J Anesth Perioper Med. 2018;5(6):333-342. https://doi.org/10.24015/ebcmed.japm.2018.0114

How Do Satellite Glial Cells Control Chronic Pain?

Xiaojuan Liu1,2, Travis Goettemoeller1, and Temugin Berta1

From the 1Pain Research Center, Department of Anesthesiology, University of Cincinnati College of Medicine, Cincinnati, OH, USA; 2Department of Pathogen Biology, Medical College, Nantong University, Nantong, China.

Correspondence to Dr. Temugin Berta at temugin.berta@uc.edu.

EBCMED ID: ebcmed.japm.2018.0114 DOI: 10.24015/ebcmed.japm.2018.0114


Aim of review
Pain afflicts more than 1.5 billion people worldwide, with hundreds of millions suffering from unrelieved chronic pain. Accumulating evidence suggests that satellite glial cells (SGCs) play active roles in the pathogenesis of pain. We review how SGCs interact with nociceptive neurons by secreting neuroactive signaling molecules that modulate pain, which may offer new therapeutic strategies for the prevention and treatment of chronic pain.

According to the available literature, we first described the morphology and physiology of SGCs in sensory ganglia and then provided an overview of the signaling molecules by which SGCs contribute to the modulation of the neuronal activity in various animal models of acute and chronic pain. Finally, we addressed some outstanding questions about SGCs that remain to be answered in future research and clinical applications.

Recent findings
Accumulating evidence has implicated structural and biochemical changes in SGCs in chronic pain: gliosis (i.e. proliferation), increase in expression of glial fibrillary acidic protein (a marker for their activation), modulation of glutamate transporters and ion channels, increases in purinergic and cytokine signaling, as well as aberrant connectivity between neighboring SGCs and sensory neurons. These changes alter the activity of sensory neurons and contribute to the development and maintenance of chronic pain. Remarkably, SGCs also participate in acute pain, and acute opioid treatment activates SGCs to mask opioid analgesia.

SGCs are now recognized players in the pathogenesis of chronic pain through the secretion of neuroactive signaling molecules and controls of nociceptive neurons. Given the inadequate treatment of chronic pain by the current “neurocentric” drugs, these recently recognized roles of SGCs and their neuroactive signaling molecules are exciting as they predict novel approaches for effective control of chronic pain. (Funded by the National Institutes of Health/National Institute of Neurological Disorders and Stroke (NIH/NINDS), and the University of Cincinnati.)

Article Type
Review Article

Declaration of Interests
The authors declare no conflicts of interest.

This study was supported by a grant (R21 NS106264) from the National Institutes of Health/National Institute of Neurological Disorders and Stroke (NIH/NINDS), and the Gardner Neuroscience Institute Pilot Award 2017 from the University of Cincinnati.

This is an open-access article, published by Evidence Based Communications (EBC). This work is licensed under the Creative Commons Attribution 4.0 International License, which permits unrestricted use, distribution, and reproduction in any medium or format for any lawful purpose. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.