Molecular mechanism of gonadotropin and prolactin release from pituitary cells

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LH-RH induces LH from anterior pituitary gland and prolactin is secreted by TRH. Bromocriptine, a dopamine agonist, is useful for the treatment of prolactinoma. This drug not only suppresses prolactin release but also reduces tumor size. The purpose of this research is to clarify the postreceptor mechanism in prolactin and LH secretion, and molecular mechanism of inhibition of prolactin release by dopamine. (METHODS) Rat anterior pituitary cells and HG_3 cell line were used for the experiment. (RESULTS) (1) Maitotoxin induced Ca^<2+> influx into the cells and prolactin release.(2) TRH stimulated-^<32>P incorporation in phosphatidyl inositol turnover. (3)Phospholipase C, Activated by calcium, dissolved phosphatidyl inositol into diacylglycerol and inocitol triphosphate, and induced prolactin release. (4) Protein kinase C in pituitary cells was activated PMA. PMA stimulated LH and prolactin secretion. TRH induced the translocation of prolactin kinase C In GH_3 cells. (5) TRH stimulated arachidonate release from the phospholipids of pituitary cells preincubated with ^3H-arachidonate. (6) Prolactin and LH was released when pituitary cells was incubated with arachidonate. (7) Products of cyclooxygenase has no effects on prolactin release, although 5-HETE and leukotriene, 5-lipoxygenase products, induced prolactin and LH secretion.(8) Dopamine inhibited prolactin release stimulated by PMA, arachidonate, phospholipase C, maitotoxin and 5-HETE. TRH- induced prolactin release was not inhibited by dopamine in GH_3 cells which has no dopamine receptor. (CONCLUSION) TRH and LH-RH stimulated prolactin and LH respectively though diacylglycerol, protein kinase and calcium, arachidonate system. Dopamine inhibit every these signals.