Effects of estrogen on prolactin and tuberoinfundibular dopaminergic neurons

Abstract

Serum prolactin concentrations and dopamine turnover in the striatum and median eminence were studied in male rats after the administration of estradiol benzoate. The alpha-methyltyrosine-induced reduction of dopamine concentrations in these brain regions was used to evaluate relative rates of turnover. Steady state dopamine concentrations in the median eminence and striatum were not altered by 1, 3 or 5 days of estradiol treatment. However, 3 or 5 days of estradiol administration enhanced dopamine turnover in the median eminence but not in the striatum. Estradiol treatment failed to alter dopamine turnover in the median eminence of hypophysectomized rats. Estradiol increased serum prolactin concentrations at all of the times examined. Although alpha-methyltyrosine also increased serum prolactin, this increase was further enhanced in estradiol-treated rats. The increased prolactin response to alpha-methyltyrosine and increased dopamine turnover in the median eminence of estradiol-treated rats suggests that tuberoinfundibular dopaminergic neurons may be part of a hormonal-neuronal negative feedback loop which functions to regulate prolactin secretion.

Oestrogen-Induced Hyperprolactinaemia in the Rat: Reduced Concentrations of Hypothalamic Dopamine and the Effects of Bromocriptine

“…Eikenburg et al (1977) showed in rats that treatment for 5 days with oestrogen resulted in approximately threefold increases in serum prolactin and increased DA turnover in the median eminence but no changes were seen in DA concentrations. The study of Eikenburg et al (1977) did not investigate the effects of chronic hyperprolactinaemia in the situation when prolactin-secreting tumours are present and the degree of hyperprolactinaemia is great. After chronic (3 months) treatment with oestradiol valerate in the rat prolactin-secreting pituitary tumours are seen associated with specific pathological changes in the hypothalamus (Brawer and Sonnenschein 1975;Brawer and Naftolin 1979).…”

“…It has also been proposed that central serotoninergic neurones mediate the effect of oestrogen on prolactin release (Caligaris and Taleisnil( 1974). Oestrogen administration depresses 'prolactin-inhibiting factor' activity in the rat hypothalamus (Ratner and Meites 1964) and since prolactin release is tonically inhibited via hypothalamic dopamine (DA) pathways which have been shown to be subject to negative feedback by prolactin, attention has recently been directed toward the role of DA in oestrogen-induced hyperprolactinaemia (Eikenburg et al 1977). Eikenburg et al (1977) showed in rats that treatment for 5 days with oestrogen resulted in approximately threefold increases in serum prolactin and increased DA turnover in the median eminence but no changes were seen in DA concentrations.…”

“…Oestrogen administration depresses 'prolactin-inhibiting factor' activity in the rat hypothalamus (Ratner and Meites 1964) and since prolactin release is tonically inhibited via hypothalamic dopamine (DA) pathways which have been shown to be subject to negative feedback by prolactin, attention has recently been directed toward the role of DA in oestrogen-induced hyperprolactinaemia (Eikenburg et al 1977). Eikenburg et al (1977) showed in rats that treatment for 5 days with oestrogen resulted in approximately threefold increases in serum prolactin and increased DA turnover in the median eminence but no changes were seen in DA concentrations. The study of Eikenburg et al (1977) did not investigate the effects of chronic hyperprolactinaemia in the situation when prolactin-secreting tumours are present and the degree of hyperprolactinaemia is great.…”

Loss of Hypothalamic Dopaminergic Control of Prolactin Secretion in the Hyperprolactinaemic Rat

“…Initially (after approximately 3 days) this results in the maintenance of basal serum prolactin levels near normal but there is an enhanced prolactin response to DA synthesis inhibition relative to controls (Eikenburg·et al 1977). However, as the E2 stimulus and lactotroph hyperplasia maintain the drive to release more prolactin, we suggest that a limit to hypothalamic DA activity is reached after which serum prolactin levels cannot be kept near normal.…”

“…In the short term, at least, the administration of exogenous prolactin or the induction of high levels of prolactin secretion in the rat result in increased dopamine (DA) turnover in the median eminence without altering steady-state concentrations of DA (GudeIsky et al 1976;Eikenburg et al 1977). When circulating prolactin levels are raised in the rat 3-5 days following oestrogen (E 2 ) administration there is a significant increase in median eminence DA turnover and an increased prolactin release from the pituitary in response to tyrosine hydroxylase inhibition with IX-methyl-tyrosine (Eikenburg et al 1977). However, we have recently presented evidence that this initial response to increased prolactin secretion is not maintained following chronic hyperprolactinaemia induced by E2 treatment in the rat (Smythe and Brandstater 1980).…”