Stimulation and inhibition of prolactin release from rat pituitary lactotrophs by the cholinomimetic carbachol in vitro. Influence of hormonal environment and intercellular contacts

Carmeliet, Peter; Maertens, Philippe; Denef, Carl

doi:10.1016/0303-7207(89)90088-9

Cited by 19 publications

(15 citation statements)

References 50 publications

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“…The ineffectivenss of ACh in diluent-pretreatment cells is consistent with the unaltered basal PRL secretion in response to carbachol observed by Campbell et al [16], using AP fragments. The inhibition by ACh on basal PRL secretion in the presence of E 2 and T 3 is similarly observed by Carmeliet et al [2]in T 3 /dexamethasone pretreated rat AP cells, and in rat pituitary tumor GH 4 C 1 cells [14]. However, we further demonstrated that the availability of E 2 and T 3 in the culture medium also influences the efficacy of ACh suppression of TRH-stimulated PRL secretion.…”

Section: Discussionsupporting

confidence: 43%

“…In addition, acetylcholine (ACh), synthesized in the pituitary, has been implicated as a local regulator of pituitary function [10, 11, 12]. The identification of cholinergic receptors in the AP [13]further supports sites of ACh action in this tissue [2, 14, 15]. …”

Section: Introductionmentioning

confidence: 99%

“…Basal PRL secretion by normal rat pituitary cells was found to be unaltered, enhanced or suppressed by cholinergic compounds, depending on the hormonal environment and close cellular association [2, 16]. In pituitary tumor GH 3 cells, ACh antagonized the vasoactive intestinal peptide (VIP)-stimulated activity of adenylate cyclase and PRL secretion [17]; however, Wang et al [18]reported the potentiation of TRH-stimulated PRL mRNA levels by ACh.…”

Section: Introductionmentioning

confidence: 99%

“…Production of prolactin (PRL) by lactotropes in the anterior pituitary (AP) gland can be regulated by many inhibitory and stimulatory factors released from the hypothalamus and synthesized in the pituitary as well as by the circulating hormones [1, 2, 3, 4, 5]. Among these factors, 17β-estradiol (E 2 ), thyroid hormones, and thyrotropin-releasing hormone (TRH) are known to affect both synthesis and secretion of PRL [1, 5, 6, 7, 8].…”

Section: Introductionmentioning

confidence: 99%

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Muscarinic Regulation of Basal versus Thyrotropin-Releasing Hormone-Induced Prolactin Secretion in Rat AnteriorPituitary Cells

Pu¹,

Tan²,

Chen³

et al. 1999

Neuroendocrinology

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Acetylcholine (ACh), synthesized in the pituitary, can act locally to modulate pituitary function. We used rat primary anterior pituitary (AP) cells to investigate how ACh affects pituitary prolactin (PRL) secretion in the presence or absence of known PRL regulators: thyrotropin-releasing hormone (TRH), 17β-estradiol (E₂) and triiodothyronine (T₃). Cultured AP cells were prepared from ovariectomized rats and pretreated with diluent, 0.6 nM E₂, 10 nM T₃, or E₂ plus T₃ for 5 days, then challenged with various doses of ACh or muscarinic receptor agonists (oxotremorine or carbachol) and TRH (100 nM) for 20 min. Significant ACh (10^–5M) suppression of both basal and TRH-induced PRL secretion was not evident in diluent-, E₂- or T₃-pretreated cells, but observed only in cells pretreated with both E₂ and T₃. Moreover, in E₂ plus T₃-pretreated cells, oxotremorine and carbachol, like ACh (10^–7–10^–5M), suppressed both responses in a dose- related manner. Pertussis toxin (PTX; 100 ng/ml) as well as atropine (a muscarinic receptor antagonist; 1 mM) blocked these effects of cholinomimetics. ACh also inhibited both PRL responses elicited by drugs elevating intracellular cAMP (10 µM forskolin) or Ca²⁺ (1 µM Bay K-8644) in a PTX-sensitive manner. ACh inhibition of basal PRL secretion was unaltered by intracellular Ca²⁺ mobilization blockers, TMB-8 (100 µM) and thapsigargin (1 µM), but abrogated by the nitric oxide synthase inhibitor (300 µM L-NAME). ACh inhibition of TRH-induced PRL secretion was accentuated by TMB-8 and alleviated by thapsigargin or L-NAME. In summary, muscarinic inhibition of either basal or TRH-induced PRL secretion was augmented by E₂ and T₃, and involved the PTX-sensitive cAMP/Ca²⁺ pathways. Furthermore, nitric oxide mediated the basal rather than TRH-induced PRL response to ACh, whereas the intracellular Ca²⁺ mobilization concerned the TRH-induced rather than the basal PRL response to ACh. Thus, ACh synthesized in the AP appears to inhibit basal vs. TRH-induced PRL secretion via different mechanisms.

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Section: Discussionsupporting

confidence: 43%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Muscarinic Regulation of Basal versus Thyrotropin-Releasing Hormone-Induced Prolactin Secretion in Rat AnteriorPituitary Cells

Pu¹,

Tan²,

Chen³

et al. 1999

Neuroendocrinology

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“…Other inhibitory and stimulatory factors synthesized in the pituitary and hormones present in the circulation (i.e., estrogens and thyroid hormones) also affect PRL secretion [Maurer, 1982;Carmeliet et al, 1989;Dymshitz et al, 1992;Ray and Melmed, 1997;Bruhn et al, 1998;Cai et al, 1998;Kanyicska et al, 1998;Pu et al, 1999]. Among the autocrine/paracrine factors in the pituitary, angiotensin II (AII) and vasoactive intestinal peptide (VIP) have been shown to stimulate, and acetylcholine (ACh) to inhibit PRL secretion [Rudnick and Dannies, 1981;Carmeliet et al, 1989;Balsa et al, 1996;Díaz-Torga et al, 1998;Pu et al, 1999]. Recently, we have further demonstrated that the suppression by ACh of both basal and TRH-induced PRL secretion was enhanced in a 17b-estradiol (E 2 )-and triiodothyronine (T 3 )-dependent manner in AP cells prepared from ovariectomized young rats [Pu et al, 1999].…”

mentioning

confidence: 99%

Differential involvement of protein kinase C in basal versus acetylcholine‐regulated prolactin secretion in rat anterior pituitary cells during aging

Pu¹,

Liu²

2002

J of Cellular Biochemistry

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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-related increase in PRL secretion, and if protein kinase C (PKC) is involved. We also determined if replenishment with aging-declined hormones such as estrogen/thyroid hormone influences the aging-caused effects on pituitary PRL responses. AP cells were prepared from old (23-24-month-old) as well as young (2-3-month-old) ovariectomized rats. Cells were pretreated for 5 days with diluent or 17beta-estradiol (E(2); 0.6 nM) in combination with or without triiodothyronine (T(3); 10 nM). Then, cells were incubated for 20 min with thyrotropin-releasing hormone (TRH; 100 nM), angiotensin II (AII; 0.2-20 nM), vasoactive intestinal peptide (VIP; 10(-9)-10(-5) M), dopamine (DA; 10(-9)-10(-5) M), or ACh (10(-7)-10(-3) M). Cells were also challenged with ACh, TRH, or phorbol 12-myristate 13-acetate (PMA; 10(-6) M) following PKC depletion by prolonged PMA (10(-6) M for 24 h) pretreatment. We found that estrogen priming of AP cells could reverse the aging-caused effects on pituitary PRL responses to AII and DA. In hormone-replenished 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-induced PRL secretion. Furthermore, ACh suppressed TRH-induced PRL secretion mainly via the PMA-sensitive PKC in the old AP cells, but via additional mechanisms in young AP cells. On the contrary, basal PRL secretion was PKC (PMA-sensitive)-independent in the old AP cells, but dependent in the young AP cells. Taken together, these results suggest differential roles of PMA-sensitive PKC in regulating basal and ACh-regulated PRL responses in old versus young AP cells. The persistent aging-induced differences in AP cell responsiveness to ACh, DA, TRH, and PMA following hormone (E(2)/T(3)) replenishment suggest an intrinsic pituitary change that may contribute, in part, to the elevated in vivo PRL secretion observed in aged rats.

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Paracrine communication in the anterior pituitary as studied in reaggregate cell cultures

Vankelecom

Denef

1997

Microsc. Res. Tech.

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Stimulation and inhibition of prolactin release from rat pituitary lactotrophs by the cholinomimetic carbachol in vitro. Influence of hormonal environment and intercellular contacts

Cited by 19 publications

References 50 publications

Muscarinic Regulation of Basal versus Thyrotropin-Releasing Hormone-Induced Prolactin Secretion in Rat AnteriorPituitary Cells

Muscarinic Regulation of Basal versus Thyrotropin-Releasing Hormone-Induced Prolactin Secretion in Rat AnteriorPituitary Cells

Differential involvement of protein kinase C in basal versus acetylcholine‐regulated prolactin secretion in rat anterior pituitary cells during aging

Paracrine communication in the anterior pituitary as studied in reaggregate cell cultures

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