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Neurohypophysial opioids and oxytocin secretion: source of inhibitory opioids
Abstract:
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.
Insights
Opioid peptides inhibit oxytocin release from the pituitary gland. Blocking these opioids with naloxone potentiates oxytocin release, suggesting opioids coexist with oxytocin or vasopressin.
Area of Science:
- Neuroendocrinology
- Peptide Hormone Research
Background:
- Electrical stimulation of the pituitary neural stalk releases oxytocin, vasopressin, and opioid peptides.
- Released opioids may inhibit oxytocin release via presynaptic inhibition.
Purpose of the Study:
- To confirm and extend findings on opioid inhibition of oxytocin release.
- To investigate the specific opioid receptor involved in this inhibition.
Main Methods:
- Stimulation of the neural stalk and supraoptic nucleus in vivo.
- Administration of opioid antagonist naloxone.
- Administration of delta-receptor antagonist ICI 174864.
- In vitro and in vivo experiments.
Main Results:
- Naloxone potentiated oxytocin release evoked by neural stalk stimulation.
- Naloxone also potentiated oxytocin release evoked by supraoptic nucleus stimulation.
- The delta-receptor antagonist ICI 174864 did not potentiate oxytocin release.
Conclusions:
- Opioid inhibition of oxytocin release is confirmed and appears to involve coexisting peptides.
- Enkephalins acting on delta-receptors are unlikely to be responsible for this opioid-mediated inhibition.