Cholinergic stimulation of phosphoinositide hydrolysis in rat anterior pituitary

Schrey, M.P.; Read, Alison M.

doi:10.1016/0303-7207(88)90039-1

Cited by 4 publications

(2 citation statements)

References 27 publications

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“…Thus, it appears that the sites of ACh action on PRL secretion are at and/or subsequent to the changes of intracellular Ca 2+ or cAMP levels. However, in normal rat AP, the PTX-insensitive PI hydrolysis was induced by carbachol [19]; perhaps this is related to the stimulatory effect of ACh on GH secretion [48]. In normal bovine AP cells, ACh-stimulated, PTX-insensitive PI hydrolysis correlated with the PTX-insensitive ACh enhancement of basal PRL secretion [49].…”

Section: Discussionmentioning

confidence: 99%

“…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. In addition, pertussis toxin (PTX)-insensitive cholinergic stimulation of phosphoinositide (PI) hydrolysis was reported in rat AP [19], whereas in GH 3 cells, cholinergic agents lowered cytosolic free Ca 2+ [20], the cAMP content [21], the PTX-sensitive voltage-dependent Ca 2+ channels [22], and PRL release [14, 23]. The rat pituitary tumor cells differ from normal AP cells in many respects, e.g.…”

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.