Suckling-Induced Prolactin Release is Suppressed by Naloxone and Simulated by β-Endorphin

Selmanoff, Michael; Gregerson, Karen A.

doi:10.1159/000124448

Cited by 79 publications

(33 citation statements)

References 24 publications

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“…Additionally, the participation of endogenous opioid peptides in the regulation of prolactin release in lactating rats has been reported by several authors (Ferland et al 1978, Selmanoff & Gregerson 1986, Baumann & Rabii 1991, Arbogast & Voogt 1998. Various studies have revealed that progesterone has an inhibitory control on prolactin release at the end of pregnancy (Vermouth & Deis 1972, 1974, Jahn et al 1986).…”

Section: Introductionmentioning

confidence: 72%

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

Soaje¹,

Nasso²,

Deis³

2002

Journal of Endocrinology

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Evidence suggests that endogenous opioid peptides are implicated in the suckling-induced prolactin rise. We explored the role of the opioid system and the participation of ovarian hormones in the regulation of prolactin induced by the suckling stimulus at the end of pregnancy in rats with developed maternal behavior, and during lactation. Suckling for 24 h induced a significant increase in serum prolactin on day 19 of pregnancy, which was increased more than three times when naloxone (2 mg/kg s.c.) or mifepristone (2 mg/kg) was administered. The combination of naloxone and mifepristone did not increase serum prolactin more than either compound alone. Administration of tamoxifen (500 µg/kg orally) on days 14 and 15 of pregnancy completely abolished the effect of naloxone, indicating a role for estrogens in establishing this inhibitory role of opioids. To examine the participation of the opioid system during lactation, we used groups of rats on days 1, 3, 5, 12 and 19 postpartum either (i) isolated from the pups for 4 h, or (ii) isolated from the pups for 3·5 h and reunited with them and suckled for 30 min. Naloxone, given just before replacing the pups, prevented the increase in serum prolactin levels observed in the suckled group of rats but had no effect on the basal levels of the isolated rats. To examine whether the participation of the opioid system in the release of prolactin is dependent on the variation of progesterone levels, rats on day 20 of pregnancy were implanted with two cannulae containing progesterone (that blocked postpartum ovulation) or cholesterol, and cesarean surgery was performed on day 21. To maintain lactation, pups (1-3 days old) were replaced every 24 h, and 4 days after the cesarean eight pups were placed in the cage at 1800 h to maintain a strong suckling stimulus during the following 24 h. Naloxone administration significantly reduced serum prolactin levels in control (cholesterol) rats but progesterone implants prevented the inhibitory effect of naloxone and this effect was not modified by treatment with estrogen.These results indicate that the opioid system modulates suckling-induced prolactin secretion, passing from an inhibitory action before delivery to a stimulatory action during lactation. This regulatory shift seems to be dependent on the fall in progesterone concentration at the end of pregnancy and the subsequent increase after the postpartum ovulation and luteal phase.

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Section: Introductionmentioning

confidence: 72%

“…Quite a bit of evidence supports these results demonstrating a participation of the opioid system on suckling-induced hormone release (Ferland et al 1978, Selmanoff & Gregerson 1986 Rabii 1991). Moreover, Arbogast & Voogt (1998) recently reported that opioidergic input is essential for normal lactation due to its effects on the TIDA neurons.…”

Section: Discussionmentioning

confidence: 88%

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

Soaje¹,

Nasso²,

Deis³

2002

Journal of Endocrinology

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“…The suckling-induced PRL surge is blocked by treatment with naloxone, a nonselective opioid antagonist (Selmanoff and Gregerson, 1986). Naloxone also decreases stress-and estrogen-induced PRL secretion (Dupont et al, 1980;Petraglia et al, 1987).…”

Section: Modulatorsmentioning

confidence: 99%

From Galactorrhea to Osteopenia: Rethinking Serotonin–Prolactin Interactions

Emiliano

Fudge

2004

Neuropsychopharmacol

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The widespread use of the selective serotonin reuptake inhibitors (SSRIs) has been accompanied by numerous reports describing a potential association with hyperprolactinemia. Antipsychotics are commonly known to elevate serum prolactin (PRL) through blockade of dopamine receptors in the pituitary. However, there is little awareness of the mechanisms by which SSRIs stimulate PRL release. Hyperprolactinemia may result in overt symptoms such as galactorrhea, which may be accompanied by impaired fertility. Long-term clinical sequelae include decreased bone density and the possibility of an increased risk of breast cancer. Through literature review, we explore the possible pathways involved in serotonin-induced PRL release. While the classic mechanism of antipsychotic-induced hyperprolactinemia directly involves dopamine cells in the tuberoinfundibular pathway, SSRIs may act on this system indirectly through GABAergic neurons. Alternate pathways involve serotonin stimulation of vasoactive intestinal peptide (VIP) and oxytocin (OT) release. We conclude with a comprehensive review of clinical sequelae associated with hyperprolactinemia, and the potential role of SSRIs in this phenomenon.

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“…, stress [10][11][12][13] and lactation [12,[14][15][16], We have reported that EOPs may also be essential in the occur rence of each nocturnal PRL surge in the pregnant rat [17]. These results however, did not identify the specific EOP involved and thus provided the precedence for the present study.…”

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confidence: 65%

Time-Dependent Changes in β-Endorphin-Stimulated Prolactin Release during Pregnancy

Sagrillo¹,

Voogt²

1992

Neuroendocrinology

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Endogenous opioid peptides (EOPs) stimulate prolactin (PRL) release in various physiological conditions in the rat. Moreover, EOPs are essential in initiating and maintaining the nocturnal PRL surges that occur over the first half of gestation in the rat. The purpose of this study was to investigate the potential role of the opioid β-endorphin (β-End) in mediating the nocturnal PRL surges. Day 8 pregnant rats received an infusion of 2.5, 10, 25 or 100 ng/µl/min β-End intracerebroventricularly (i.c.v.) for 15 min at 12.00 h, an intersurge period. PRL increased in a dose-dependent manner and from this, the largest dose was used in subsequent experiments to ensure maximal opioid receptor stimulation. The next experiment defined the temporal sensitivity of the neuroendocrine system regulating PRL surges to exogenous β-End. Day 8 pregnant rats showed dramatic PRL responses to β-End when given at midnight (presurge) or 12.00 h (intersurge), but greatly attenuated responses at 02.00 h (early surge) and 04.00 h (late surge). Animals treated at 06.00 h (postsurge) showed recovered responsiveness to β-End. To determine what may account for the significantly lower PRL increases to β-End during the surge, day 8 pregnant rats received 100 ng/µl/min β-End i.c.v. for 15 min at 10.00 h, and then again at 12.00 h. All animals showed PRL increases greater than 1,140 ng/ml at 10.00 h, but the subsequent response to β-End at 12.00 h was reduced by 70%. In another experiment, β-End was infused at midnight and the animals were monitored for a subsequent endogenous nocturnal PRL surge. Although all animals showed a rapid increase in PRL following β-End treatment, 5 of 8 animals did not have a nocturnal PRL surge. This suggests that the initial β-End may downregulate its receptors, and therefore account for the much lower PRL response to β-End during the surge. To determine whether an insufficient amount of pituitary PRL may account for the small response to β-End during the surge, hemipituitary PRL concentration was measured. Pituitary PRL concentration was found to be lower at 04.00 h, when the incremental increase in plasma PRL to β-End was smallest, compared to the concentration at midnight, when the response was highest. However, at 02.00 h, pituitary PRL levels were similar to those at midnight, yet the PRL response to β-End differed greatly at these 2 times. Based on these results, lower pituitary PRL concentration during the nocturnal surge may only partially account for the attenuated PRL response to β-End. Downregulation of β-end receptors or less dopamine available for inhibition by β-End in the tuberoinfundibular dopamine neurons also are likely explanations.

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Suckling-Induced Prolactin Release is Suppressed by Naloxone and Simulated by β-Endorphin

Cited by 79 publications

References 24 publications

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

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

From Galactorrhea to Osteopenia: Rethinking Serotonin–Prolactin Interactions

Time-Dependent Changes in β-Endorphin-Stimulated Prolactin Release during Pregnancy

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