{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2023,10,12]],"date-time":"2023-10-12T21:41:42Z","timestamp":1697146902903},"reference-count":53,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2002,5,22]],"date-time":"2002-05-22T00:00:00Z","timestamp":1022025600000},"content-version":"vor","delay-in-days":141,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Cellular Biochemistry"],"published-print":{"date-parts":[[2002,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Although it is well known that plasma concentration of prolactin (PRL) increases during aging in rats, how the anterior pituitary (AP) aging per se affects PRL secretion remains obscure. The objectives of this study were to determine if changes in the pituitary PRL responsiveness to acetylcholine (ACh; a paracrine factor in the AP), as compared with that to other PRL stimulators or inhibitors, contribute to the known age\u2010related increase in PRL secretion, and if protein kinase C (PKC) is involved. We also determined if replenishment with aging\u2010declined hormones such as estrogen\/thyroid hormone influences the aging\u2010caused effects on pituitary PRL responses. AP cells were prepared from old (23\u201324\u2010month\u2010old) as well as young (2\u20133\u2010month\u2010old) ovariectomized rats. Cells were pretreated for 5 days with diluent or 17\u03b2\u2010estradiol (E<jats:sub>2<\/jats:sub>; 0.6 nM) in combination with or without triiodothyronine (T<jats:sub>3<\/jats:sub>; 10 nM). Then, cells were incubated for 20 min with thyrotropin\u2010releasing hormone (TRH; 100 nM), angiotensin II (AII; 0.2\u201320 nM), vasoactive intestinal peptide (VIP; 10<jats:sup>\u22129<\/jats:sup>\u201310<jats:sup>\u22125<\/jats:sup> M), dopamine (DA; 10<jats:sup>\u22129<\/jats:sup>\u201310<jats:sup>\u22125<\/jats:sup> M), or ACh (10<jats:sup>\u22127<\/jats:sup>\u201310<jats:sup>\u22123<\/jats:sup> M). Cells were also challenged with ACh, TRH, or phorbol 12\u2010myristate 13\u2010acetate (PMA; 10<jats:sup>\u22126<\/jats:sup> M) following PKC depletion by prolonged PMA (10<jats:sup>\u22126<\/jats:sup> M for 24 h) pretreatment. We found that estrogen priming of AP cells could reverse the aging\u2010caused effects on pituitary PRL responses to AII and DA. In hormone\u2010replenished cells aging enhanced the stimulation of PRL secretion by TRH and PMA, but not by AII and VIP. Aging also reduced the responsiveness of cells to ACh and DA in suppressing basal PRL secretion, and attenuated ACh inhibition of TRH\u2010induced PRL secretion. Furthermore, ACh suppressed TRH\u2010induced PRL secretion mainly via the PMA\u2010sensitive PKC in the old AP cells, but via additional mechanisms in young AP cells. On the contrary, basal PRL secretion was PKC (PMA\u2010sensitive)\u2010independent in the old AP cells, but dependent in the young AP cells. Taken together, these results suggest differential roles of PMA\u2010sensitive PKC in regulating basal and ACh\u2010regulated PRL responses in old versus young AP cells. The persistent aging\u2010induced differences in AP cell responsiveness to ACh, DA, TRH, and PMA following hormone (E<jats:sub>2<\/jats:sub>\/T<jats:sub>3<\/jats:sub>) replenishment suggest an intrinsic pituitary change that may contribute, in part, to the elevated in vivo PRL secretion observed in aged rats. J. Cell. Biochem. 86: 268\u2013276, 2002. \u00a9 2002 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jcb.10213","type":"journal-article","created":{"date-parts":[[2002,10,6]],"date-time":"2002-10-06T11:34:39Z","timestamp":1033904079000},"page":"268-276","source":"Crossref","is-referenced-by-count":1,"title":["Differential involvement of protein kinase C in basal versus acetylcholine\u2010regulated prolactin secretion in rat anterior pituitary cells during aging"],"prefix":"10.1002","volume":"86","author":[{"given":"Hsiao\u2010Fung","family":"Pu","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tsuei\u2010Chu","family":"Liu","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2002,6,24]]},"reference":[{"key":"e_1_2_6_2_1","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1522-2683(20000101)21:2<452::AID-ELPS452>3.0.CO;2-L"},{"key":"e_1_2_6_3_1","first-page":"223","article-title":"c\u2010AMP concentration in various organs of female rats and in human ovaries with aging","volume":"34","author":"Arima M","year":"1982","journal-title":"Acta Obstet Gynaecol Jpn"},{"key":"e_1_2_6_4_1","doi-asserted-by":"publisher","DOI":"10.1210\/endo-129-4-2231"},{"key":"e_1_2_6_5_1","doi-asserted-by":"publisher","DOI":"10.1016\/0014-5793(81)80523-6"},{"key":"e_1_2_6_6_1","doi-asserted-by":"crossref","first-page":"144","DOI":"10.1210\/endo.137.1.8536606","article-title":"Autocrine and\/or paracrine action of vasoactive intestinal peptide on thyrotropin\u2010releasing hormone\u2010induced prolactin release","volume":"137","author":"Balsa JA","year":"1996","journal-title":"Endocrinology"},{"key":"e_1_2_6_7_1","doi-asserted-by":"publisher","DOI":"10.1159\/000124714"},{"key":"e_1_2_6_8_1","doi-asserted-by":"publisher","DOI":"10.1016\/0303-7207(88)90193-1"},{"key":"e_1_2_6_9_1","doi-asserted-by":"crossref","first-page":"3453","DOI":"10.1210\/endo.130.6.1534540","article-title":"Dopamine receptor activation inhibits estrogen\u2010stimulated transforming growth factor\u2010\u03b1 gene expression and growth in anterior pituitary, but not in uterus","volume":"130","author":"Borgundvaag B","year":"1992","journal-title":"Endocrinology"},{"key":"e_1_2_6_10_1","doi-asserted-by":"crossref","first-page":"3416","DOI":"10.1210\/endo.139.8.6146","article-title":"Thyrotropin\u2010releasing hormone gene expression in the anterior pituitary. 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