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 microdissect ed supraoptic (SO) and paraventricular (PV) nuclei of ovariectomised f emale rats. An initial period of electrical stimulation (S1) applied t hrough a pair of platinum electrodes evoked an increase in peptide rel ease, however, subsequent periods of stimulation (S2, S3, S4) were inc reasingly less effective, suggesting depletion of releasable stores. H owever; addition of the opioid antagonist, naloxone (5 x 10(-5) M), du ring periods S2 and S3 potentiated this stimulated oxytocin release, i ndicating the presence of an endogenous opioid inhibition. Tissue from ovariectomised animals pre-treated with progesterone for 3 days showe d increased basal secretion but no naloxone-induced potentiation of el ectrically-stimulated release. However, increasing the naloxone concen tration (5 x 10(-4) M) again revealed a potentiation, indicating that progesterone had caused a shift in the effective dose of the antagonis t. These data demonstrate that, like their axon terminals in the neuro hypophysis, the dendrites of magnocellular oxytocin neurones are under control of endogenous opioids, and that progesterone causes an increa se in this opioid tone. This may function to regulate intranuclear oxy tocin secretion in the pregnant and periparturient animal.