Effect of dynorphin-(1-13) and related peptides on respiratory rate and morphine-induced respiratory rate depression

Eur J Pharmacol. 1983 Dec 9;96(1-2):117-22. doi: 10.1016/0014-2999(83)90537-x.

Abstract

Previous studies from our laboratory have shown that the opioid peptide dynorphin-(1-13), although not analgesic when given by itself, can inhibit morphine-induced analgesia in naive mice and potentiate it in morphine tolerant mice. In the present study, we examined the effect of dynorphin-(1-13) with two other dynorphin-like peptides, alpha-neoendorphin and dynorphin-(1-10) amide, on respiration. Our results show that none of the peptides studied had any significant activity on the respiratory rate in mice when given alone. However, in the presence of morphine, dynorphin-(1-13) antagonized the morphine-induced respiratory rate depression in morphine-tolerant animals; alpha-neoendorphin enhanced the morphine-induced respiratory rate depression in naive but had no effect in morphine-tolerant animals and dynorphin-(1-10) amide had no modulatory effect on the morphine-induced respiratory rate depression in either group of animals.

Publication types

  • Comparative Study
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Drug Tolerance
  • Dynorphins*
  • Endorphins / pharmacology*
  • Male
  • Mice
  • Mice, Inbred ICR
  • Morphine / antagonists & inhibitors*
  • Peptide Fragments / pharmacology*
  • Protein Precursors / pharmacology
  • Respiration / drug effects*

Substances

  • Endorphins
  • Peptide Fragments
  • Protein Precursors
  • alpha-neoendorphin
  • dynorphin (1-13)
  • Dynorphins
  • Morphine
  • dynorphin amide (1-10)