Source:http://linkedlifedata.com/resource/pubmed/id/19520130
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
9
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| pubmed:dateCreated |
2009-8-5
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| pubmed:abstractText |
The present study sought to examine the mechanism of substance P to modulate the antinociceptive action of intrathecal (i.t.) morphine in paw-licking/biting response evoked by subcutaneous injection of capsaicin into the plantar surface of the hindpaw in mice. The i.t. injection of morphine inhibited capsaicin-induced licking/biting response in a dose-dependent manner. Substance P (25 and 50 pmol) injected i.t. alone did not alter capsaicin-induced nociception, whereas substance P at a higher dose of 100 pmol significantly reduced the capsaicin response. Western blots showed the constitutive expression of endopeptidase-24.11 in the dorsal and ventral parts of lumbar spinal cord of mice. The N-terminal fragment of substance P (1-7), which is known as a major product of substance P by endopeptidase-24.11, was more effective than substance P on capsaicin-induced nociception. Combination treatment with substance P (50 pmol) and morphine at a subthreshold dose enhanced the antinociceptive effect of morphine. The enhanced effect of the combination of substance P with morphine was reduced significantly by co-administration of phosphoramidon, an inhibitor of endopeptidase-24.11. Administration of D-isomer of substance P (1-7), [D-Pro(2), D-Phe(7)]substance P (1-7), an inhibitor of [(3)H] substance P (1-7) binding, or antisera against substance P (1-7) reversed the enhanced antinociceptive effect by co-administration of substance P and morphine. Taken together these data suggest that morphine-induced antinociception may be enhanced through substance P (1-7) formed by the enzymatic degradation of i.t. injected substance P in the spinal cord.
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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/Antibodies,
http://linkedlifedata.com/resource/pubmed/chemical/Capsaicin,
http://linkedlifedata.com/resource/pubmed/chemical/Glycopeptides,
http://linkedlifedata.com/resource/pubmed/chemical/Morphine,
http://linkedlifedata.com/resource/pubmed/chemical/Neprilysin,
http://linkedlifedata.com/resource/pubmed/chemical/Peptide Fragments,
http://linkedlifedata.com/resource/pubmed/chemical/Protease Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Substance P,
http://linkedlifedata.com/resource/pubmed/chemical/phosphoramidon,
http://linkedlifedata.com/resource/pubmed/chemical/substance P (1-7),
http://linkedlifedata.com/resource/pubmed/chemical/substance P (1-7), Pro(2)-Phe(7)-,
http://linkedlifedata.com/resource/pubmed/chemical/substance P (5-11)
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| pubmed:status |
MEDLINE
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| pubmed:month |
Sep
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| pubmed:issn |
1873-5169
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| pubmed:author | |
| pubmed:issnType |
Electronic
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| pubmed:volume |
30
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| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
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| pubmed:pagination |
1689-96
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| pubmed:meshHeading |
pubmed-meshheading:19520130-Animals,
pubmed-meshheading:19520130-Antibodies,
pubmed-meshheading:19520130-Capsaicin,
pubmed-meshheading:19520130-Dose-Response Relationship, Drug,
pubmed-meshheading:19520130-Drug Synergism,
pubmed-meshheading:19520130-Glycopeptides,
pubmed-meshheading:19520130-Injections, Spinal,
pubmed-meshheading:19520130-Male,
pubmed-meshheading:19520130-Mice,
pubmed-meshheading:19520130-Mice, Inbred Strains,
pubmed-meshheading:19520130-Morphine,
pubmed-meshheading:19520130-Neprilysin,
pubmed-meshheading:19520130-Pain,
pubmed-meshheading:19520130-Pain Measurement,
pubmed-meshheading:19520130-Peptide Fragments,
pubmed-meshheading:19520130-Protease Inhibitors,
pubmed-meshheading:19520130-Spinal Cord,
pubmed-meshheading:19520130-Substance P
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| pubmed:year |
2009
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| pubmed:articleTitle |
Intrathecal substance P augments morphine-induced antinociception: possible relevance in the production of substance P N-terminal fragments.
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| pubmed:affiliation |
First Department of Pharmacology, Daiichi College of Pharmaceutical Sciences, 22-1 Tamagawa-cho, Minami-ku, Fukuoka, Japan.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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