Neurohypophysial opioids and oxytocin secretion: source of inhibitory opioids.
When electrical stimuli are applied to the neural stalk of the pituitary, oxytocin, vasopressin, and probably several opioid peptides also contained in nerve terminals in the gland are released: one action of the released opioids appears to be to inhibit oxytocin release by an action that has been likened to pre-synaptic inhibition. Thus, when Clarke et al. (1979) stimulated the neural stalk following intravenous injection of the opioid antagonist naloxone, they observed that the evoked oxytocin release was potentiated. In the present study we confirm this result and show that oxytocin release evoked by stimulation of the supraoptic nucleus is similarly potentiated by naloxone. This finding is consistent with the hypothesis that the opioid responsible for inhibition of oxytocin release coexists with either oxytocin or vasopressin. We further report that the specific delta-receptor antagonist ICI 174864 does not potentiate oxytocin release either in vivo or in vitro. Thus, it seems unlikely that the enkephalins, putative delta-receptor agonists present in neurohypophysial fibres, are the opioids responsible for the observed inhibition of oxytocin release.
D000818:Animals; D004558:Electric Stimulation; D004723:Endorphins / Q000502:physiology*; D004743:Enkephalin, Leucine / Q000031:analogs & derivatives / Q000494:pharmacology; D005260:Female; D007774:Lactation; D009270:Naloxone / Q000494:pharmacology; D009433:Neural Inhibition; D010121:Oxytocin / Q000378:metabolism*; D010904:Pituitary Gland, Posterior / Q000378:metabolism*; D011247:Pregnancy; D051381:Rats; D011957:Receptors, Opioid / Q000502:physiology*; D017465:Receptors, Opioid, delta; D013495:Supraoptic Nucleus / Q000502:physiology*
D004723:Endorphins; D011957:Receptors, Opioid; D017465:Receptors, Opioid, delta; D009270:Naloxone; D010121:Oxytocin; D004743:Enkephalin, Leucine; C040643:N,N-diallyl-tyrosyl-alpha-aminoisobutyric acid-phenylalanyl-leucine