Opioids influence neurohypophysial but not central oxytocin release following direct hyperosmotic stimulation of the supraoptic nucleus in urethane-anaesthetised rats

G Munro, M Ludwig, R Landgraf, J A Russell

Research output: Contribution to journalArticlepeer-review

Abstract

Microdialysis was used to apply an osmotic stimulus (0.5 M NaCl-aCSF) into both supraoptic nuclei (SON) to investigate the role of endogenous opioid peptides in the control of both central and peripheral oxytocin release in response to this stimulus. There were no differences in central peptide release during direct hyperosmotic stimulation between groups of rats given either vehicle, morphine (5 mg/kg) or naloxone (5 mg/kg) intravenously. Naloxone potentiated oxytocin release into blood; this suggests that endogenous opioid peptides at the level of the neurohypophysis, but not in the SON are important modulators of oxytocin release to this stimulus. However morphine blocked oxytocin release into blood indicative of a central inhibitory action on the firing rate of oxytocin neurones, contrasted with insensitivity to morphine of oxytocin secretion from the dendrites stimulated directly by hyperosmolarity.

Original languageEnglish
Pages (from-to)121-7
Number of pages7
JournalNeuropeptides
Volume27
Issue number2
Publication statusPublished - Aug 1994

Keywords / Materials (for Non-textual outputs)

  • Animals
  • Female
  • Microdialysis
  • Morphine
  • Naloxone
  • Opioid Peptides
  • Osmotic Pressure
  • Oxytocin
  • Pituitary Gland, Posterior
  • Rats
  • Rats, Sprague-Dawley
  • Stimulation, Chemical
  • Supraoptic Nucleus
  • Urethane

Fingerprint

Dive into the research topics of 'Opioids influence neurohypophysial but not central oxytocin release following direct hyperosmotic stimulation of the supraoptic nucleus in urethane-anaesthetised rats'. Together they form a unique fingerprint.

Cite this