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Antagonism of Oxytocin Prevents Suckling- and Estradiol-Induced, But Not Progesterone-Induced, Secretion of Prolactin

Department of Biological Science (J.E.K., M.O.P., C.A.F., M.E.F.) and Program in Neuroscience (J.E.K., M.E.F.), Florida State University, Tallahassee, Florida 32306

Address all correspondence and requests for reprints to: Dr. Marc Freeman, Department of Biological Science, Program in Neuroscience, Florida State University, Tallahassee, Florida 32306. E-mail: freeman{at}neuro.fsu.edu.

In female rats, estradiol (E₂) and suckling induce prolactin (PRL) secretion. This involves inhibition of hypothalamic dopaminergic tone and stimulation by a PRL-releasing hormone, possibly oxytocin (OT). Infusing an OT antagonist (OTA) iv, we evaluated the role of OT on suckling- and E₂-induced PRL secretion. Three days after parturition at 0900 h, lactating dams were fitted with 24-h osmotic minipumps filled with saline or OTA. On d 5 of lactation, pups were separated from their dams for 6 h. Immediately or 20 min after the resumption of suckling, dam trunk blood was collected. Also, ovariectomized (OVX) rats were treated with E₂ (OVE) and OTA at 1000 h on d 1. Blood samples were obtained from 1300 to 2100 h on d 2 for PRL measurements. Additionally, OVX rats were evaluated on d 2 after receiving progesterone (P₄). OTA blocked suckling and E₂-induced release of PRL but not that induced by E₂+P₄. Pups from treated dams failed to gain weight when allowed to nurse for 20 min on d 5 but gained more than 7 g when nursed on d 7 of lactation, indicating that the OTA was active 48 h later. Western blot analysis showed that E₂ treatment increased OT receptors in the anterior pituitary when compared with OVX animals. No further increase was observed in response to the P₄, suggesting that the enhancing effect of P₄ on E₂-induced PRL release may act through mechanisms independent of OT. These data demonstrate the role of OT in the control of suckling and steroid-induced PRL secretion.