Arcuate Nucleus and Preoptic Area Involvement in Beta‐Endorphin‐lnduced Release of Prolactin in Conscious Ovariectomized Rats†

Voogt, James L.; Reseh, Garth; Turkington, Susan

doi:10.1111/j.1365-2826.1989.tb00146.x

Cited by 11 publications

(5 citation statements)

References 29 publications

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“…Although extrahypothalamic site(s) whereby endogenous opioids alter prolactin secretion cannot be excluded, the prevailing view of the locus of endogenous opioids' action asserts that it takes place at the hypothalamic level (1485,1836,1880). Indeed, chemical lesions within the arcuate nucleus by neonatal administration of monosodium glutamate impairs the ability of morphine to induce prolactin secretion (49) while the opiate antagonist naloxone diminishes the release of prolactin evoked by electrical stimulation of the medial basal hypothalamus (48).…”

Section: Neuropeptidesmentioning

confidence: 99%

Hypothalamic Prolactin Receptor Messenger Ribonucleic Acid Levels, Prolactin Signaling, and Hyperprolactinemic Inhibition of Pulsatile Luteinizing Hormone Secretion Are Dependent on Estradiol

et al. 2007

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Hyperprolactinemia can reduce fertility and libido. Although central prolactin actions are thought to contribute to this, the mechanisms are poorly understood. We first tested whether chronic hyperprolactinemia inhibited two neuroendocrine parameters necessary for female fertility: pulsatile LH secretion and the estrogen-induced LH surge. Chronic hyperprolactinemia induced by the dopamine antagonist sulpiride caused a 40% reduction LH pulse frequency in ovariectomized rats, but only in the presence of chronic low levels of estradiol. Sulpiride did not affect the magnitude of a steroid-induced LH surge or the percentage of GnRH neurons activated during the surge. Estradiol is known to influence expression of the long form of prolactin receptors (PRL-R) and components of prolactin's signaling pathway. To test the hypothesis that estrogen increases PRL-R expression and sensitivity to prolactin, we next demonstrated that estradiol greatly augments prolactin-induced STAT5 activation. Lastly, we measured PRL-R and suppressor of cytokine signaling (SOCS-1 and -3 and CIS, which reflect the level of prolactin signaling) mRNAs in response to sulpiride and estradiol. Sulpiride induced only SOCS-1 in the medial preoptic area, where GnRH neurons are regulated, but in the arcuate nucleus and choroid plexus, PRL-R, SOCS-3, and CIS mRNA levels were also induced. Estradiol enhanced these effects on SOCS-3 and CIS. Interestingly, estradiol also induced PRL-R, SOCS-3, and CIS mRNA levels independently. These data show that GnRH pulse frequency is inhibited by chronic hyperprolactinemia in a steroid-dependent manner. They also provide evidence for estradiol-dependent and brain region-specific regulation of PRL-R expression and signaling responses by prolactin.

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Section: Neuropeptidesmentioning

confidence: 99%

Hypothalamic Prolactin Receptor Messenger Ribonucleic Acid Levels, Prolactin Signaling, and Hyperprolactinemic Inhibition of Pulsatile Luteinizing Hormone Secretion Are Dependent on Estradiol

et al. 2007

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“…It seems that the endogenous opioid peptides exert their action at the hypothalamic level to alter PRL secretion (23)(24)(25). Although a nondopaminergic mechanism(s) may also be involved in the opiate stimulation of PRL release (26,27), a number of studies indicate that the endogenous opioid peptides interact with the TIDA neurons.…”

mentioning

confidence: 99%

Endogenous Opioid Peptides Contribute to Suckling-Induced Prolactin Release by Suppressing Tyrosine Hydroxylase Activity and Messenger Ribonucleic Acid Levels in Tuberoinfundibular Dopaminergic Neurons*

Arbogast

Voogt

1998

Endocrinology

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The endogenous opioid peptides have been implicated in the control of the suckling-induced PRL rise during lactation. This study examined the role of the endogenous opioid peptides in suppressing tuberoinfundibular dopaminergic neuronal activity during lactation. In the first experiment, lactating rats were constantly exposed to pups. Naloxone (NAL; 60 mg/kg x h; i.v.), an opioid receptor antagonist, or saline was infused for 12 h. Blood was collected before and at 2-h intervals during the infusion. NAL suppressed circulating PRL levels to less than 36% of control values at 4, 6, 8, and 12 h after the onset of the infusion. Tyrosine hydroxylase (TH) activity in the stalk-median eminence and TH messenger RNA signal levels in the arcuate nucleus were determined at the end of the NAL infusion. TH activity and TH messenger RNA signal levels were increased 2.5- and 2.7-fold, respectively, after the 12-h NAL infusion. Even though the time spent with their pups was similar between the two groups, the pups in the NAL-treated group failed to gain weight during the 12-h NAL infusion period, whereas the control litters (8 pups) gained 5 g. In a second experiment, pups were removed from the dams before the 12-h NAL infusion and were returned after 11 h. Blood was collected before the infusion, at 3-h intervals during the pup separation period, and at 15-min intervals after reunion with the pups. Plasma PRL in control and NAL-treated rats was low (1-15 ng/ml) and similar during the separation period. The suckling-induced PRL surge in NAL-treated rats was markedly attenuated to 9-25% of control levels (350-650 ng/ml). After a 1-h suckling episode, TH activity in the stalk-median eminence of NAL-treated rats was 4.5-fold greater than controls. Litter weight gains were significantly less in NAL-treated rats during the 1-h suckling episode. These data indicate that the endogenous opioid peptides are an integral component for increasing PRL release in response to suckling and they act to decrease tuberoinfundibular dopaminergic neuronal activity during lactation, in part, by suppressing TH gene expression.

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“…Decreased responsiveness to a second infusion of (3-End was first reported when ovariectomized rats were treated with two perfusions of [3-End, 90 min apart, into the arcuate nucleus. A separate experiment showed that elevated PRL levels, in response to a 120-min perfusion of P-End, decreased dramatically after only 60 min of treatment [46]. Reduced sensitivity to [3-End could have perhaps taken place at the receptor level.…”

Section: Discussionmentioning

confidence: 95%

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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Arcuate Nucleus and Preoptic Area Involvement in Beta‐Endorphin‐lnduced Release of Prolactin in Conscious Ovariectomized Rats†

Cited by 11 publications

References 29 publications

Hypothalamic Prolactin Receptor Messenger Ribonucleic Acid Levels, Prolactin Signaling, and Hyperprolactinemic Inhibition of Pulsatile Luteinizing Hormone Secretion Are Dependent on Estradiol

Hypothalamic Prolactin Receptor Messenger Ribonucleic Acid Levels, Prolactin Signaling, and Hyperprolactinemic Inhibition of Pulsatile Luteinizing Hormone Secretion Are Dependent on Estradiol

Endogenous Opioid Peptides Contribute to Suckling-Induced Prolactin Release by Suppressing Tyrosine Hydroxylase Activity and Messenger Ribonucleic Acid Levels in Tuberoinfundibular Dopaminergic Neurons*

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

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