The Inhibition of Phosphatidylinositol Turnover: A Possible Postreceptor Mechanism for the Prolactin Secretion-Inhibiting Effect of Dopamine*
- 1 July 1983
- journal article
- research article
- Published by The Endocrine Society in Endocrinology
- Vol. 113 (1), 7-14
- https://doi.org/10.1210/endo-113-1-7
Abstract
The association between the inhibition of phosphatidylinositol (PI) turnover and the inhibition of PRL [prolactin] secretion in the presence of dopamine was studied. The incorporation of radiolabeled phosphate into anterior pituitary gland PI as well as serum PRL levels were significantly (P < 0.01) greater in female than in male rats. No significant sex-related difference was found in the incorporation by pituitary tissue of 32P into phosphatidylcholine (PC) or phosphatidylethanolamine (PE). Dopamine decreased the incorporation of 32P into PI, but not into PC or PE, by female rat pituitary glands; this effect was reversed by 2 dopamine receptor-blocking agents, haloperidol and pimozide. After dopamine was removed from the incubation medium, basal 32P incorporation into PI was restored within 10 min. The administration of bromocriptine (500 .mu./kg, i.p., 4 h earlier) significantly reduced pituitary PI turnover. Conversely, in vivo injection of .alpha.-methyl-p-tyrosine (.alpha.MpT; 200 mg, i.p., 2.5 h before death), an inhibitor of catecholamine biosynthesis, dramatically increased serum PRL levels. In vivo incorporation of 32P into PI, but not into PC or PE, increased (+130%) when these glands were incubated for 30 min with radiolabeled phosphate. The in vitro addition of 0.5 .mu.M dopamine to glands from .alpha.MpT-treated rats counteracted the stimulation of 32P incorporation into PI produced by .alpha.MpT treatment. In rats bearing the transplantable PRL-secreting tumor MtTW15, the hyperprolactinemia produced by the tumor stimulates hypothalamic turnover of dopamine, with a consequent inhibition of pituitary gland PRL secretion. 32P incorporation into PI, but not into PC or Pe, was significantly (P < 0.01) inhibited (-41%) in pituitary glands from these rats. The injection of .alpha.MpT (200 mg/kg, i.p.) or haloperidol (2 mg/kg, i.p.) 12 and 3 h before death into MtTW15 tumor-bearing rats abolished the inhibition of 32P incorporation into pituitary PI. Dopamine also decreased PI turnover in the 7315a PRL-secreting pituitary tumor. The PI cycle may be an intracellular mechanism controlling PRL release in the rat and the changes in its cleavage and turnover may be an early postreceptor event responsible for the inhibition of PRL secretion produced by factors such as dopamine.This publication has 24 references indexed in Scilit:
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