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.
journal_name
Proc Natl Acad Sci U S Aauthors
Inoue M,Kobayashi M,Kozaki S,Zimmer A,Ueda Hdoi
10.1073/pnas.95.18.10949subject
Has Abstractpub_date
1998-09-01 00:00:00pages
10949-53issue
18eissn
0027-8424issn
1091-6490journal_volume
95pub_type
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