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Peripheral and Central Mechanisms of Persistent Orofacial Pain

Neuroplastic changes in the neuronal networks involving the trigeminal ganglion (TG), trigeminal spinal subnucleus caudalis (Vc), and upper cervical spinal cord (C1/C2) are considered the mechanisms underlying the ectopic orofacial hypersensitivity associated with trigeminal nerve injury or orofacia...

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Autores principales: Shinoda, Masamichi, Kubo, Asako, Hayashi, Yoshinori, Iwata, Koichi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6863776/
https://www.ncbi.nlm.nih.gov/pubmed/31798407
http://dx.doi.org/10.3389/fnins.2019.01227
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author Shinoda, Masamichi
Kubo, Asako
Hayashi, Yoshinori
Iwata, Koichi
author_facet Shinoda, Masamichi
Kubo, Asako
Hayashi, Yoshinori
Iwata, Koichi
author_sort Shinoda, Masamichi
collection PubMed
description Neuroplastic changes in the neuronal networks involving the trigeminal ganglion (TG), trigeminal spinal subnucleus caudalis (Vc), and upper cervical spinal cord (C1/C2) are considered the mechanisms underlying the ectopic orofacial hypersensitivity associated with trigeminal nerve injury or orofacial inflammation. It has been reported that peripheral nerve injury causes injury discharges in the TG neurons, and a barrage of action potentials is generated in TG neurons and conveyed to the Vc and C1/C2 after trigeminal nerve injury. Long after trigeminal nerve injury, various molecules are produced in the TG neurons, and these molecules are released from the soma of TG neurons and are transported to the central and peripheral terminals of TG neurons. These changes within the TG cause neuroplastic changes in TG neurons and they become sensitized. The neuronal activity of TG neurons is further accelerated, and Vc and C1/C2 neurons are also sensitized. In addition to this cascade, non-neuronal glial cells are also involved in the enhancement of the neuronal activity of TG, Vc, and C1/C2 neurons. Satellite glial cells and macrophages are activated in the TG after trigeminal nerve injury and orofacial inflammation. Microglial cells and astrocytes are also activated in the Vc and C1/C2 regions. It is considered that functional interaction between non-neuronal cells and neurons in the TG, Vc, and C1/C2 regions is a key mechanism involved in the enhancement of neuronal excitability after nerve injury or inflammation. In this article, the detailed mechanisms underlying ectopic orofacial hyperalgesia associated with trigeminal nerve injury and orofacial inflammation are addressed.
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spelling pubmed-68637762019-12-03 Peripheral and Central Mechanisms of Persistent Orofacial Pain Shinoda, Masamichi Kubo, Asako Hayashi, Yoshinori Iwata, Koichi Front Neurosci Neuroscience Neuroplastic changes in the neuronal networks involving the trigeminal ganglion (TG), trigeminal spinal subnucleus caudalis (Vc), and upper cervical spinal cord (C1/C2) are considered the mechanisms underlying the ectopic orofacial hypersensitivity associated with trigeminal nerve injury or orofacial inflammation. It has been reported that peripheral nerve injury causes injury discharges in the TG neurons, and a barrage of action potentials is generated in TG neurons and conveyed to the Vc and C1/C2 after trigeminal nerve injury. Long after trigeminal nerve injury, various molecules are produced in the TG neurons, and these molecules are released from the soma of TG neurons and are transported to the central and peripheral terminals of TG neurons. These changes within the TG cause neuroplastic changes in TG neurons and they become sensitized. The neuronal activity of TG neurons is further accelerated, and Vc and C1/C2 neurons are also sensitized. In addition to this cascade, non-neuronal glial cells are also involved in the enhancement of the neuronal activity of TG, Vc, and C1/C2 neurons. Satellite glial cells and macrophages are activated in the TG after trigeminal nerve injury and orofacial inflammation. Microglial cells and astrocytes are also activated in the Vc and C1/C2 regions. It is considered that functional interaction between non-neuronal cells and neurons in the TG, Vc, and C1/C2 regions is a key mechanism involved in the enhancement of neuronal excitability after nerve injury or inflammation. In this article, the detailed mechanisms underlying ectopic orofacial hyperalgesia associated with trigeminal nerve injury and orofacial inflammation are addressed. Frontiers Media S.A. 2019-11-13 /pmc/articles/PMC6863776/ /pubmed/31798407 http://dx.doi.org/10.3389/fnins.2019.01227 Text en Copyright © 2019 Shinoda, Kubo, Hayashi and Iwata. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Neuroscience
Shinoda, Masamichi
Kubo, Asako
Hayashi, Yoshinori
Iwata, Koichi
Peripheral and Central Mechanisms of Persistent Orofacial Pain
title Peripheral and Central Mechanisms of Persistent Orofacial Pain
title_full Peripheral and Central Mechanisms of Persistent Orofacial Pain
title_fullStr Peripheral and Central Mechanisms of Persistent Orofacial Pain
title_full_unstemmed Peripheral and Central Mechanisms of Persistent Orofacial Pain
title_short Peripheral and Central Mechanisms of Persistent Orofacial Pain
title_sort peripheral and central mechanisms of persistent orofacial pain
topic Neuroscience
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6863776/
https://www.ncbi.nlm.nih.gov/pubmed/31798407
http://dx.doi.org/10.3389/fnins.2019.01227
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