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This Article Accepted manuscript (PDF) All Versions of this Article: JOE-08-0486v1 202/1/153    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Trott, J. Articles by Hovey, R. Search for Related Content PubMed PubMed Citation Articles by Trott, J. Articles by Hovey, R.

J Trott, Animal Science, University of California, Davis, Davis, United States
K Horigan, Animal Science, University of Vermont, Burlington, United States
J Gloviczki, Animal Science, University of California, Davis, Davis, United States
K Costa, Animal Science, University of Vermont, Burlington, United States
B Freking, U.S. Meat Animal Research Center, USDA, Clay Center, United States
C Farmer, Agriculture and Agri-Food Canada, Sherbrooke, Quebec, Canada
K Hayashi, Department of Physiology, Southern Illinois University School of Medicine, Carbondale, United States
T Spencer, Animal Science, Texas A&M University, College Station, United States
J Morabito, Animal Science, University of Vermont, Burlington, United States
R Hovey, Animal Science, University of California, Davis, Davis, 95616-8521, United States

Correspondence: Russell Hovey, Email: rchovey{at}ucdavis.edu

Prolactin (PRL) acts through its receptor (PRLR) via both endocrine and local paracrine/autocrine pathways to regulate biological processes including reproduction and lactation. We analyzed the tissue- and stage of gestation-specific regulation of PRL and PRLR expression in various tissues of pigs. Abundance of pPRLR-long form (LF) mRNA increased in the mammary gland and endometrium during gestation while in other tissues it remained constant. There was a parallel increase in the abundance of the pPRLR-LF protein in mammary gland and endometrium during gestation. We determined the hormonal regulation of pPRLR-LF mRNA expression in various tissues from ovariectomized, hypoprolactinemic gilts given combinations of the replacement hormones estrogen (E), progestin (P) and/or haloperidol-induced PRL. Abundance of pPRLR-LF mRNA in kidney and liver was unaffected by hormone treatments. Expression of uterine pPRLR-LF mRNA was induced by E whereas the effect of E was abolished by co-administering P. The expression of pPRLR-LF mRNA in the mammary gland stroma was induced by PRL, whereas E induced its expression in the epithelium. In contrast to these changes in pPRLR expression, pPRL expression was relatively constant and low during gestation in all tissues except the pituitary. Taken together, these data reveal that specific combinations of E, P and PRL differentially regulated pPRLR-LF expression in the endometrium and mammary glands, and that the action of PRL on its target tissues is dependant upon pPRLR-LF abundance moreso than local PRL expression.