1016/j.autneu.2019.102584

Cited by 11 publications

(9 citation statements)

References 73 publications

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“…SGCs in sensory ganglia are not sensitive to ACh 129 , which is consistent with the idea that there is a match between chemical messengers in neurons and the receptors in adjacent glia. A later work showed that selective injury to sympathetic nerve terminals activated SGCs in superior cervical ganglia, but not in sensory ones 130 . Conversely, LPS-induced inflammation, which activated SGCs in sensory ganglia, had no effect on SGCs in the superior cervical ganglia 130 .…”

Section: Sgcs In Sympathetic Gangliamentioning

confidence: 97%

“…A later work showed that selective injury to sympathetic nerve terminals activated SGCs in superior cervical ganglia, but not in sensory ones 130 . Conversely, LPS-induced inflammation, which activated SGCs in sensory ganglia, had no effect on SGCs in the superior cervical ganglia 130 . This selective activation correlates with the presence of TLR4 in sensory neurons, and their absence in sympathetic ones.…”

Section: Sgcs In Sympathetic Gangliamentioning

confidence: 97%

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Emerging importance of satellite glia in nervous system function and dysfunction

2020

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Satellite glial cells (SGCs) closely envelop cell bodies of neurons in sensory, sympathetic and parasympathetic ganglia. This unique organization is not found elsewhere in the nervous system. SGCs in sensory ganglia are activated by numerous types of nerve injury and inflammation. The activation includes upregulation of glial fibrillary acidic protein, stronger gap junction-mediated SGC–SGC and neuron–SGC coupling, increased sensitivity to ATP, downregulation of Kir4.1 potassium channels and increased cytokine synthesis and release. There is evidence that these changes in SGCs contribute to chronic pain by augmenting neuronal activity and that these changes are consistent in various rodent pain models and likely also in human pain. Therefore, understanding these changes and the resulting abnormal interactions of SGCs with sensory neurons could provide a mechanistic approach that might be exploited therapeutically in alleviation and prevention of pain. We describe how SGCs are altered in rodent models of four common types of pain: systemic inflammation (sickness behaviour), post-surgical pain, diabetic neuropathic pain and post-herpetic pain.

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Section: Sgcs In Sympathetic Gangliamentioning

confidence: 97%

Section: Sgcs In Sympathetic Gangliamentioning

confidence: 97%

Emerging importance of satellite glia in nervous system function and dysfunction

2020

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“…The authors suggested that this pattern difference between these ganglia may provide information about contribution of macrophages in neuronal insult and post injury hyperexcitability ( 92 ). Another study ( 93 ) demonstrated that when the sympathetic nerves in the superior cervical ganglia were damaged, SGCs became activated and underwent alterations consisting of coupling, higher sensitivity to ATP, and less responsiveness to acetylcholine. Interestingly, in this study, SGCs of the TG were not affected ( 93 ).…”

Section: Future Directions For Satellite Glial Cells In Pain Researchmentioning

confidence: 99%

Satellite Glial Cells in Pain Research: A Targeted Viewpoint of Potential and Future Directions

Gazerani

2021

Front. Pain Res.

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Chronic pain is known to be caused by sensitization within the pain circuits. An imbalance occurs between excitatory and inhibitory transmission that enables this sensitization to form. In addition to neurons, the contribution of central glia, especially astrocytes and microglia, to the pathogenesis of pain induction and maintenance has been identified. This has led to the targeting of astrogliosis and microgliosis to restore the normal functions of astrocytes and microglia to help reverse chronic pain. Gliosis is broadly defined as a reactive response of glial cells in response to insults to the central nervous system (CNS). The role of glia in the peripheral nervous system (PNS) has been less investigated. Accumulating evidence, however, points to the contribution of satellite glial cells (SGCs) to chronic pain. Hence, understanding the potential role of these cells and their interaction with sensory neurons has become important for identifying the mechanisms underlying pain signaling. This would, in turn, provide future therapeutic options to target pain. Here, a viewpoint will be presented regarding potential future directions in pain research, with a focus on SGCs to trigger further research. Promising avenues and new directions include the potential use of cell lines, cell live imaging, computational analysis, 3D tissue prints and new markers, investigation of glia–glia and macrophage–glia interactions, the time course of glial activation under acute and chronic pathological pain compared with spontaneous pain, pharmacological and non-pharmacological responses of glia, and potential restoration of normal function of glia considering sex-related differences.

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“…Wild-type and genetically-engineered mice are widely used to understand the mechanisms by which hypoxic challenges elicit carotid body-dependent and -independent ventilatory responses (He et al, 2000(He et al, , 2002(He et al, , 2003Kline and Prabhakar, 2000;Pérez-García et al, 2004;Kline et al, 2005;Pichard et al, 2015;Gao et al, 2017;Wang et al, 2017;Ortega-Sáenz et al, 2018;Peng et al, 2018;Prabhakar et al, 2018). The morphology, neurophysiology and neuropharmacology of the mouse CSC-SCG has received considerable investigation over the years (Black et al, 1972;Yokota and Yamauchi, 1974;Banks and Walter, 1975;Inoue, 1975;Lewis and Burton, 1977;Forehand, 1985;Kidd and Heath, 1988;Gibbins, 1991;Kasa et al, 1991;Little and Heath, 1994;Jobling and Gibbins, 1999;El-Fadaly and Kummer, 2003;David et al, 2010;Cadaveira-Mosquera et al, 2012;Pashai et al, 2012;Alberola-Die et al, 2013;Liu and Bean, 2014;Martinez-Pinna et al, 2018;Mitsuoka et al, 2018;Feldman-Goriachnik and Hanani, 2019;Simeone et al, 2019;Rivas-Ramírez et al, 2020). Mouse tissues that receive post-ganglionic projections from the SCG have also been heavily investigated (Krieger et al, 1976;García et al, 1988;…”

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confidence: 99%

Loss of Cervical Sympathetic Chain Input to the Superior Cervical Ganglia Affects the Ventilatory Responses to Hypoxic Challenge in Freely-Moving C57BL6 Mice

et al. 2021

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The cervical sympathetic chain (CSC) innervates post-ganglionic sympathetic neurons within the ipsilateral superior cervical ganglion (SCG) of all mammalian species studied to date. The post-ganglionic neurons within the SCG project to a wide variety of structures, including the brain (parenchyma and cerebral arteries), upper airway (e.g., nasopharynx and tongue) and submandibular glands. The SCG also sends post-ganglionic fibers to the carotid body (e.g., chemosensitive glomus cells and microcirculation), however, the function of these connections are not established in the mouse. In addition, nothing is known about the functional importance of the CSC-SCG complex (including input to the carotid body) in the mouse. The objective of this study was to determine the effects of bilateral transection of the CSC on the ventilatory responses [e.g., increases in frequency of breathing (Freq), tidal volume (TV) and minute ventilation (MV)] that occur during and following exposure to a hypoxic gas challenge (10% O2 and 90% N2) in freely-moving sham-operated (SHAM) adult male C57BL6 mice, and in mice in which both CSC were transected (CSCX). Resting ventilatory parameters (19 directly recorded or calculated parameters) were similar in the SHAM and CSCX mice. There were numerous important differences in the responses of CSCX and SHAM mice to the hypoxic challenge. For example, the increases in Freq (and associated decreases in inspiratory and expiratory times, end expiratory pause, and relaxation time), and the increases in MV, expiratory drive, and expiratory flow at 50% exhaled TV (EF50) occurred more quickly in the CSCX mice than in the SHAM mice, although the overall responses were similar in both groups. Moreover, the initial and total increases in peak inspiratory flow were higher in the CSCX mice. Additionally, the overall increases in TV during the latter half of the hypoxic challenge were greater in the CSCX mice. The ventilatory responses that occurred upon return to room-air were essentially similar in the SHAM and CSCX mice. Overall, this novel data suggest that the CSC may normally provide inhibitory input to peripheral (e.g., carotid bodies) and central (e.g., brainstem) structures that are involved in the ventilatory responses to hypoxic gas challenge in C57BL6 mice.

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The effects of sympathetic nerve damage on satellite glial cells in the mouse superior cervical ganglion

Cited by 11 publications

References 73 publications

Emerging importance of satellite glia in nervous system function and dysfunction

Emerging importance of satellite glia in nervous system function and dysfunction

Satellite Glial Cells in Pain Research: A Targeted Viewpoint of Potential and Future Directions

Loss of Cervical Sympathetic Chain Input to the Superior Cervical Ganglia Affects the Ventilatory Responses to Hypoxic Challenge in Freely-Moving C57BL6 Mice

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