{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,20]],"date-time":"2026-07-20T14:19:57Z","timestamp":1784557197662,"version":"3.55.0"},"reference-count":41,"publisher":"Bioscientifica","issue":"1","content-domain":{"domain":["joe.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2012,7]]},"abstract":"<jats:p>\n                    The neurotransmitter dopamine (DA) is known to inhibit prolactin (PRL) secretion and the proliferation of lactotropes in the pituitary gland. Dopamine-2 (D2) receptor short (D2S) isoform is expressed in a reduced level while the D2 receptor long (D2L) isoform is expressed in an elevated level during estradiol (E\n                    <jats:sub>2<\/jats:sub>\n                    )-induced PRL production and cell proliferation in lactotropes. To evaluate the role of these D2 receptor isoforms in E\n                    <jats:sub>2<\/jats:sub>\n                    -regulated lactotropic cell function, we compared E\n                    <jats:sub>2<\/jats:sub>\n                    effects on the level of PRL, cell proliferation, and G proteins in enriched lactotropes and lactotrope-derived PR1 cells containing only D2S isoform (D2S cells), D2L isoform (D2L cells), or no D2 receptor (V cells). Additionally, we determined the effects of G protein blockade on the E\n                    <jats:sub>2<\/jats:sub>\n                    -induced PRL production and cell proliferation in these cells. We here show that E\n                    <jats:sub>2<\/jats:sub>\n                    actions on G proteins, PRL production, and cell proliferation were maximally achieved in D2S cells, oppositely or marginally achieved in D2L cells, and absent in V cells. We also show that the DA and pertussis toxin modulations of E\n                    <jats:sub>2<\/jats:sub>\n                    actions on PRL, G proteins, and cell proliferation were maximally achieved in D2S cells compared with in D2L or V cells. Furthermore, we provide evidence for the existence of an inhibitory action of Gi3 on Gs that is under the control of the D2S receptor and is inhibited by E\n                    <jats:sub>2<\/jats:sub>\n                    . These results suggest that the suppression of D2S-regulated Gi3 inhibition of Gs protein may be one of the mechanisms controlling E\n                    <jats:sub>2<\/jats:sub>\n                    -activated PRL synthesis and cell proliferation in lactotropes.\n                  <\/jats:p>","DOI":"10.1530\/joe-12-0125","type":"journal-article","created":{"date-parts":[[2012,5,10]],"date-time":"2012-05-10T00:43:46Z","timestamp":1336610626000},"page":"67-78","update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-1","source":"Crossref","is-referenced-by-count":5,"title":["Estrogen inhibits D2S receptor-regulated Gi3 and Gs protein interactions to stimulate prolactin production and cell proliferation in lactotropic cells"],"prefix":"10.1530","volume":"214","author":[{"given":"A","family":"Sengupta","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"D 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