Hypothalamic catecholamine biosynthesis and pituitary gonadotropin secretion in vitro: effect of hyperprolactinemia

The effect of hyperprolactinemia on central catecholamine biosynthesis and anterior pituitary hormone release was studied using an in vitro methodology. The incorporation of [3H]tyrosine into hypothalamic and neurohypophyseal catecholamines was determined using a new method which combines high performance liquid chromatography (HPLC) with amperometric detection (LCEC). Elevated plasma prolactin levels, induced by pituitary transplants, resulted in increased in vitro biosynthesis of medial basal hypothalamic (MBH) dopamine (DA), but not norepinephrine (NE). Neurohypophyseal DA biosynthesis (including the intermediate lobe) was not affected. Plasma LH levels were depressed by hyperprolactinemia although the content of hypothalamic luteinizing hormone-releasing hormone (LHRH) was not changed. In parallel studies, the anterior pituitaries from these animals were incubated in vitro using a paired-half technique and LH and PRL release measured. While the basal release of prolactin was not altered by hyperprolactinemia, LH release was significantly decreased. Gonadotroph responsiveness to LHRH was significantly increased, while the inhibition of prolactin by dopamine was not altered. There was a decrease in pituitary prolactin content with normal LH levels. These experiments confirm several in vivo reports which show that hypothalamic dopaminergic but not noradrenergic activity is increased by prolactin. This action is specifically localized in the tuberoinfundibular dopaminergic neurons. Furthermore, these experiments suggest that these central changes result in alterations in both gonadotroph and mammotroph function.