The stimulatory effect of dopamine (DA) on the release of oxytocin (OT) in lactating rats is exerted at the D-1 DA receptor subtype. Because the neural loci mediating this effect have not been identified, the objective of the present studies was to test whether OT release in the lactating rat would be elevated after central administration of a D-1 DA receptor agonist into the third ventricle (3V) or directly into either the rostral paraventricular/anterior commissural nucleus area (PVN/ACN), the central paraventricular nucleus area, or the supraoptic nucleus (SON), all of which contain OT neurosecretory cells. Lactating rats were implanted with a stainless steel cannula directed into one of the above areas or into the arcuate-ventromedial region of the medial basal hypothalamus (MBH), or sites dorsal to the PVN/ACN or SON, which served as anatomical controls. After 6-7 days of recovery, each animal received an intra-atrial cannula for sequential blood sampling, and was used in experiments 24 h later. Animals were separated from their litters, and following a period of basal blood sampling, received central microinjections of either vehicle, the D-1 DA receptor agonist SKF-38393, or the D-2 DA receptor agonist quinpirole, and blood samples were removed periodically for 60 min. An injection of angiotensin II (Ang II, 100 ng) was made into each site as a positive control for OT release. Injection of SKF-38393 (12.5 or 50 µg/5 µl) into the 3V resulted in a statistically significant and dose-releated increase in plasma OT concentrations, which was attenuated by intravenous pretreatment with the specific D-1 DA receptor antagonist, SCH-23390 (1.2 mg/kg). Unilateral injection of SKF-38393 (8 µg) into the SON region also produced a significant increase in plasma OT concentrations, while more modest increases followed injection of this agent into the PVN sites. Systemic pretreatment with the D-1 DA antagonist also blocked the effect of SKF-38393 in the SON. Plasma OT concentrations were not significantly changed after administration of SKF-38393 into the MBH or to dorsal control sites, or after any central injections of vehicle or the D-2 agonist quinpirole. Ang II markedly stimulated OT release after administration to 3V, PVN, SON and MBH, but not to the control sites dorsal to the PVN and SON. The present findings extend previous observations that D-1 DA receptors mediate the central dopaminergic stimulation of OT secretion in the lactating rat, and suggest that the SON region may be an important locus for this effect.

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