Effects of general anesthetics on visceral pain transmission in the spinal cord
<p>Abstract</p> <p>Current evidence suggests an analgesic role for the spinal cord action of general anesthetics; however, the cellular population and intracellular mechanisms underlying anti-visceral pain by general anesthetics still remain unclear. It is known that visceral nocic...
Main Authors: | , , , , , |
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Format: | Article |
Language: | English |
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SAGE Publishing
2008-10-01
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Series: | Molecular Pain |
Online Access: | http://www.molecularpain.com/content/4/1/50 |
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author | Yue Yun Nauta HJ Lin Qing Wu Jing Wang Yun Fang Li |
author_facet | Yue Yun Nauta HJ Lin Qing Wu Jing Wang Yun Fang Li |
author_sort | Yue Yun |
collection | DOAJ |
description | <p>Abstract</p> <p>Current evidence suggests an analgesic role for the spinal cord action of general anesthetics; however, the cellular population and intracellular mechanisms underlying anti-visceral pain by general anesthetics still remain unclear. It is known that visceral nociceptive signals are transmited via post-synaptic dorsal column (PSDC) and spinothalamic tract (STT) neuronal pathways and that the PSDC pathway plays a major role in visceral nociception. Animal studies report that persistent changes including nociception-associated molecular expression (e.g. neurokinin-1 (NK-1) receptors) and activation of signal transduction cascades (such as the protein kinase A [PKA]-c-AMP-responsive element binding [CREB] cascade)-in spinal PSDC neurons are observed following visceral pain stimulation. The clinical practice of interruption of the spinal PSDC pathway in patients with cancer pain further supports a role of this group of neurons in the development and maintenance of visceral pain. We propose the hypothesis that general anesthetics might affect critical molecular targets such as NK-1 and glutamate receptors, as well as intracellular signaling by CaM kinase II, protein kinase C (PKC), PKA, and MAP kinase cascades in PSDC neurons, which contribute to the neurotransmission of visceral pain signaling. This would help elucidate the mechanism of antivisceral nociception by general anesthetics at the cellular and molecular levels and aid in development of novel therapeutic strategies to improve clinical management of visceral pain.</p> |
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id | doaj.art-d7306c14210a409a840e17de051ac15b |
institution | Directory Open Access Journal |
issn | 1744-8069 |
language | English |
last_indexed | 2024-04-14T04:15:44Z |
publishDate | 2008-10-01 |
publisher | SAGE Publishing |
record_format | Article |
series | Molecular Pain |
spelling | doaj.art-d7306c14210a409a840e17de051ac15b2022-12-22T02:12:51ZengSAGE PublishingMolecular Pain1744-80692008-10-01415010.1186/1744-8069-4-50Effects of general anesthetics on visceral pain transmission in the spinal cordYue YunNauta HJLin QingWu JingWang YunFang Li<p>Abstract</p> <p>Current evidence suggests an analgesic role for the spinal cord action of general anesthetics; however, the cellular population and intracellular mechanisms underlying anti-visceral pain by general anesthetics still remain unclear. It is known that visceral nociceptive signals are transmited via post-synaptic dorsal column (PSDC) and spinothalamic tract (STT) neuronal pathways and that the PSDC pathway plays a major role in visceral nociception. Animal studies report that persistent changes including nociception-associated molecular expression (e.g. neurokinin-1 (NK-1) receptors) and activation of signal transduction cascades (such as the protein kinase A [PKA]-c-AMP-responsive element binding [CREB] cascade)-in spinal PSDC neurons are observed following visceral pain stimulation. The clinical practice of interruption of the spinal PSDC pathway in patients with cancer pain further supports a role of this group of neurons in the development and maintenance of visceral pain. We propose the hypothesis that general anesthetics might affect critical molecular targets such as NK-1 and glutamate receptors, as well as intracellular signaling by CaM kinase II, protein kinase C (PKC), PKA, and MAP kinase cascades in PSDC neurons, which contribute to the neurotransmission of visceral pain signaling. This would help elucidate the mechanism of antivisceral nociception by general anesthetics at the cellular and molecular levels and aid in development of novel therapeutic strategies to improve clinical management of visceral pain.</p>http://www.molecularpain.com/content/4/1/50 |
spellingShingle | Yue Yun Nauta HJ Lin Qing Wu Jing Wang Yun Fang Li Effects of general anesthetics on visceral pain transmission in the spinal cord Molecular Pain |
title | Effects of general anesthetics on visceral pain transmission in the spinal cord |
title_full | Effects of general anesthetics on visceral pain transmission in the spinal cord |
title_fullStr | Effects of general anesthetics on visceral pain transmission in the spinal cord |
title_full_unstemmed | Effects of general anesthetics on visceral pain transmission in the spinal cord |
title_short | Effects of general anesthetics on visceral pain transmission in the spinal cord |
title_sort | effects of general anesthetics on visceral pain transmission in the spinal cord |
url | http://www.molecularpain.com/content/4/1/50 |
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