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How Is Peripheral Injury Signaled to Satellite Glial Cells in Sensory Ganglia?
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 somat...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2022
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8833977/ https://www.ncbi.nlm.nih.gov/pubmed/35159321 http://dx.doi.org/10.3390/cells11030512 |
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author | Hanani, Menachem |
author_facet | Hanani, Menachem |
author_sort | Hanani, Menachem |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-8833977 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-88339772022-02-12 How Is Peripheral Injury Signaled to Satellite Glial Cells in Sensory Ganglia? Hanani, Menachem Cells Review 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. MDPI 2022-02-01 /pmc/articles/PMC8833977/ /pubmed/35159321 http://dx.doi.org/10.3390/cells11030512 Text en © 2022 by the author. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Hanani, Menachem How Is Peripheral Injury Signaled to Satellite Glial Cells in Sensory Ganglia? |
title | How Is Peripheral Injury Signaled to Satellite Glial Cells in Sensory Ganglia? |
title_full | How Is Peripheral Injury Signaled to Satellite Glial Cells in Sensory Ganglia? |
title_fullStr | How Is Peripheral Injury Signaled to Satellite Glial Cells in Sensory Ganglia? |
title_full_unstemmed | How Is Peripheral Injury Signaled to Satellite Glial Cells in Sensory Ganglia? |
title_short | How Is Peripheral Injury Signaled to Satellite Glial Cells in Sensory Ganglia? |
title_sort | how is peripheral injury signaled to satellite glial cells in sensory ganglia? |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8833977/ https://www.ncbi.nlm.nih.gov/pubmed/35159321 http://dx.doi.org/10.3390/cells11030512 |
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