Inhibitory effects of centrally administered |ASU1–7| eel calcitonin on basal and stimulated prolactin release in rats

Sibilia, V.; Netti, C.; Guidobono, F.; Villa, Isabella; Pecile, A.

doi:10.1007/bf03348612

Cited by 5 publications

(4 citation statements)

References 20 publications

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“…Calcitonin-like peptides lower prolactin secretion induced by stress in prepubertal female rats or by the suckling stimulus in lactating animals (495, 1348). Intracerebroventricular administration of a calcitonin analog lowers basal as well as stress-or morphine-induced prolactin secretion (1633). These data suggest that, in addition to its direct effects in the pituitary, calcitonin has central inhibitory activity on prolactin secretion as well, probably through enhancement of hypothalamic inhibitory pathways controlling prolactin secretion (1308,1633).…”

Section: Neuropeptidesmentioning

confidence: 95%

“…Intracerebroventricular administration of a calcitonin analog lowers basal as well as stress-or morphine-induced prolactin secretion (1633). These data suggest that, in addition to its direct effects in the pituitary, calcitonin has central inhibitory activity on prolactin secretion as well, probably through enhancement of hypothalamic inhibitory pathways controlling prolactin secretion (1308,1633). It has been suggested that calcitonin has a potential role as neuromodulator in the CNS (1679) and it may decrease prolactin secretion by activating the TIDA system (341).…”

Section: Neuropeptidesmentioning

confidence: 99%

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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: 95%

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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“…The premise for this hypothesis has been provided by the recent discovery of other neural regulators of bone, including leptin and neuropeptide Y, whose actions originate from the hypothalamus and are mediated via efferent neural pathways to regulate bone turnover 54, 55. Evidence supporting this hypothesis is the high level of CTR expression and calcitonin binding within the arcuate nucleus of the hypothalamus,56–58 together with the observations that calcitonin and CGRP act via the central nervous system (CNS) to inhibit appetite and gastric acid secretion, to modulate hormone secretion, to exert analgesic effects, and to control the secretion of prolactin 59–62. It remains to be tested whether calcitonin acting in the hypothalamus can influence bone metabolism.…”

Section: The Physiological Role Of Calcitoninmentioning

confidence: 99%

Calcitonin: Physiology or fantasy?

Davey

Findlay

2013

Journal of Bone and Mineral Research

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Calcitonin, a potent hypocalcemic hormone produced by the C-cells of the thyroid, was first discovered by Harold Copp in 1962. The physiological significance of calcitonin has been questioned, but recent studies using genetically modified mouse models have uncovered additional actions of calcitonin acting through its receptor (CTR) that are of particular significance to the regulation of bone and calcium homeostasis. Mice in which the CTR is deleted in osteoclasts are more susceptible to induced hypercalcemia and exogenous calcitonin is able to lower serum calcium in younger animals. These data are consistent with the hypothesis that calcitonin can regulate serum calcium by inhibiting the efflux of calcium from bone, and that this action is most important when bone turnover is high. Calcitonin has also been implicated in protecting the skeleton from excessive loss of bone mineral during times of high calcium demand, such as lactation. This action may be linked to an intriguing and as yet unexplained observation that calcitonin inhibits bone formation, because deletion of the CTR leads to increased bone formation. We propose several mechanisms by which calcitonin could protect the skeleton by regulating bone turnover, acting within the bone and/or centrally. A new more holistic notion of the physiological role of calcitonin in bone and calcium homeostasis is required and we have highlighted some important knowledge gaps so that future calcitonin research will help to achieve such an understanding.

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“…There is also evidence for calcitonin actions in the kidney, with reports demonstrating an action to decrease tubular reabsorption of calcium (4,5) and others showing that calcitonin can facilitate renal calcium and magnesium reabsorption (6). A number of actions for calcitonin have also been described in the brain and hypothalamus (7,8). Calcitonin mediates its actions by binding to its G protein-coupled cell surface receptor, the calcitonin receptor (CTR), to which it binds with the highest affinity.…”

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confidence: 99%

A Role for the Calcitonin Receptor to Limit Bone Loss During Lactation in Female Mice by Inhibiting Osteocytic Osteolysis

et al. 2015

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During lactation, the large transfer of calcium from the mother to the milk is primarily sourced from the maternal skeleton. To determine whether the calcitonin receptor (CTR) plays a physiological role to protect the skeleton from excessive resorption during lactation, we assessed the maternal skeleton of global CTR knockout (CTRKO) and littermate control mice at the end of lactation (postnatal day 21). Micro-computed tomography analyses showed no effect on trabecular or cortical bone in the distal femur and L1 vertebra of maternal global CTR deletion at the end of lactation in global CTRKO mice compared with that in control mice. Bone resorption, as assessed by osteoclast number and activity at the end of lactation, was unaffected by maternal CTR deletion. Cathepsin K, carbonic anhydrase 2, matrix metalloproteinase 13, and receptor activator of nuclear factor-κB ligand mRNA levels, however, were markedly elevated by 3- to 6.5-fold in whole bone of lactating global CTRKO females. Because these genes have been shown to be up-regulated in osteocytes during lactation when osteocytes resorb their surrounding bone matrix, together with their reported expression of the CTR, we determined the osteocyte lacunar area in cortical bone. After lactation, the top 20% of osteocyte lacunar area in global CTRKO mice was 10% larger than the top 20% in control mice. These data are consistent with an increased osteocytic osteolysis in global CTRKO mice during lactation, which is further supported by the increased serum calcium observed in global CTRKO mice after lactation. These results provide evidence for a physiological role for the CTR to protect the maternal skeleton during lactation by a direct action on osteocytes to inhibit osteolysis.

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Inhibitory effects of centrally administered |ASU1–7| eel calcitonin on basal and stimulated prolactin release in rats

Cited by 5 publications

References 20 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

Calcitonin: Physiology or fantasy?

A Role for the Calcitonin Receptor to Limit Bone Loss During Lactation in Female Mice by Inhibiting Osteocytic Osteolysis

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