Tri-iodothyronine and phenytoin reduce prolactin messenger RNA levels in cultured rat pituitary cells

Abstract

Thyroid hormones may regulate prolactin gene transcription. We have previously found that phenytoin inhibits tri-iodothyronine (T₃) nuclear binding, and have suggested that phenytoin may act as a partial T₃ agonist. We have therefore investigated the effects of phenytoin and T₃ on prolactin release and gene transcription, using the technique of cytoplasmic dot hybridization with complementary DNA probes to estimate prolactin messenger (m) RNA concentrations in cytoplasm from cultured rat pituitary cells. Tri-iodothyronine treatment led to a small but significant fall in prolactin release by 72 h, but caused marked dose- and time-dependent reductions in prolactin mRNA levels at 48–72 h. Phenytoin, however, caused more rapid falls in both prolactin release and mRNA concentrations. Neither T₃ nor phenytoin significantly altered GH mRNA levels. These studies suggest effects of phenytoin similar, but not identical, to those of T₃ in the lactotroph. J. Endocr. (1986) 109, 359–364