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However, the functions of these receptors in the pituitary have not been reported to date. In the present study, we show that the expression of mPR<\/jats:styled-content><\/jats:italic>\u03b1 was the highest among the mPR<\/jats:styled-content>s<\/jats:italic> in the rat anterior pituitary gland. Immunostaining of mPR<\/jats:styled-content>\u03b1 was detected in somatotrophs, gonadotrophs and lactotrophs. Interestingly, 63% of mPR<\/jats:styled-content>\u03b1\u2010positive cells within the pituitary were lactotrophs, suggesting that mPR<\/jats:styled-content>\u03b1 is involved in controlling prolactin (PRL<\/jats:styled-content>) secretion in the pituitary. To test this hypothesis, rat pituitaries were incubated (1\u00a0hour) with either progesterone (P4) or the mPR<\/jats:styled-content>\u03b1\u2010specific agonist Org OD<\/jats:styled-content> 02\u20100. PRL<\/jats:styled-content> secretion was then measured by radioimmunoassay. The results of this experiment revealed that both P4 and Org OD<\/jats:styled-content> 02\u20100 decreased PRL<\/jats:styled-content> secretion. Moreover, the results from the GH<\/jats:styled-content>3 cell line (CCL<\/jats:styled-content>\u201082.1) showed that P4 and Org OD<\/jats:styled-content> 02\u20100 inhibited PRL<\/jats:styled-content> release, although the nuclear PR<\/jats:styled-content> agonist R5020 was ineffective. Our investigation of the cellular mechanisms behind mPR<\/jats:styled-content>\u03b1 activity indicated that both P4 and Org OD<\/jats:styled-content> 02\u20100 decreased cAMP<\/jats:styled-content> accumulation, whereas R5020 was ineffective. In addition, the Org OD<\/jats:styled-content> 02\u20100\u2010effect on PRL<\/jats:styled-content> release was blocked by pretreatment with pertussis toxin, an inhibitor of Go\/Gi proteins. Because transforming growth factor (TGF)<\/jats:styled-content>\u03b21 is a potent inhibitor of PRL<\/jats:styled-content> secretion in lactotrophs, we lastly evaluated whether TGF<\/jats:styled-content>\u03b21 was activated by progesterone and whether this effect was mediated by mPR<\/jats:styled-content>\u03b1. Our results showed that P4 and Org OD<\/jats:styled-content> 02\u20100, but not R5020, increased active TGF<\/jats:styled-content>\u03b21 levels. This effect was not observed when cells were transfected with mPR<\/jats:styled-content>\u03b1\u2010small interfering RNA<\/jats:styled-content>. Taken together, these data provide new evidence suggesting that mPR<\/jats:styled-content>\u03b1 mediates the progesterone inhibitory effect on PRL<\/jats:styled-content> secretion through both decreases in cAMP<\/jats:styled-content> levels and activation of TGF<\/jats:styled-content>\u03b21 in the lactotroph population.<\/jats:p>","DOI":"10.1111\/jne.12614","type":"journal-article","created":{"date-parts":[[2018,6,5]],"date-time":"2018-06-05T11:15:46Z","timestamp":1528197346000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":22,"title":["Participation of membrane progesterone receptor \u03b1 in the inhibitory effect of progesterone on prolactin secretion"],"prefix":"10.1111","volume":"30","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5160-5523","authenticated-orcid":false,"given":"M. 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