| 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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MedLine Citation:
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PMID: 19917879 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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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Authors:
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Ana Campillo; Ana Gonz?lez-Cuello; David Caba?ero; Paula Garcia-Nogales; Asunci?n Romero; M Victoria Milan?s; M Luisa Laorden; Margarita M Puig |
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Publication Detail:
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Type: Comparative Study; Journal Article; Research Support, Non-U.S. Gov't Date: 2009-11-16 |
Journal Detail:
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Title: Molecular pharmacology Volume: 77 ISSN: 1521-0111 ISO Abbreviation: Mol. Pharmacol. Publication Date: 2010 Feb |
Date Detail:
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Created Date: 2010-01-20 Completed Date: 2010-02-11 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0035623 Medline TA: Mol Pharmacol Country: United States |
Other Details:
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Languages: eng Pagination: 185-94 Citation Subset: IM |
Affiliation:
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Department of Anesthesiology, Hospital Universitari del Mar, Universitat Aut?noma de Barcelona, Passeig Mar?tim 25-29, E-08003 Barcelona, Spain. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Anesthetics, Intravenous
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pharmacology,
therapeutic use Animals Dynorphins / biosynthesis* Genes, fos / physiology* Male Mice Mitogen-Activated Protein Kinase 1 / biosynthesis* Mitogen-Activated Protein Kinase 3 / biosynthesis* Pain Measurement / drug effects, methods Pain, Postoperative / metabolism*, prevention & control Piperidines / pharmacology, therapeutic use* Spinal Cord / drug effects, metabolism |
| Chemical | |
Reg. No./Substance:
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0/Anesthetics, Intravenous; 0/Piperidines; 132875-61-7/remifentanil; 74913-18-1/Dynorphins; EC 2.7.11.24/Mitogen-Activated Protein Kinase 1; EC 2.7.11.24/Mitogen-Activated Protein Kinase 3 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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