Kisspeptin Regulates Prolactin Release through Hypothalamic Dopaminergic Neurons

Szawka, Raphael E.; Ribeiro, Aline Barbosa; Leite, Cristiane Mota; Helena, Cleyde; Franci, Celso Rodrigues; Anderson, Greg M.; Hoffman, Gloria E.; Anselmo-Franci, Janete Aparecida

doi:10.1210/en.2009-1414

Cited by 86 publications

(45 citation statements)

References 61 publications

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“…In mice, kisspeptin regulates the prolactin release through the inhibition of hypothalamic dopaminergic neurons, whereas this mechanism depends on estradiol in female rodents [49]. These results confirm the important role played by kisspeptin in physiological regulation of HPG axis.…”

Section: Function In Puberty and Reproductive Systemsupporting

confidence: 69%

Kisspeptin/GPR54 System: What Do We Know About Its Role in Human Reproduction?

Trevisan

Montagna

Oliveira

et al. 2018

Cell Physiol Biochem

101

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Kisspeptin is involved in the control of human reproduction bridging the gap between the sex steroid levels and feedback mechanisms that control the gonadotropin releasing hormone (GnRH) secretion; however, studies considering this peptide and infertility are limited. We conducted a review and critical assessment of available evidence considering kisspeptin structure, physiology, function in puberty and reproduction, its role in assisted reproduction treatments, kisspeptin dosage and the impact on KISS1 and GPR54 genes. Literature searches were conducted in PubMed using keywords related to: (i) kisspeptin or receptors, kisspeptin-1 (ii) reproduction or infertility or fertility (iii) gene and (iv) dosage or measurement or quantification or serum level, in human. Kisspeptin is a product of KISS1 gene that binds to a G-protein-coupled receptor (GPR54/KISS1R) stimulating the release of GnRH by hypothalamic neurons, leading to secretion of pituitary gonadotropins (LH and FSH) and sexual steroids, which in turn will act in the gonads to produce the gametes. Kisspeptin is being recognized as a crucial regulator of the onset of puberty, the regulation of sex hormone mediated secretion of gonadotropins, and the control of fertility. Inactivating and activating mutations in both KISS1 or GPR54 genes were associated with hypogonadotropic hypogonadism and precocious puberty. Despite this, studies considering kisspeptin and infertility are scarce. The understanding of the role of kisspeptin may lead to its use as a biomarker in infertility treatments and use in controlled ovarian hyperstimulation.

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Section: Function In Puberty and Reproductive Systemsupporting

confidence: 69%

Kisspeptin/GPR54 System: What Do We Know About Its Role in Human Reproduction?

Trevisan

Montagna

Oliveira

et al. 2018

Cell Physiol Biochem

101

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“…Suckling stimulus suppresses the expression of tyrosine hydroxylase, a key enzyme of dopamine production, in TIDA neurons, which results in the secretion of PRL from the pituitary (Berghorn et al 2001). Recent studies have shown that kisspeptin neurons in the ARC directly project their axons to TIDA neurons (Sawai et al 2012), and that kisspeptin suppresses the activity of TIDA neurons (Szawka et al 2010). The afferent input from the SPFpc to kisspeptin neurons in the ARC observed in this study indicates a new regulatory mechanism of PRL secretion via a SPFpc-kisspeptin neuron-TIDA neuron feedback pathway.…”

Section: Discussionmentioning

confidence: 99%

Rapid modulation of hypothalamic Kiss1 levels by the suckling stimulus in the lactating rat

Higo¹,

Aikawa²,

Iijima³

et al. 2015

Journal of Endocrinology

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In mammals, lactation suppresses GnRH/LH secretion resulting in transient infertility. In rats, GnRH/LH secretion is rescued within 18-48 h after pup separation (PS) and rapidly re-suppressed by subsequent re-exposure of pups. To elucidate the mechanisms underlying these rapid modulations, changes in the expression of kisspeptin, a stimulator of GnRH secretion, in several lactating conditions (normal-lactating; 4-h PS; 18-h PS; 4-h PS C1-h re-exposure of pups; non-lactating) were examined using in situ hybridization. PS for 4 h or 18 h increased Kiss1 expressing neurons in both the anteroventral periventricular nucleus (AVPV) and the arcuate nucleus (ARC), and subsequent exposure of pups re-suppressed Kiss1 in the AVPV. A change in Kiss1 expression was observed prior to the reported time of the change in GnRH/LH, indicating that the change in GnRH/LH results from changes in kisspeptin. We further examined the mechanisms underlying the rapid modulation of Kiss1. We first investigated the possible involvement of ascending sensory input during the suckling stimulus. Injection of the anterograde tracer to the subparafascicular parvocellular nucleus (SPFpc) in the midbrain, which relays the suckling stimulus, revealed direct neuronal connections between the SPFpc and kisspeptin neurons in both the AVPV and ARC. We also examined the possible involvement of prolactin (PRL). Administration of PRL for 1 h suppressed Kiss1 expression in the AVPV but not in the ARC. These results indicate that suckling stimulus rapidly modulates Kiss1 expression directly via neuronal connections and indirectly through serum PRL, resulting in modulation in GnRH/LH secretion.

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“…Monoamines and metabolites were identified based on their peak retention times. Quantification was performed using the internal standard method based on the area under the peak (Rizelio et al, 2010;Szawka et al, 2010). All samples from each brain area were measured in the same analysis.…”

Section: Neurotransmitter Analysesmentioning

confidence: 99%