Source:http://linkedlifedata.com/resource/pubmed/id/19917879
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
2010-1-20
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pubmed:abstractText |
In humans, remifentanil anesthesia enhances nociceptive sensitization in the postoperative period. We hypothesized that activation of extracellular signal-regulated kinases 1 and 2 (ERK1/2) and the expression of c-Fos, prodynorphin (mRNA), and dynorphin in the spinal cord could participate in the molecular mechanisms underlying postoperative opioid-induced sensitization. In a mouse model of incisional pain, we evaluated thermal (Hargreaves test) and mechanical (von Frey) hyperalgesia during the first 21 postoperative days. Moreover, prodynorphin (mRNA, real-time polymerase chain reaction), dynorphin (enzymatic immunoassay), c-Fos expression, and ERK1/2 phosphorylation (both by immunohistochemistry) in the lumbar spinal cord were assessed. Surgery performed under remifentanil anesthesia induced a maximal decrease in nociceptive thresholds between 4 h and 2 days postoperatively (p < 0.001) that lasted 10 to 14 days compared with noninjured animals. In the same experimental conditions, a significant increase in prodynorphin mRNA expression (at 2 and 4 days) followed by a sustained increase of dynorphin (days 2 to 10) in the spinal cord was observed. We also identified an early expression of c-Fos immunoreactivity in the superficial laminae of the dorsal horn of the spinal cord (peak at 4 h; p < 0.001), together with a partial activation of ERK1/2 (4 h; p < 0.001). These findings suggest that activated ERK1/2 could induce c-Fos expression and trigger the transcription of prodynorphin in the spinal cord. This in turn would result in long-lasting increased levels of dynorphin that, in our model, could participate in the persistence of pain but not in the manifestation of first pain.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Anesthetics, Intravenous,
http://linkedlifedata.com/resource/pubmed/chemical/Dynorphins,
http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinase 1,
http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinase 3,
http://linkedlifedata.com/resource/pubmed/chemical/Piperidines,
http://linkedlifedata.com/resource/pubmed/chemical/remifentanil
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
1521-0111
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
77
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
185-94
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pubmed:meshHeading |
pubmed-meshheading:19917879-Anesthetics, Intravenous,
pubmed-meshheading:19917879-Animals,
pubmed-meshheading:19917879-Dynorphins,
pubmed-meshheading:19917879-Genes, fos,
pubmed-meshheading:19917879-Male,
pubmed-meshheading:19917879-Mice,
pubmed-meshheading:19917879-Mitogen-Activated Protein Kinase 1,
pubmed-meshheading:19917879-Mitogen-Activated Protein Kinase 3,
pubmed-meshheading:19917879-Pain, Postoperative,
pubmed-meshheading:19917879-Pain Measurement,
pubmed-meshheading:19917879-Piperidines,
pubmed-meshheading:19917879-Spinal Cord
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pubmed:year |
2010
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pubmed:articleTitle |
Increased spinal dynorphin levels and phospho-extracellular signal-regulated kinases 1 and 2 and c-Fos immunoreactivity after surgery under remifentanil anesthesia in mice.
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pubmed:affiliation |
Department of Anesthesiology, Hospital Universitari del Mar, Universitat Autònoma de Barcelona, Passeig Marítim 25-29, E-08003 Barcelona, Spain.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
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