Nociceptin/orphanin FQ-induced nociceptive responses through substance P release from peripheral nerve endings in mice.

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.

authors

Inoue M,Kobayashi M,Kozaki S,Zimmer A,Ueda H

doi

10.1073/pnas.95.18.10949

subject

Has Abstract

pub_date

1998-09-01 00:00:00

pages

10949-53

issue

18

eissn

0027-8424

issn

1091-6490

journal_volume

95

pub_type

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