Long-term potentiation in spinal nociceptive pathways as a novel target for pain therapy

<p>Abstract</p> <p>Long-term potentiation (LTP) in nociceptive spinal pathways shares several features with hyperalgesia and has been proposed to be a cellular mechanism of pain amplification in acute and chronic pain states. Spinal LTP is typically induced by noxious input and has...

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Main Authors: Liu Xian-Guo, Drdla Ruth, Wilder-Smith Oliver, Ruscheweyh Ruth, Sandkühler Jürgen
Format: Article
Language:English
Published: SAGE Publishing 2011-03-01
Series:Molecular Pain
Online Access:http://www.molecularpain.com/content/7/1/20
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spelling doaj-150cdf9dc0ca4df18025c600b67f31422020-11-25T03:28:29ZengSAGE PublishingMolecular Pain1744-80692011-03-01712010.1186/1744-8069-7-20Long-term potentiation in spinal nociceptive pathways as a novel target for pain therapyLiu Xian-GuoDrdla RuthWilder-Smith OliverRuscheweyh RuthSandkühler Jürgen<p>Abstract</p> <p>Long-term potentiation (LTP) in nociceptive spinal pathways shares several features with hyperalgesia and has been proposed to be a cellular mechanism of pain amplification in acute and chronic pain states. Spinal LTP is typically induced by noxious input and has therefore been hypothesized to contribute to acute postoperative pain and to forms of chronic pain that develop from an initial painful event, peripheral inflammation or neuropathy. Under this assumption, preventing LTP induction may help to prevent the development of exaggerated postoperative pain and reversing established LTP may help to treat patients who have an LTP component to their chronic pain. Spinal LTP is also induced by abrupt opioid withdrawal, making it a possible mechanism of some forms of opioid-induced hyperalgesia. Here, we give an overview of targets for preventing LTP induction and modifying established LTP as identified in animal studies. We discuss which of the various symptoms of human experimental and clinical pain may be manifestations of spinal LTP, review the pharmacology of these possible human LTP manifestations and compare it to the pharmacology of spinal LTP in rodents.</p> http://www.molecularpain.com/content/7/1/20
collection DOAJ
language English
format Article
sources DOAJ
author Liu Xian-Guo
Drdla Ruth
Wilder-Smith Oliver
Ruscheweyh Ruth
Sandkühler Jürgen
spellingShingle Liu Xian-Guo
Drdla Ruth
Wilder-Smith Oliver
Ruscheweyh Ruth
Sandkühler Jürgen
Long-term potentiation in spinal nociceptive pathways as a novel target for pain therapy
Molecular Pain
author_facet Liu Xian-Guo
Drdla Ruth
Wilder-Smith Oliver
Ruscheweyh Ruth
Sandkühler Jürgen
author_sort Liu Xian-Guo
title Long-term potentiation in spinal nociceptive pathways as a novel target for pain therapy
title_short Long-term potentiation in spinal nociceptive pathways as a novel target for pain therapy
title_full Long-term potentiation in spinal nociceptive pathways as a novel target for pain therapy
title_fullStr Long-term potentiation in spinal nociceptive pathways as a novel target for pain therapy
title_full_unstemmed Long-term potentiation in spinal nociceptive pathways as a novel target for pain therapy
title_sort long-term potentiation in spinal nociceptive pathways as a novel target for pain therapy
publisher SAGE Publishing
series Molecular Pain
issn 1744-8069
publishDate 2011-03-01
description <p>Abstract</p> <p>Long-term potentiation (LTP) in nociceptive spinal pathways shares several features with hyperalgesia and has been proposed to be a cellular mechanism of pain amplification in acute and chronic pain states. Spinal LTP is typically induced by noxious input and has therefore been hypothesized to contribute to acute postoperative pain and to forms of chronic pain that develop from an initial painful event, peripheral inflammation or neuropathy. Under this assumption, preventing LTP induction may help to prevent the development of exaggerated postoperative pain and reversing established LTP may help to treat patients who have an LTP component to their chronic pain. Spinal LTP is also induced by abrupt opioid withdrawal, making it a possible mechanism of some forms of opioid-induced hyperalgesia. Here, we give an overview of targets for preventing LTP induction and modifying established LTP as identified in animal studies. We discuss which of the various symptoms of human experimental and clinical pain may be manifestations of spinal LTP, review the pharmacology of these possible human LTP manifestations and compare it to the pharmacology of spinal LTP in rodents.</p>
url http://www.molecularpain.com/content/7/1/20
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