Potentiation of prolactin secretion following lactotrope escape from dopamine action. II. Phosphorylation of the alpha(1) subunit of L-type, voltage-dependent calcium channels.

摘要: Modulation of Ca(2+) channels has been shown to alter cellular functions. It can play an important role in the amplification signals endocrine system, including pleiotropically regulated pituitary lactotropes. Prolactin (PRL) secretion is tonically inhibited by dopamine (DA), escape from which triggers acute episodes hormone secretion. The magnitude these explained a potentiation PRL-releasing action secretagogues such as thyrotropin-releasing (TRH). While mechanisms this are not fully understood, it known be mimicked dihydropyridine, L-type channel agonist Bay K 8644 and blocked nifedipine methoxyverapamil. also inhibitors cyclic AMP-dependent protein kinase C. We recently described that tonic actions DA results increased macroscopic currents GH(4)C(1) lactotropic clonal cells transfected with cDNA encoding long form human D(2)-DA receptor. Here we show withdrawal potentiates TRH GH(4)C(1)/D(2)-DAR same extent enriched lactotropes primary culture. In both experimental models low density dihydropyridine receptors was (+)-[(3)H]PN200-110 binding. Photoaffinity labelling [(3)H]azidopine revealed consistent alpha(1) subunit 165-170 kDa. models, facilitation triggered correlated enhanced rate phosphorylation putative subunit, nature further supported immunoprecipitation selective antibodies directed against alpha(1C) alpha(1D) voltage-gated calcium channels. propose PKA- PKC-dependent high voltage activated, responsible for lactotropes, hence secretagogue-mediated PRL Thus, may mechanism regulation various functions