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Review
. 2022 Feb 1;11(3):512.
doi: 10.3390/cells11030512.

How Is Peripheral Injury Signaled to Satellite Glial Cells in Sensory Ganglia?

Menachem Hanani  1
Affiliations
Review

How Is Peripheral Injury Signaled to Satellite Glial Cells in Sensory Ganglia?

Menachem Hanani. Cells. .

Abstract

Injury or inflammation in the peripheral branches of neurons of sensory ganglia causes changes in neuronal properties, including excessive firing, which may underlie chronic pain. The main types of glial cell in these ganglia are satellite glial cells (SGCs), which completely surround neuronal somata. SGCs undergo activation following peripheral lesions, which can enhance neuronal firing. How neuronal injury induces SGC activation has been an open question. Moreover, the mechanisms by which the injury is signaled from the periphery to the ganglia are obscure and may include electrical conduction, axonal and humoral transport, and transmission at the spinal level. We found that peripheral inflammation induced SGC activation and that the messenger between injured neurons and SGCs was nitric oxide (NO), acting by elevating cyclic guanosine monophosphate (cGMP) in SGCs. These results, together with work from other laboratories, indicate that a plausible (but not exclusive) mechanism for neuron-SGCs interactions can be formulated as follows: Firing due to peripheral injury induces NO formation in neuronal somata, which diffuses to SGCs. This stimulates cGMP synthesis in SGCs, leading to their activation and to other changes, which contribute to neuronal hyperexcitability and pain. Other mediators such as proinflammatory cytokines probably also contribute to neuron-SGC communications.

Keywords: axonal transport; gliosis; neurons; nitric oxide; pain; satellite glial cells; sensory ganglia.

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Conflict of interest statement

The author declares no conflict of interest.

Figures

Figure 1
Figure 1
Diagram describing some of the ideas on how signals from peripheral injury reach satellite glial cells (SGCs) in sensory ganglia. Signals from the periphery travel in the axon of the sensory ganglion (by electrical conduction or axonal transport). Electrical activity in the neuronal somata induces the synthesis of nitric oxide (NO), which diffuses to SGCs and evokes the synthesis of cyclic guanosine monophosphate (cGMP) in them. This in turn induces SGC activation that leads to the release of cytokines from SGCs, which can increase neuronal excitability. Other pathways from the periphery to the ganglia include circulating substances such as cytokines and the transmission of electrical signals to contralateral ganglia across the spinal cord.
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