Direct Effects of Sex Steroids on Prolactin Release at the Anterior Pituitary Level: Interactions with Dopamine, Thyrotropin-Releasing Hormone, and Isobutylmethylxanthine

Giguère, Vincent; Meunier, Hélène; Veilleux, Raymonde; Labrie, Fernand

doi:10.1210/endo-111-3-857

Cited by 63 publications

(28 citation statements)

References 35 publications

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“…It is known that estrogen is a potent stimulator of prolactin secretion, acting at two levels. On pituitary lactotropes, estradiol directly regulates transcription of the prolactin gene [26, 27], acts as a potent antidopaminergic agent [28] and modifies the response of the lactotrope to physiological stimulators of prolactin secretion [29]. At hypothalamic levels, estrogen decreases TIDA neuronal activity [24, 25, 30, 31].…”

Section: Discussionmentioning

confidence: 99%

Pituitary Changes Involved in Prolactin Secretion Induced by Mifepristone and Naloxone during Late Pregnancy

Gabutti

Ezquer²,

Deis³

et al. 2008

Neuroendocrinology

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Background/Aims: The antiprogesterone mifepristone facilitates prolactin release, an effect enhanced by administration of the opioid antagonist naloxone. The present study explores ultrastructural changes in lactotropes after mifepristone and naloxone administration, correlating them with the expression of pituitary prolactin. Methods/Results: Rats were sacrificed at 18:00 h on day 19 of pregnancy. Prolactin immunoelectron microscopy of lactotropes from control rats showed characteristics of quiescent cells with numerous small and spherical secretory granules. Naloxone administration did not modify lactotrope morphology or prolactin expression in terms of mRNA or protein abundances. Mifepristone treatment induced lactotrope activation with development of the rough endoplasmic reticulum and Golgi complex with prolactin immunoreactive small newly formed and large mature secretory granules. Mifepristone increased prolactin mRNA and protein expression. Naloxone administration to mifepristone-treated rats potentiated lactotrope activation compared with mifepristone alone showing exocytotic images of prolactin granules and some cells with evident signs of involution. Conclusions: (1) Blockade of progesterone action by mifepristone activated the lactotrope, increased significantly prolactin mRNA and protein expression and prepared the pituitary for naloxone action. (2) The high serum prolactin levels induced by mifepristone and naloxone may regulate negatively lactotrope activity as suggested by the presence of regressing cells neighboring the actively secreting cells.

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Section: Discussionmentioning

confidence: 99%

Pituitary Changes Involved in Prolactin Secretion Induced by Mifepristone and Naloxone during Late Pregnancy

Gabutti

Ezquer²,

Deis³

et al. 2008

Neuroendocrinology

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“…A de crease rather than an increase in DA receptor number during preovulatory PRL surge could mediate the change of the lactotroph sensitivity to DA observed in our study. However, the lactotroph resonsiveness might also be regulated at a step sub sequent to the binding of DA to its membrane receptors as it was shown in estradiol-induced alterations o f lactotroph sensi tivity to DA [12,23],…”

Section: Discussionmentioning

confidence: 98%

Changes of Prolactin Response to Dopamine during the Rat Estrous Cycle

et al. 1990

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The effects of dopamine (DA) on prolactin (PRL) secretion in anterior pituitary tissue from rats selected during various stages of the estrous cycle were analyzed under in vitro conditions. The results were examined in relation to plasma PRL, estradiol and progesterone levels. During the estrous cycle there was a marked variation in the responsiveness of the lactotrophs to the inhibitory action of DA. Rapid changes occurred during proestrus: pituitary lactotrophs were not sensitive to the inhibitory action of 10 nM DA at 15.00 and 17.00 h and were less sensitive to 1 µM DA compared to 09.00 h (p < 0.01), 12.00 h (p < 0.05) and 19.00 h (p < 0.05). This lowest PRL response to DA was associated with the preovulatory PRL surge. The recovery of a higher PRL response at 19.00 h coincided with the decrease of plasma PRL levels. During the remainder of the cycle, plasma PRL levels remained low in estrus, diestrus 1 and diestrus 2. Lactotrophs were sensitive to 1 µM and 10 nM DA during estrus and diestrus 2 but a significant lower PRL response to 1 µM DA (p < 0.05) and no PRL response to 10 nM DA was observed in diestrus 1. These data show that alterations in the sensitivity of the lactotrophs’ responsiveness to DA occur in the anterior pituitary gland during the rat estrous cycle and can lead to the removal of DA inhibition in the presence of physiological DA concentrations. This phenomenon is consistent with the fact that DA could be involved in the preovulatory PRL surge during the estrous cycle.

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“…The fact that NKA stimulated PRL release when the anterior pituitary cells from OVX rats were cultured in the presence of estradiol suggests that estrogens may exert an enabling action at the pituitary level. Indeed, it has been reported that estradiol modulates the responsiveness of lactotropes to other PRL-releasing peptides such as TRH (Giguere et al 1982) and VIP (Pizzi et al 1991). In the male rat, endogenous concentrations of sex steroids could be high enough to induce an NKA action.…”

Section: Discussionmentioning

confidence: 99%

The hormonal status modulates the effect of neurokinin A on prolactin secretion in female rats

Pisera

Theas²,

Laurentiis³

et al. 1998

Journal of Endocrinology

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We have previously reported that neurokinin A (NKA), a tachykinin closely related to substance P, increases the release of prolactin (PRL) from the anterior pituitary gland of male rats, but not from pituitaries of ovariectomized (OVX) female rats. In this study, we evaluated the influence of estrogens in the action of NKA on PRL secretion in female rats. NKA stimulated the in vitro release of PRL from pituitary glands of OVX-chronically estrogenized rats, and of proestrus and estrus rats, but had no effect in anterior pituitaries of diestrus rats. In addition, we observed that cultured anterior pituitary cells of OVX rats responded to NKA only when they were incubated for 3 days in the presence of estradiol 10 9 M. This effect was blocked by L-659,877, an NK-2 receptor antagonist. We also studied the action of NKA on PRL release during lactation. The response of anterior pituitary cells to NKA was variable over this period. The maximal sensitivity to NKA was observed at day 10 of lactation. Furthermore, the blockade of endogenous NKA by the administration of an anti-NKA serum to lactating rats reduced the PRL surge induced by the suckling stimulus. These results show that the responsiveness of the anterior pituitary gland of female rats to NKA is modulated by the endocrine environment, and suggest that NKA may participate in the control of PRL secretion during the estrus cycle and lactation.

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Direct Effects of Sex Steroids on Prolactin Release at the Anterior Pituitary Level: Interactions with Dopamine, Thyrotropin-Releasing Hormone, and Isobutylmethylxanthine

Cited by 63 publications

References 35 publications

Pituitary Changes Involved in Prolactin Secretion Induced by Mifepristone and Naloxone during Late Pregnancy

Pituitary Changes Involved in Prolactin Secretion Induced by Mifepristone and Naloxone during Late Pregnancy

Changes of Prolactin Response to Dopamine during the Rat Estrous Cycle

The hormonal status modulates the effect of neurokinin A on prolactin secretion in female rats

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