Tachykinins and the hypothalamo–pituitary–gonadal axis: An update

Lasaga, Mercedes; Debéljuk, Luciano

doi:10.1016/j.peptides.2011.07.009

Cited by 59 publications

(45 citation statements)

References 99 publications

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“…Thus, our findings provide a reasonable explanation for the developmental and reproductive toxicity of triptolide. Interestingly, estradiol is not only responsible for follicular maturation, but also regulate secretion of LH and folliclestimulating hormone (FSH) from the pituitary through positive and negative feedback on the hypothalamus and pituitary [39]. Decreased estradiol release from triptolide-treated granulosa cells would remove the negative feedback control, resulting in higher serum levels of FSH and LH, as was observed in triptolidetreated female SD rats [12].…”

Section: Discussionmentioning

confidence: 99%

Effect of triptolide on estradiol release from cultured rat granulosa cells

Zhang

Liu

et al. 2012

Endocr J

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Section: Discussionmentioning

confidence: 99%

Effect of triptolide on estradiol release from cultured rat granulosa cells

Zhang

Liu

et al. 2012

Endocr J

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“…4 ). Furthermore, the TAC1 gene, implicated in the control of the GnRH pulse generator and thus LH secretion, plays a critical role in the neuroendocrine regulation of reproduction, mediating its biological effects via 3 G-protein-coupled receptors [Lasaga and Debeljuk, 2011;Kalil et al, 2016]. The observed increases in TAC1 and TAC3 gene expression following GnRHa treatment indicates that both their protein products, together with the EGRs, PROK2, PROP1 , LEP, and PITX1, may participate in orchestrating LH secretion (online suppl.…”

Section: The Differential Rna Profiles Of Hir/lir Versus Gnrha-treatementioning

confidence: 99%

GnRHa Treatment of Cryptorchid Boys Affects Genes Involved in Hormonal Control of the HPG Axis and Fertility

Hadžiselimović¹,

Gegenschatz‐Schmid²,

Verkauskas

et al. 2017

Sex Dev

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The gonadotropin-releasing hormone agonist (GnRHa; Buserelin) rescues fertility during adulthood in the majority of high infertility risk cryptorchid boys presenting with defective mini-puberty. However, the molecular events governing this effect are not understood. We report the outcome of an RNA profiling analysis of testicular biopsies from 4 operated patients who were treated with GnRHa for 6 months versus 3 operated controls who were not treated. GnRHa induces a significant transcriptional response, including protein-coding genes involved in pituitary development, the hypothalamic-pituitary-gonadal axis, and testosterone synthesis. Furthermore, we observed an increased abundance of long noncoding RNAs (lncRNAs) participating in epigenetic processes, including AIRN, FENDRR, XIST, and HOTAIR. These data are consistent with the hypothesis that hypogonadotropic hypogonadism in boys with altered mini-puberty is the consequence of a profoundly altered gene expression program involving protein-coding genes and lncRNAs. Our results point to molecular mechanisms that underlie the ability of GnRHa to rescue fertility.

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“…Accumulating evidence showed that the subpopulation neurons located in ARC, named KNDy neurons, coexpress kisspeptin, neurokinin B [NKB; also known as tachykinin 2 (TAC2)], and dynorphin and send projections to the GnRH neurons in the preoptic area (21,38). In particular, many lines of rodents and human studies have documented potent stimulatory effects of NKB on puberty onset (21,40) and reproduction (7,15).…”

mentioning

confidence: 99%

“…In particular, many lines of rodents and human studies have documented potent stimulatory effects of NKB on puberty onset (21,40) and reproduction (7,15). Both male and female pubertal failure cases resulting from NKB mutation are responsive to pulsatile administration of GnRH (42).…”

mentioning

confidence: 99%

Agouti-related peptide plays a critical role in leptin's effects on female puberty and reproduction

Sheffer-Babila

Sun

Israel

et al. 2013

American Journal of Physiology-Endocrinology and Metabolism

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Deficient leptin signaling causes infertility via reduced activity of GnRH neurons, causing a hypogonadal state in both rodents and humans. Because GnRH neurons do not express leptin receptors, leptin's effect on GnRH neurons must be indirect. Neurons within the hypothalamic arcuate nucleus that coexpress AGRP and NPY are considered to be important intermediate neurons involved in leptin regulation of GnRH neurons. Previously, we reported that the absence of AGRP and haploinsufficiency of MC4R in leptin receptor mutant (Lepr db/db ) females result in restoration of fertility and lactation despite the persistence of obesity and insulin resistance. The overarching hypothesis in the present study is that the absence or reduction of leptin's inhibition of AGRP/NPY neurons leads to suppression of GnRH release in cases of leptin signaling deficiency. Since TAC2 (NKB)-TAC3R signaling plays a role in puberty maturation and is modulated by metabolic status, the other aim of this study is to test whether TAC2/NKB neurons in ARC regulated by melanocortinergic signals herein affect leptin's action on puberty and reproduction. Our data showed that AGRP deficiency in Lepr db/db females restores normal timing of vaginal opening and estrous cycling, although uterine weight gain and mammary gland development are morphologically delayed. Nonetheless, Agrp Ϫ/Ϫ Lepr db/db females are fertile and sustain adequate nutrition of pups with lactation to weaning age. AGRP deficiency results in advanced vaginal opening in wild-type female mice. The postpubertal increase in hypothalamic TAC2 mRNA was not observed in Lepr db/db females, whereas AGRP deficiency restored it in Lepr db/db females. Additionally, MC4R activation with MTII induced FOS expression in TAC2 neurons, supporting the concept of melanocortinergic regulation of TAC2 neurons. These studies suggest that AGRP imposes an inhibitory effect on puberty and that TAC2 neurons may transmit melanocortinergic inhibition of GnRH neurons.agouti-related peptide; leptin; puberty; reproduction THE ONSET OF PUBERTY is the culmination of a subtle shift in balance of stimulatory and inhibitory neurotransmission within a complex neural network. Whereas the intrinsic pulsatility of GnRH neurons points toward a cell-autonomous function of gonadotropin-releasing hormone (GnRH) secretion, extrinsic signals are likely to be required to trigger activity in quiescent GnRH neurons. There is undoubtedly a link between metabolic status and GnRH activity (34). In the context of normal leptin signaling, a role has been implicated on the basis of a direct correlation between puberty onset and body weight (8, 16). Additionally, cases of defective leptin signaling in both humans and rodents result in hypogonadotropic hypogonadism (13). In a case report of a girl with leptin deficiency, treatment with leptin appeared to reverse the hypogonadal state (12). In cases of lipodystrophy with attendant hypoleptinemia, leptin therapy normalized pituitary hormone release (29) and restored menstrual cycles to all treat...

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Tachykinins and the hypothalamo–pituitary–gonadal axis: An update

Cited by 59 publications

References 99 publications

Effect of triptolide on estradiol release from cultured rat granulosa cells

Effect of triptolide on estradiol release from cultured rat granulosa cells

GnRHa Treatment of Cryptorchid Boys Affects Genes Involved in Hormonal Control of the HPG Axis and Fertility

Agouti-related peptide plays a critical role in leptin's effects on female puberty and reproduction

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