The Influence of Oestrogen Administration in Vivo on in Vitro Prolactin Release

Abstract

The influence of oestrogen administered to the ovariectomized rat on the interaction between dopamine (DA) and thyrotrophin releasing hormone (TRH) on the release of radioimmunoassayable (RIA) and [3H] leucine incorporated into prolactin ([3H]PRL) was examined in vitro. Dopamine had a more marked suppressing effect on newly synthetized PRL (80 %), as determined [3H]PRL, than on total PRL (50 %), as determined by RIA\x=req-\ PRL. The administration of 5 \g=m\g of oestradiolbenzoate (OeB) for 7 days resulted in blocking the suppressing effect of DA when RIA-PRL was measured but not when [3H]PRL was measured. The administration of 5 \g=m\g of OeB enabled TRH to partially override the suppressing effect of DA and the degree of response was more marked when RIA-PRL was measured than when [3H]PRL was measured. The administration of 50 \g=m\g of OeB for 3 days enabled TRH to override the DA blockade of prolactin release to levels comparable to that of the control when RIA-PRL was measured but had little to no effect on [3H]PRL. The results are discussed in relation to the two storage pools of PRL in the pituitary and the data suggest that DA acts predominantly to suppress the newly synthetized, rapidly releasable pool. Oestrogen acts to block DA action on the older more stable PRL pool. The ability of TRH to override the DA blockade of PRL release depends upon the presence of oestrogen; here TRH acts predominantly on the older more stable pool of PRL. Oestrogen's action on disrupting the DA suppression of PRL release appears to be related to the time of day the hormone is administered subsequent to when the pituitary is exposed to DA in vitro.

Evaluation of GnRH administration on the prolactin response to thyrotrophin-releasing hormone in normal women.

“…In the median eminence, an axo-axonic contact between GnRH and a dopamine-neuronal system has been suggested (McNeill et al, 1978), and dopamine has been thought to reduce gonadotrophin secretion by affecting GnRH-secreting neurons in men (Huseman et al, 1980) and women (Pehrson et al, 1983), Conversely, the acute administration of GnRH results in a rapid decrease in plasma concentrations of dopamine in normal men (Van Loon 1978). Furthermore, dopamine has been reported to inhibit the PRL response to TRH in men (Besses et al, 1975) and in rats in in vitro experiments (Jaques et al, 1979). Therefore, perhaps a high endogenous or exogenous GnRH tone leads to a decrease in the secretion of dopamine into hypophysial portal blood which consequently results in decreased inhibition of PRL release from the lactotroph in response to TRH as observed in our study.…”

Chronic estradiol exposure induces oxidative stress in the hypothalamus to decrease hypothalamic dopamine and cause hyperprolactinemia

“…Several estrogenic preparations, including estradiol benzoate (22), estradiol valerate (5), and estradiol 17␤ (25) are known to stimulate PRL secretion. This is known to be brought about by either a direct stimulatory action on the pituitary gland (1) and through a reduction in hypothalamic DA, especially DA that is produced by TIDA neurons (37).…”

Oestrogen–bromocriptine interaction in the control of luteinizing hormone and prolactin secretion in the neonatally oestrogenized female rat

“…The ability of oestrogen to stimulate prolactin secretion has been reported both in vivo and in vitro (Yamamoto, Kasai & Ieri, 1975;Jacques & Gala, 1979). Oestrogen seems to increase prolactin secretion either by changing endogenous dopamine release (Cramer, Parker & Porter, 1979) or by decreasing its turnover (Eikenburg, Ravitz, Gudelsky & Moore, 1977), thus allowing the accumulation of dopamine in the hypothalamus .…”