Endogenous opioid control of somatodendritic oxytocin release from the hypothalamic supraoptic and paraventricular nuclei in vitro.

Oxytocin release was measured in a perifusion system from microdissected supraoptic (SO) and paraventricular (PV) nuclei of ovariectomised female rats. An initial period of electrical stimulation (S1) applied through a pair of platinum electrodes evoked an increase in peptide release, however, subsequent periods of stimulation (S2, S3, S4) were increasingly less effective, suggesting depletion of releasable stores. However, addition of the opioid antagonist, naloxone (5 x 10(-5) M), during periods S2 and S3 potentiated this stimulated oxytocin release, indicating the presence of an endogenous opioid inhibition. Tissue from ovariectomised animals pre-treated with progesterone for 3 days showed increased basal secretion but no naloxone-induced potentiation of electrically-stimulated release. However, increasing the naloxone concentration (5 x 10(-5) M) again revealed a potentiation, indicating that progesterone had caused a shift in the effective dose of the antagonist. These data demonstrate that, like their axon terminals in the neurohypophysis, the dendrites of magnocellular oxytocin neurones are under control of endogenous opioids, and that progesterone causes an increase in this opioid tone. This may function to regulate intranuclear oxytocin secretion in the pregnant and periparturient animal.