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Antinociceptive eff...
Antinociceptive effect produced by intracerebroventricularly administered dynorphin A is potentiated by p-hydroxymercuribenzoate or phosphoramidon in the mouse formalin test
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Tan-No, Koichi (författare)
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Ohshima, Kiyoshi (författare)
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Taira, Aki (författare)
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Inoue, Makoto (författare)
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Niijima, Fukie (författare)
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Nakagawasai, Osamu (författare)
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Tadano, Takeshi (författare)
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- Nylander, Ingrid (författare)
- Uppsala universitet,Institutionen för farmaceutisk biovetenskap,Pharmacology
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Silberring, Jerzy (författare)
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Terenius, Lars (författare)
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Kisara, Kensuke (författare)
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(creator_code:org_t)
- 2001
- 2001
- Engelska.
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Ingår i: Brain Research. - 0006-8993 .- 1872-6240. ; 891:1-2, s. 274-280
- Relaterad länk:
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https://urn.kb.se/re...
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https://doi.org/10.1...
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Abstract
Ämnesord
Stäng
- The antinociceptive effects of intracerebroventricularly (i.c.v.) administered dynorphin A, an endogenous agonist for kappa-opioid receptors, in combination with various protease inhibitors were examined using the mouse formalin test in order to clarify the nature of the proteases involved in the degradation of dynorphin A in the mouse brain. When administered i.c.v. 15 min before the injection of 2% formalin solution into the dorsal surface of a hindpaw, 1-4 nmol dynorphin A produced a dose-dependent reduction of the nociceptive behavioral response consisting of licking and biting of the injected paw during both the first (0-5 min) and second (10-30 min) phases. When co-administered with p-hydroxymercuribenzoate (PHMB), a cysteine protease inhibitor, dynorphin A at the subthreshold dose of 0.5 nmol significantly produced an antinociceptive effect during the second phase. This effect was significantly antagonized by nor-binaltorphimine, a selective kappa-opioid receptor antagonist, but not by naltrindole, a selective delta-opioid receptor antagonist. At the same dose of 0.5 nmol, dynorphin A in combination with phosphoramidon, an endopeptidase 24.11 inhibitor, produced a significant antinociceptive effect during both phases. The antinociceptive effect was significantly antagonized by naltrindole, but not by nor-binaltorphimine. Phenylmethanesulfonyl fluoride (PMSF), a serine protease inhibitor, bestatin, a general aminopeptidase inhibitor, and captopril, an angiotensin-converting enzyme inhibitor, were all inactive. The degradation of dynorphin A by mouse brain extracts in vitro was significantly inhibited only by the cysteine protease inhibitors PHMB and N-ethylmaleimide, but not by PMSF, phosphoramidon, bestatin or captopril. The present results indicate that cysteine proteases as well as endopeptidase 24.11 are involved in two steps in the degradation of dynorphin A in the mouse brain, and that phosphoramidon inhibits the degradation of intermediary delta-opioid receptor active fragments enkephalins which are formed from dynorphin A.
Ämnesord
- MEDICIN OCH HÄLSOVETENSKAP -- Medicinska och farmaceutiska grundvetenskaper -- Farmaceutiska vetenskaper (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Basic Medicine -- Pharmaceutical Sciences (hsv//eng)
Nyckelord
- dynorphin A
- p-hydroxymercuribenzoate
- phosphoramidon
- cysteine protease
- endopeptidase 24.11
- formalin test
- intracerebroventricular administration
- mouse
- PHARMACY
- FARMACI
Publikations- och innehållstyp
- ref (ämneskategori)
- art (ämneskategori)
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Tan-No, Koichi
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Ohshima, Kiyoshi
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Taira, Aki
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Inoue, Makoto
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Niijima, Fukie
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Nakagawasai, Osa ...
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visa fler...
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Tadano, Takeshi
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Nylander, Ingrid
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Silberring, Jerz ...
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Terenius, Lars
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Kisara, Kensuke
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visa färre...
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Uppsala universitet