Cargando…

Peripheral mechanisms of neuropathic pain – involvement of lysophosphatidic acid receptor-mediated demyelination

Recent advances in pain research provide a clear picture for the molecular mechanisms of acute pain; substantial information concerning plasticity that occurs during neuropathic pain has also become available. The peripheral mechanisms responsible for neuropathic pain are found in the altered gene/p...

Descripción completa

Detalles Bibliográficos
Autor principal: Ueda, Hiroshi
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2008
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2365930/
https://www.ncbi.nlm.nih.gov/pubmed/18377664
http://dx.doi.org/10.1186/1744-8069-4-11
_version_ 1782154241960312832
author Ueda, Hiroshi
author_facet Ueda, Hiroshi
author_sort Ueda, Hiroshi
collection PubMed
description Recent advances in pain research provide a clear picture for the molecular mechanisms of acute pain; substantial information concerning plasticity that occurs during neuropathic pain has also become available. The peripheral mechanisms responsible for neuropathic pain are found in the altered gene/protein expression of primary sensory neurons. With damage to peripheral sensory fibers, a variety of changes in pain-related gene expression take place in dorsal root ganglion neurons. These changes, or plasticity, might underlie unique neuropathic pain-specific phenotype modifications – decreased unmyelinated-fiber functions, but increased myelinated A-fiber functions. Another characteristic change is observed in allodynia, the functional change of tactile to nociceptive perception. Throughout a series of studies, using novel nociceptive tests to characterize sensory-fiber or pain modality-specific nociceptive behaviors, it was demonstrated that communication between innocuous and noxious sensory fibers might play a role in allodynia mechanisms. Because neuropathic pain in peripheral and central demyelinating diseases develops as a result of aberrant myelination in experimental animals, demyelination seems to be a key mechanism of plasticity in neuropathic pain. More recently, we discovered that lysophosphatidic acid receptor activation initiates neuropathic pain, as well as possible peripheral mechanims of demyelination after nerve injury. These results lead to further hypotheses of physical communication between innocuous Aβ- and noxious C- or Aδ-fibers to influence the molecular mechanisms of allodynia.
format Text
id pubmed-2365930
institution National Center for Biotechnology Information
language English
publishDate 2008
publisher BioMed Central
record_format MEDLINE/PubMed
spelling pubmed-23659302008-05-03 Peripheral mechanisms of neuropathic pain – involvement of lysophosphatidic acid receptor-mediated demyelination Ueda, Hiroshi Mol Pain Review Recent advances in pain research provide a clear picture for the molecular mechanisms of acute pain; substantial information concerning plasticity that occurs during neuropathic pain has also become available. The peripheral mechanisms responsible for neuropathic pain are found in the altered gene/protein expression of primary sensory neurons. With damage to peripheral sensory fibers, a variety of changes in pain-related gene expression take place in dorsal root ganglion neurons. These changes, or plasticity, might underlie unique neuropathic pain-specific phenotype modifications – decreased unmyelinated-fiber functions, but increased myelinated A-fiber functions. Another characteristic change is observed in allodynia, the functional change of tactile to nociceptive perception. Throughout a series of studies, using novel nociceptive tests to characterize sensory-fiber or pain modality-specific nociceptive behaviors, it was demonstrated that communication between innocuous and noxious sensory fibers might play a role in allodynia mechanisms. Because neuropathic pain in peripheral and central demyelinating diseases develops as a result of aberrant myelination in experimental animals, demyelination seems to be a key mechanism of plasticity in neuropathic pain. More recently, we discovered that lysophosphatidic acid receptor activation initiates neuropathic pain, as well as possible peripheral mechanims of demyelination after nerve injury. These results lead to further hypotheses of physical communication between innocuous Aβ- and noxious C- or Aδ-fibers to influence the molecular mechanisms of allodynia. BioMed Central 2008-04-01 /pmc/articles/PMC2365930/ /pubmed/18377664 http://dx.doi.org/10.1186/1744-8069-4-11 Text en Copyright © 2008 Ueda; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review
Ueda, Hiroshi
Peripheral mechanisms of neuropathic pain – involvement of lysophosphatidic acid receptor-mediated demyelination
title Peripheral mechanisms of neuropathic pain – involvement of lysophosphatidic acid receptor-mediated demyelination
title_full Peripheral mechanisms of neuropathic pain – involvement of lysophosphatidic acid receptor-mediated demyelination
title_fullStr Peripheral mechanisms of neuropathic pain – involvement of lysophosphatidic acid receptor-mediated demyelination
title_full_unstemmed Peripheral mechanisms of neuropathic pain – involvement of lysophosphatidic acid receptor-mediated demyelination
title_short Peripheral mechanisms of neuropathic pain – involvement of lysophosphatidic acid receptor-mediated demyelination
title_sort peripheral mechanisms of neuropathic pain – involvement of lysophosphatidic acid receptor-mediated demyelination
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2365930/
https://www.ncbi.nlm.nih.gov/pubmed/18377664
http://dx.doi.org/10.1186/1744-8069-4-11
work_keys_str_mv AT uedahiroshi peripheralmechanismsofneuropathicpaininvolvementoflysophosphatidicacidreceptormediateddemyelination