Abstract
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.
Highlights
Abstract | Satellite glial cells (SGCs) closely envelop cell bodies of neurons in sensory, sympathetic and parasympathetic ganglia
We describe how satellite glial cells (SGCs) are altered in rodent models of four common types of pain: systemic inflammation, post-surgical pain, diabetic neuropathic pain and post-herpetic pain
We have proposed a scheme to explain how increased gap junctional communication and sensitization to ATP can explain the role of SGCs in neuronal hyperexcitability in pain models[45], based on the ‘ignition theory’ formulated to account for trigeminal neuralgia[84]
Summary
Sympathetic ganglia Clusters of neuron cell bodies that innervate smooth muscles, heart and glands; paravertebral ganglia are arranged along the spinal column, and prevertebral ones are located in the abdomen. It was found that nerve damage or inflammation activates SGCs in sensory ganglia This included upregulation of the astrocyte marker glial fibrillary acidic. Activated SGCs release pro-inflammatory cytokines IL-1β, IL-6, TNF and fractalkine[2,32,33,34,35,36], which can act on the neurons and increase their excitability and firing In this Review, we describe the normal properties of SGCs and how they change in animal pain models. Lineage and plasticity: SGCs are derived from the neural crest They contain cadherin 19, which is a Schwann cell marker[144], and it was proposed that SGCs represent a subpopulation of cells in the Schwann cell lineage whose further differentiation is arrested due to contact with sensory neuron somata[145]. SGC responses to injury, such as growing new processes[25,27], may be related to this plasticity a Neuron b
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