Opioids influence neurohypophysial but not central oxytocin release following direct hyperosmotic stimulation of the supraoptic nucleus in urethane-anaesthetised rats.
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.
Munro
G
G
Department of Physiology, University Medical School, Edinburgh, UK.
Ludwig
M
M
Landgraf
R
R
Russell
J A
JA
D000818:Animals; D005260:Female; D017551:Microdialysis; D009020:Morphine / Q000494:pharmacology*; D009270:Naloxone / Q000494:pharmacology*; D018847:Opioid Peptides / Q000502:physiology*; D009997:Osmotic Pressure; D010121:Oxytocin / Q000378:metabolism*; D010904:Pituitary Gland, Posterior / Q000187:drug effects* / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D013268:Stimulation, Chemical; D013495:Supraoptic Nucleus / Q000187:drug effects* / Q000378:metabolism; D014520:Urethane
D018847:Opioid Peptides; D009270:Naloxone; D014520:Urethane; D010121:Oxytocin; D009020:Morphine