Opioid Receptor Subtypes Involved in the Regulation of Prolactin Secretion During Pregnancy and Lactation

Andrews, Zane B.; Grattan, David R.

doi:10.1046/j.1365-2826.2003.00975.x

Cited by 59 publications

(44 citation statements)

References 84 publications

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“…There are many evidence showing that the effect of PRL-releasing factors (PRFs), such as TRH (Samson et al 2003), are dependent on a decrease in the dopaminergic tone that is not sufficient to stimulate PRL release per se, but that multiplies the release elicited by the PRF (Freeman et al 2000, Ben-Jonathan & Hnasko 2001, Voogt et al 2001. There are other neurotransmitters involved in the release of PRL at the end of pregnancy, such as norepinephrine (Jahn & Deis 1991), serotonin (Jahn & Deis 1987, Jahn et al 1999, and opioid peptides (Soaje & Deis 1994, Soaje et al 2004, Andrews & Grattan 2003) that participate in the stimulation of PRL release after the progesterone fall and that may be responsible for the similar response observed in the two strains, in spite of the elevated dopaminergic tone of the OFA rats at the end of pregnancy.…”

Section: Discussionmentioning

confidence: 99%

Hormonal profile and reproductive performance in lactation deficient (OFA hr/hr) and normal (Sprague–Dawley) female rats

Valdéz¹,

Penissi²,

Deis³

et al. 2007

Reproduction

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Lactation deficiency may have important consequences on infant health, particularly in populations of low socioeconomic status. The OFA hr/hr (OFA) strain of rats, derived from Sprague-Dawley (SD) rats, has deficient lactation and is a good model of lactation failure. We examined the reproductive performance and hormonal profiles in OFA and SD strains to determine the cause(s) of the lactation failure of the OFA strain. We measured hormonal (PRL, GH, gonadotropins, oxytocin, and progesterone) levels by RIA in cycling, pregnant, and lactating rats and in response to suckling. Dopaminergic metabolism was assessed by determination of mediobasal hypothalamic dopamine and dihydroxyphenylacetic acid (DOPAC) concentrations by HPLC and tyrosine hydroxylase expression by immunocytochemistry and western blot. OFA rats have normal fertility but 50% of the litters die of malnutrition on early lactation; only 6% of the mothers show normal lactation. The OFA rats showed lower circulating PRL during lactation, increased hypothalamic dopamine and DOPAC, and impaired milk ejection with decreased PRL and oxytocin response to suckling. Before parturition, PRL release and lactogenesis were normal, but dopaminergic metabolism was altered, suggesting activation of the dopaminergic system in OFA but not in SD rats. The number of arcuate and periventricular neurons expressing tyrosine hydroxylase was higher in SD rats, but hypothalamic expression of TH was higher in OFA rats at the end of pregnancy and early lactation. These results suggest that the OFA rats have impaired PRL release linked with an augmented dopaminergic tone which could be partially responsible for the lactational failure.

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Section: Discussionmentioning

confidence: 99%

Hormonal profile and reproductive performance in lactation deficient (OFA hr/hr) and normal (Sprague–Dawley) female rats

Valdéz¹,

Penissi²,

Deis³

et al. 2007

Reproduction

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“…Opioids act on a hypothalamic level, although a direct effect on the pituitary has not been completely excluded (Enjalbert et al, 1979). Endogenous opioid peptides and synthetic opiates suppress TH activity and m-RNA levels in the TIDA neurons (Arbogast and Voogt, 1998;Deyo et al, 1979;Reymond et al, 1983;Andrews and Grattan, 2003). Therefore, one established mechanism of opioid-induced PRL secretion is through inhibition of TIDA neuronal activity, probably modulated by the opioid receptor subtypes m and k (see review, Ben-Jonathan, 1994;Soaje and Deis, 1994).…”

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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“…Although the results obtained after U50,488H treatment are not in agreement with previous reports [43], there are evidences suggesting that the effects of U50,488H treatment on prolactin are quite variable [38]. Moreover, we have recently demonstrated that the administration of a ĸ-agonist did not modify the serum prolactin concentration on day 3 of pregnancy [39].…”

Section: Discussionmentioning

confidence: 56%

“…The effect of DAMGO was abolished by the administration of the antagonist naloxone, suggesting that the activation of µ-opioid receptors is involved in the stimulation of prolactin secretion at the end of pregnancy. In a recent study [43], it has been shown that opioid regulation of prolactin during pregnancy and lactation is mediated by the activation of both µ- and ĸ-opioid receptors. However, in our experiments, we could not demonstrate the participation of ĸ-opioid receptors in the regulation of prolactin secretion at the end of pregnancy, although our results confirm the participation of µ-opioid receptors.…”

Section: Discussionmentioning

confidence: 99%

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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Opioid Receptor Subtypes Involved in the Regulation of Prolactin Secretion During Pregnancy and Lactation

Cited by 59 publications

References 84 publications

Hormonal profile and reproductive performance in lactation deficient (OFA hr/hr) and normal (Sprague–Dawley) female rats

Hormonal profile and reproductive performance in lactation deficient (OFA hr/hr) and normal (Sprague–Dawley) female rats

From Galactorrhea to Osteopenia: Rethinking Serotonin–Prolactin Interactions

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

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