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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Zimmer, A. Kobayashi, M. Inoue, M. Kozaki, S. Ueda, H. |
| Description | Author Affiliation: Inoue M ( Department of Molecular Pharmacology and Neuroscience, Nagasaki University School of Pharmaceutical Sciences, Nagasaki 852-8521, Japan.); |
| Abstract | We have studied the in vivo signaling mechanisms involved in nociceptin/orphanin FQ (Noci)-induced pain responses by using a flexor-reflex paradigm. Noci was 10,000 times more potent than substance P (SP) in eliciting flexor responses after intraplantar injection into the hind limb of mice, but the action of Noci seems to be mediated by SP. Mice pretreated with an NK1 tachykinin receptor antagonist or capsaicin, or mice with a targeted disruption of the tachykinin 1 gene no longer respond to Noci. The action of Noci appears to be mediated by the Noci receptor, a pertussis toxin-sensitive G protein-coupled receptor that stimulates inositol trisphosphate receptor and Ca2+ influx. These findings suggest that Noci indirectly stimulates nerve endings of nociceptive primary afferent neurons through a local SP release. |
| ISSN | 00278424 |
| e-ISSN | 10916490 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Issue Number | 18 |
| Volume Number | 95 |
| Language | English |
| Publisher | National Academy of Sciences |
| Publisher Date | 1998-09-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Nerve Endings Drug Effects Opioid Peptides Pharmacology Substance P Metabolism Animals Calcium GTP-Binding Proteins Inositol 1,4,5-Trisphosphate Ion Transport Mice Mutation Oligonucleotides, Antisense Pertussis Toxin Receptors, Opioid Agonists Tachykinins Genetics Virulence Factors, Bordetella Research Support, Non-U.S. Gov't Multidisciplinary |
| Content Type | Text |
| Resource Type | Article |
| Subject | Multidisciplinary |
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