Superoxide signaling in pain is independent of nitric oxide signaling

Hee Young Kim, Jigong Wang, Ying Lu, Jin Chung, Kyungsoon Chung

Research output: Contribution to journalArticle

23 Citations (Scopus)

Abstract

Two reactive oxygen species (ROS), nitric oxide (NO) and superoxide (O2), contribute to persistent pain. Using three different animal models where ROS mediate pain, this study examined whether NO and O2 converge to peroxynitrite (ONOO) or whether each has an independent signaling pathway to produce hyperalgesia. The hyperalgesia after spinal nerve ligation was attenuated by removing O2 by TEMPOL or inhibiting NO production by L-NAME, but not by removing peroxynitrite with FeTMPyP. Nitric oxide-induced hyperalgesia was not affected by removing O2 but was reduced by a guanyl cyclase inhibitor. Superoxide-induced hyperalgesia was not affected by inhibiting NO production but was suppressed by a protein kinase C inhibitor. The data suggest that NO and O2 operate independently to generate pain.

Original languageEnglish (US)
Pages (from-to)1424-1428
Number of pages5
JournalNeuroReport
Volume20
Issue number16
DOIs
StatePublished - Oct 28 2009

Fingerprint

Superoxides
Nitric Oxide
Hyperalgesia
Pain
Peroxynitrous Acid
Reactive Oxygen Species
Spinal Nerves
Protein C Inhibitor
Guanylate Cyclase
NG-Nitroarginine Methyl Ester
Protein Kinase Inhibitors
Protein Kinase C
Ligation
Animal Models

Keywords

  • Hyperalgesia
  • Pain signaling pathway
  • Peroxynitrite
  • Reactive oxygen species

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Superoxide signaling in pain is independent of nitric oxide signaling. / Kim, Hee Young; Wang, Jigong; Lu, Ying; Chung, Jin; Chung, Kyungsoon.

In: NeuroReport, Vol. 20, No. 16, 28.10.2009, p. 1424-1428.

Research output: Contribution to journalArticle

Kim, Hee Young ; Wang, Jigong ; Lu, Ying ; Chung, Jin ; Chung, Kyungsoon. / Superoxide signaling in pain is independent of nitric oxide signaling. In: NeuroReport. 2009 ; Vol. 20, No. 16. pp. 1424-1428.
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