Antagonism of oxytocin prevents suckling- and estradiol-induced, but not progesterone-induced, secretion of prolactin.

Authors: Kennett, JE  Poletini, MO  Fitch, CA  Freeman, ME 
Citation: Kennett JE, etal., Endocrinology. 2008 Dec 23.
Pubmed: (View Article at PubMed) PMID:19106214
DOI: Full-text: DOI:10.1210/en.2008-1611

In female rats, estradiol (E2)-administration and suckling induce secretion of prolactin (PRL). This involves inhibition of hypothalamic dopaminergic tone and stimulation by a PRL-releasing-hormone, possibly oxytocin (OT). Using an OT antagonist (OTA), we evaluated the role of OT on suckling- and E2-induced secretion of PRL. Three days after parturition, lactating dams were fitted with 24h Alzet osmotic minipumps filled with saline or OTA. On day 5 of lactation, pups were separated from their dams for 6h. Immediately or 20 minutes after the resumption of suckling, trunk blood was collected by decapitation of the dams. Also, OVX rats treated with E2 (OVE) and OTA and blood samples were obtained from 1300-2100 h on day 2 for PRL measurements. Additionally, OVE rats were evaluated after receiving progesterone (P4) on day 2. OTA blocked suckling and E2-induced release of PRL but not that induced by E2+P4. Pups from OTA-treated dams failed to gain weight when allowed to nurse for 20 minutes on day 5 but gained over 7 g when nursed on day 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 to 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 possible role of OT in the control of two physiological states of PRL secretion, suckling- and steroid-induced.

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CRRD ID: 2303958
Created: 2009-03-02
Species: All species
Last Modified: 2009-03-02
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.