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A new mechanistic approach for the treatment of chronic neuropathic pain with nitrous oxide integrated from a systems biology narrative review

The limitations of the currently available treatments for chronic neuropathic pain highlight the need for safer and more effective alternatives. The authors carried out a focused review using a systems biology approach to integrate the complex mechanisms of nociception and neuropathic pain, and to d...

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Autores principales: Bessière, Baptiste, Iris, François, Milet, Aude, Beopoulos, Athanasios, Billoet, Catherine, Farjot, Géraldine
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Wolters Kluwer - Medknow 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8103977/
https://www.ncbi.nlm.nih.gov/pubmed/33642336
http://dx.doi.org/10.4103/2045-9912.310058
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author Bessière, Baptiste
Iris, François
Milet, Aude
Beopoulos, Athanasios
Billoet, Catherine
Farjot, Géraldine
author_facet Bessière, Baptiste
Iris, François
Milet, Aude
Beopoulos, Athanasios
Billoet, Catherine
Farjot, Géraldine
author_sort Bessière, Baptiste
collection PubMed
description The limitations of the currently available treatments for chronic neuropathic pain highlight the need for safer and more effective alternatives. The authors carried out a focused review using a systems biology approach to integrate the complex mechanisms of nociception and neuropathic pain, and to decipher the effects of nitrous oxide (N(2)O) on those pathways, beyond the known effect of N(2)O on N-methyl-D-aspartate receptors. This review identified a number of potential mechanisms by which N(2)O could impact the processes involved in peripheral and central sensitization. In the ascending pathway, the effects of N(2)O include activating TWIK-related K(+) channel 1 potassium channels on first-order neurons, blocking voltage-dependent calcium channels to attenuate neuronal excitability, attenuating postsynaptic glutamatergic receptor activation, and possibly blocking voltage-dependent sodium channels. In the descending pathway, N(2)O induces the release of endogenous opioid ligands and stimulates norepinephrine release. In addition, N(2)O may mediate epigenetic changes by inhibiting methionine synthase, a key enzyme involved in DNA and RNA methylation. This could explain why this short-acting analgesic has shown long-lasting anti-pain sensitization effects in animal models of chronic pain. These new hypotheses support the rationale for investigating N(2)O, either alone or in combination with other analgesics, for the management of chronic neuropathic pain.
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spelling pubmed-81039772021-06-02 A new mechanistic approach for the treatment of chronic neuropathic pain with nitrous oxide integrated from a systems biology narrative review Bessière, Baptiste Iris, François Milet, Aude Beopoulos, Athanasios Billoet, Catherine Farjot, Géraldine Med Gas Res Review The limitations of the currently available treatments for chronic neuropathic pain highlight the need for safer and more effective alternatives. The authors carried out a focused review using a systems biology approach to integrate the complex mechanisms of nociception and neuropathic pain, and to decipher the effects of nitrous oxide (N(2)O) on those pathways, beyond the known effect of N(2)O on N-methyl-D-aspartate receptors. This review identified a number of potential mechanisms by which N(2)O could impact the processes involved in peripheral and central sensitization. In the ascending pathway, the effects of N(2)O include activating TWIK-related K(+) channel 1 potassium channels on first-order neurons, blocking voltage-dependent calcium channels to attenuate neuronal excitability, attenuating postsynaptic glutamatergic receptor activation, and possibly blocking voltage-dependent sodium channels. In the descending pathway, N(2)O induces the release of endogenous opioid ligands and stimulates norepinephrine release. In addition, N(2)O may mediate epigenetic changes by inhibiting methionine synthase, a key enzyme involved in DNA and RNA methylation. This could explain why this short-acting analgesic has shown long-lasting anti-pain sensitization effects in animal models of chronic pain. These new hypotheses support the rationale for investigating N(2)O, either alone or in combination with other analgesics, for the management of chronic neuropathic pain. Wolters Kluwer - Medknow 2021-02-26 /pmc/articles/PMC8103977/ /pubmed/33642336 http://dx.doi.org/10.4103/2045-9912.310058 Text en Copyright: © 2021 Medical Gas Research https://creativecommons.org/licenses/by-nc-sa/4.0/This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms.
spellingShingle Review
Bessière, Baptiste
Iris, François
Milet, Aude
Beopoulos, Athanasios
Billoet, Catherine
Farjot, Géraldine
A new mechanistic approach for the treatment of chronic neuropathic pain with nitrous oxide integrated from a systems biology narrative review
title A new mechanistic approach for the treatment of chronic neuropathic pain with nitrous oxide integrated from a systems biology narrative review
title_full A new mechanistic approach for the treatment of chronic neuropathic pain with nitrous oxide integrated from a systems biology narrative review
title_fullStr A new mechanistic approach for the treatment of chronic neuropathic pain with nitrous oxide integrated from a systems biology narrative review
title_full_unstemmed A new mechanistic approach for the treatment of chronic neuropathic pain with nitrous oxide integrated from a systems biology narrative review
title_short A new mechanistic approach for the treatment of chronic neuropathic pain with nitrous oxide integrated from a systems biology narrative review
title_sort new mechanistic approach for the treatment of chronic neuropathic pain with nitrous oxide integrated from a systems biology narrative review
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8103977/
https://www.ncbi.nlm.nih.gov/pubmed/33642336
http://dx.doi.org/10.4103/2045-9912.310058
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