Nociceptin (1 - 7) antagonizes nociceptin-induced hyperalgesia in mice.

Nociceptin and its N-terminal fragment, nociceptin (1 7), were administered intrathecally (i.t.) into conscious mice. Nociceptin (3.0 fmol) produced a significant reduction in the nociceptive thermal threshold (hyperalgesia) measured as the tail-flick and paw-withdrawal responses. Nociceptin (1-7), injected i.t., at 150-1200 fmol had no significant effect. However, when nociceptin (1-7) (150 1200 fmol) was injected simultaneously with nociceptin (3.0 fmol), nociceptin-induced hyperalgesia was significantly reduced. Analgesia induced by a high dose (1200 pmol) of nociceptin was not antagonized by co-administration of nociceptin (1-7) (1200 fmol). These results suggest that N-terminal fragments of nociceptin formed endogenously could modulate the hyperalgesic action of nociceptin in the spinal cord.
AuthorsT Sakurada, S Sakurada, S Katsuyama, C Sakurada, K Tan-No, L Terenius
JournalBritish journal of pharmacology (Br J Pharmacol) Vol. 128 Issue 5 Pg. 941-4 (Nov 1999) ISSN: 0007-1188 [Print] ENGLAND
PMID10556929 (Publication Type: Journal Article)
Chemical References
  • Opioid Peptides
  • Peptide Fragments
  • Receptors, Opioid
  • nociceptin
  • nociceptin receptor
  • Amino Acid Sequence
  • Animals
  • Hyperalgesia (chemically induced, prevention & control)
  • Injections, Intraventricular
  • Injections, Spinal
  • Male
  • Mice
  • Molecular Sequence Data
  • Opioid Peptides (antagonists & inhibitors)
  • Pain Measurement (drug effects)
  • Peptide Fragments (administration & dosage, chemical synthesis, pharmacology)
  • Reaction Time (drug effects)
  • Receptors, Opioid (metabolism)
  • Spinal Cord (drug effects, metabolism)

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