Regulation by endogenous opioids of suckling-induced prolactin secretion in pregnant and lactating rats: role of ovarian steroids

Soaje, Marta; Nasso, Elina G. de Di; Deis, R. P.

doi:10.1677/joe.0.1720255

Cited by 18 publications

(24 citation statements)

References 35 publications

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“…We may suggest that the ability of the hypophysis to release prolactin is lower at the end of pregnancy. Although this is a hypothesis based on our present and previous results [5, 6, 63]and results obtained by others [62], experiments in course suggest that the secretory activity of the lactotropes on day 19 of pregnancy is in an inhibited state characterized by the appearance of atypical cells with predominance of small dense spherical secretory granules instead of the typical large granules seen in actively secreting cells. We cannot rule out that this effect may be a consequence of the increased dopaminegic tone that characterizes the end of pregnancy [64].…”

Section: Discussioncontrasting

confidence: 43%

“…Although we have described an important increase in serum prolactin levels after mifepristone and naloxone treatment on day 19 of pregnancy [5, 6, 63], this response is lower than that observed under different physiological conditions such as early pregnancy or during lactation. We may suggest that the ability of the hypophysis to release prolactin is lower at the end of pregnancy.…”

Section: Discussionmentioning

confidence: 93%

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Neurotransmitters Involved in the Opioid Regulation of Prolactin Secretion at the End of Pregnancy in Rats

Soaje

Bregonzio²,

Carón³

et al. 2004

Neuroendocrinology

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Using a pharmacological approach, we explored potential mechanisms for the regulation of prolactin secretion by opioid peptides at the end of pregnancy in rats. On day 19 of pregnancy, intracereboventricular administration of the µ-opioid receptor agonist (D-Ala², NMe-Phe⁴, Gly-ol⁵)-enkephalin (DAMGO) or β-endorphin (β-END) induced a dose-related increase in serum prolactin levels 30 min later. Pretreatment with the opioid antagonist naloxone abolished the increase induced by DAMGO injection. At lower doses, DAMGO and β-END did not modify the 3,4-dihydroxyphenylacetic acid/dopamine ratio, but at higher doses, the µ-agonists evoked a significant increase of the dopaminergic activity as compared with saline control. The time course of the effects of β-END (2.5 µg/rat) showed a higher increase in serum prolactin levels at 15 min than at 30 min after treatment. The 3,4-dihydroxyphenylacetic acid/dopamine ratio increased 15 min after β-END administration and was even higher 30 min later. Neither the selective ĸ-agonist U50,488H nor the selective δ-agonist (D-Pen², D-Pen⁵)- enkephalin were able to modify the serum prolactin levels at the doses studied.To evaluate potential neurotransmitters involved in the regulation of prolactin secretion at the end of pregnancy, we combined the administration of serotoninergic or GABAergic antagonists with the opioid agonist DAMGO. The serotonin 5-HT₂ receptor antagonist ketanserin increased the serum prolactin levels and potentiated the effect of DAMGO. The intracerebroventricular administration of SR-95531 did not modify the serum prolactin concentration under basal conditions, but partially prevented the increase induced by DAMGO injection. The intracerebroventricular administration of the GABA_B receptor antagonist phaclofen had no effect on the serum prolactin levels either in naive or DAMGO-treated rats. The present results support the proposal that activation of µ-opioid receptors stimulates prolactin secretion at the end of pregnancy. Although the exact mechanisms by which the opioid system modulates prolactin secretion at the end of pregnancy are unclear, these results suggest an interaction of the opioidergic system with serotoninergic and GABAergic systems, without ruling out a direct or indirect action on dopaminergic neurons. In conclusion, the opioid system may regulate prolactin secretion at the end of pregnancy through either stimulatory (present results) or inhibitory actions previously described.

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Section: Discussioncontrasting

confidence: 43%

Section: Discussionmentioning

confidence: 93%

Neurotransmitters Involved in the Opioid Regulation of Prolactin Secretion at the End of Pregnancy in Rats

Soaje

Bregonzio²,

Carón³

et al. 2004

Neuroendocrinology

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“…However, late pregnancy seems to be a particular endocrine period with respect to the regulation of prolactin secretion by the opioid system. In previous reports [8,9,10], we demonstrated that the blockade of the central inhibitory action of progesterone on prolactin release by the antiprogesterone mifepristone [11] facilitated prolactin release in rats on day 19 of pregnancy. The effect of mifepristone was enhanced by the administration of the opioid antagonist naloxone, suggesting an inhibitory-neuromodulatory role of the opioid system at the end of pregnancy [8, 9].…”

Section: Introductionmentioning

confidence: 76%

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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“…In pregnant rats, the opioid system modulates prolactin secretion in a complex manner. Both stimulatory and inhibitory actions of opioids may result, acting through different regulatory pathways, in an elevation of prolactin levels [6,7,8,9,10,11]. Interestingly, progesterone plays an important role in this regulation.…”

Section: Introductionmentioning

confidence: 99%

Dopaminergic Mechanisms Involved in Prolactin Release after Mifepristone and Naloxone Treatment during Late Pregnancy in the Rat

et al. 2006

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Background/Aims: During late pregnancy, the antiprogesterone mifepristone facilitates prolactin release. This effect is enhanced by administration of the opioid antagonist naloxone, suggesting an inhibitory-neuromodulatory role of the opioid system. Since hypothalamic dopamine (DA) is the main regulator of prolactin release, in this study we explored the role of DA on prolactin release induced by mifepristone and naloxone treatment. Methods/Results: Rats on day 19 of pregnancy were used. Naloxone treatment did not modify the 3,4-dihydroxyphenylacetic acid/DA (DOPAC/DA) ratio or serum prolactin concentration in control rats. After mifepristone treatment, DA activity diminished significantly without modifying serum prolactin levels. Naloxone administration to antiprogesterone-treated rats did not change the DOPAC/DA ratio but increased serum prolactin. Tyrosine hydroxylase (TH) expression in medial basal hypothalamus (MBH) protein extracts was lowered by pretreatment with mifepristone, with no additional effect of naloxone. While mifepristone decreased the intensity of TH immunoreactivity in the arcuate and periventricular nuclei and in fibers of the median eminence, naloxone treatment had no further effect. Conclusions: (1) A reduction of tuberoinfundibular dopaminergic (TIDA) neuron activity is suggested by the fall of the DOPAC/DA ratio and the low expression of MBH TH; (2) this reduction facilitates prolactin secretion by naloxone, indicating that progesterone stimulates DA neurons to maintain low serum prolactin; (3) naloxone action seems to depend on a previous decrease of DA tone induced by mifepristone, without involve a direct effect on neuronal DA activity, and (4) endogenous opioids may inhibit prolactin secretion through a non-dopaminergic neuronal system that regulates prolactin secretion in which as yet undetermined prolactin-releasing factors may participate.

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Regulation by endogenous opioids of suckling-induced prolactin secretion in pregnant and lactating rats: role of ovarian steroids

Cited by 18 publications

References 35 publications

Neurotransmitters Involved in the Opioid Regulation of Prolactin Secretion at the End of Pregnancy in Rats

Neurotransmitters Involved in the Opioid Regulation of Prolactin Secretion at the End of Pregnancy in Rats

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

Dopaminergic Mechanisms Involved in Prolactin Release after Mifepristone and Naloxone Treatment during Late Pregnancy in the Rat

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