Lack of Functional GABA&lt;sub&gt;B&lt;/sub&gt; Receptors Alters &lt;b&gt;&lt;i&gt;Kiss1&lt;/i&gt;&lt;/b&gt;, &lt;b&gt;&lt;i&gt;Gnrh1 &lt;/i&gt;&lt;/b&gt;and &lt;b&gt;&lt;i&gt;Gad1&lt;/i&gt;&lt;/b&gt; mRNA Expression in the Medial Basal Hypothalamus at Postnatal Day 4

Giorgio, Noelia Paula Di; Catalano, Paolo N.; López, Paula V.; González, Betina; Semaan, Sheila J.; López, Gabriela C.; Kauffman, Alexander S.; Rulli, Susana B.; Somoza, Gustavo M.; Bettler, Bernhard; Libertun, Carlos; Lux‐Lantos, Victoria

doi:10.1159/000355631

Cited by 31 publications

(23 citation statements)

References 65 publications

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“…We studied four treatments in each genotype: control (Krebs‐Ringer), Kiss‐10 (Kiss1r agonist; Phoenix Pharmaceuticals Inc., Belmont, CA, USA; 1 × 10 −7 mol L ‐1 ), Kiss‐234 (Kiss1r antagonist; Sigma‐Aldrich; 1 × 10 −7 mol L ‐1 ) and the combination of agonist and antagonist (Kiss‐10 + Kiss‐234; 1 × 10 −7 mol L ‐1 each). Media were frozen until GnRH content was measured by RIA (n = 4‐7).…”

Section: Methodsmentioning

confidence: 99%

“…Each sample was analysed in duplicate along with non‐template (water) and non‐RT controls to monitor contaminating DNA. Quantitative differences in the cDNA target between samples were determined as described previously using the mathematical model of Pfaffl, which refers expression to a single randomly selected WT female.…”

Section: Methodsmentioning

confidence: 99%

“…Serum LH and FSH levels were determined by RIA with kits from the National Hormone and Pituitary Program, National Institute of Diabetes and Digestive and Kidney Diseases (Bethesda, MD, USA) and Dr A. F. Parlow (National Hormone and Pituitary Program, Torrance, CA, USA) as previously described . The results were expressed in terms of RP3 rat LH and FSH standards because these systems recognise mouse proteins.…”

Section: Methodsmentioning

confidence: 99%

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Multiple failures in the lutenising hormone surge generating system in GABAB1KO female mice

Giorgio

Bizzozzero-Hiriart

Surkin

et al. 2019

J Neuroendocrinology

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Female mice lacking GABAB receptors, GABAB1KO, show disrupted oestrous cycles, reduced pregnancies and increased hypothalamic Gnrh1 mRNA expression, whereas anteroventral periventricular/periventricular preoptic nucleus (AVPV/PeN) Kiss1 mRNA was not affected. In the present study, we characterise the important components of the gonadotrophic preovulatory surge, aiming to unravel the origin of this reproductive impairment. In GABAB1KO and wild-type (WT) females, we determined: (i) hypothalamic oestrogen receptor (ER)α and β and aromatase mRNA and protein expression; (ii) ovulation index and oestrus serum follicle-stimulating hormone (FSH) and pituitary Gnrh1r expression; (iii) in ovariectomised-oestradiol valerate-treated mice, we evaluated ex vivo hypothalamic gonadotrophin-releasing hormone (GnRH) pulsatility in the presence/absence of kisspeptin (Kiss-10, constant or pulsatile) and oestradiol (constant); and (iv) in ovariectomised-oestradiol silastic capsule-treated mice (proestrous-like environment), we evaluated morning and evening kisspeptin neurone activation (c-Fos+) and serum luteinising homrone (LH). In the medial basal hypothalamus of oestrus GABAB1KOs, aromatase and ERα mRNA and protein were increased, whereas ERβ was decreased. In GABAB1KOs, the ovulation index was decreased together with decreased first oestrus serum FSH and increased pituitary Gnrh1r mRNA. Under constant Kiss-10 stimulation, hypothalamic GnRH pulse frequency did not vary, although GnRH mass/pulse was increased in GABAB1KOs.In WTs, pulsatile Kiss-10 together with constant oestradiol significantly increased GnRH pulsatility, whereas, in GABAB1KOs, oestradiol alone increased GnRH pulsatility and this was reversed by pulsatile Kiss-10 addition. In GABAB1KOs AVPV/PeN kisspeptin neurones were similarly activated (c-Fos+) in the morning and evening, whereas WTs showed the expected, marked evening stimulation. LH correlated with activated kisspeptin cells in WT mice, whereas GABAB1KO mice showed high, similar LH levels both in the morning and evening. Taken together, all of these alterations point to impairment in the trigger of the preovulatory GnRH surge that entails the reproductive alterations described. K E Y W O R D SGABAB1KO mice, GnRH pulsatility, kisspeptin, oestrogen receptors, ovulation

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Multiple failures in the lutenising hormone surge generating system in GABAB1KO female mice

Giorgio

Bizzozzero-Hiriart

Surkin

et al. 2019

J Neuroendocrinology

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“…GnRH concentration was determined by radioimmunoassay (RIA) as previously described in mouse, Mus musculus (Di Giorgio et al. ), and validated in the vizcacha (Dorfman et al. ; Charif et al.…”

Section: Methodsmentioning

confidence: 99%

Local production of neurostradiol affects gonadotropin-releasing hormone (GnRH) secretion at mid-gestation inLagostomus maximus(Rodentia, Caviomorpha)

et al. 2017

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Females of the South American plains vizcacha, Lagostomus maximus, show peculiar reproductive features such as massive polyovulation up to 800 oocytes per estrous cycle and an ovulatory process around mid‐gestation arising from the reactivation of the hypothalamic–hypophyseal–ovary (H.H.O.) axis. Estradiol (E2) regulates gonadotropin‐releasing hormone (GnRH) expression. Biosynthesis of estrogens results from the aromatization of androgens by aromatase, which mainly occurs in the gonads, but has also been described in the hypothalamus. The recently described correlation between GnRH and ER α expression patterns in the hypothalamus of the vizcacha during pregnancy, with coexpression in the same neurons of the medial preoptic area, suggests that hypothalamic synthesis of E2 may affect GnRH neurons and contribute with systemic E2 to modulate GnRH delivery during the gestation. To elucidate this hypothesis, hypothalamic expression and the action of aromatase on GnRH release were evaluated in female vizcachas throughout pregnancy. Aromatase and GnRH expression was increased significantly in mid‐pregnant and term‐pregnant vizcachas compared to early‐pregnant and nonpregnant females. In addition, aromatase and GnRH were colocalized in neurons of the medial preoptic area of the hypothalamus throughout gestation. The blockage of the negative feedback of E2 induced by the inhibition of aromatase resulted in a significant increment of GnRH‐secreted mass by hypothalamic explants. E2 produced in the same neurons as GnRH may drive intracellular E2 to higher levels than those obtained from systemic circulation alone. This may trigger for a prompt GnRH availability enabling H.H.O. activity at mid‐gestation with ovulation and formation of accessory corpora lutea with steroidogenic activity that produce the necessary progesterone to maintain gestation to term and guarantee the reproductive success.

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“…Thirdly, KP can act per se on in vitro GnRH-secreting cells to heighten their firing rates (Quaynor et al 2007, Dumalska et al 2008, Pielecka-Fortuna et al 2008. Fourthly, there has been recent evidence suggest that KP can communicate indirectly with GnRH neurons through other neurons such as glutamatergic and GABAergic neurons (Pielecka-Fortuna et al 2008, García-Galiano et al 2012, Di Giorgio et al 2013.…”

Section: Role Of Kp In Regulation Of Reproductionmentioning

confidence: 99%

The involvement of gonadotropin inhibitory hormone and kisspeptin in the metabolic regulation of reproduction

Wahab¹,

Shahab²,

Behr³

2015

Journal of Endocrinology

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Recently, kisspeptin (KP) and gonadotropin inhibitory hormone (GnIH), two counteracting neuropeptides, have been acknowledged as significant regulators of reproductive function. KP stimulates reproduction while GnIH inhibits it. These two neuropeptides seem to be pivotal for the modulation of reproductive activity in response to internal and external cues. It is well-documented that the current metabolic status of the body is closely linked to its reproductive output. However, how reproductive function is regulated by the body's energy status is less clear. Recent studies have suggested an active participation of hypothalamic KP and GnIH in the modulation of reproductive function according to available metabolic cues. Expression of KISS1, the KP encoding gene, is decreased while expression of RFRP (NPVF), the gene encoding GnIH, is increased in metabolic deficiency conditions. The lower levels of KP, as suggested by a decrease in KISS1 gene mRNA expression, during metabolic deficiency can be corrected by administration of exogenous KP, which leads to an increase in reproductive hormone levels. Likewise, administration of RF9, a GnIH receptor antagonist, can reverse the inhibitory effect of fasting on testosterone in monkeys. Together, it is likely that the integrated function of both these hypothalamic neuropeptides works as a reproductive output regulator in response to a change in metabolic status. In this review, we have summarized literature from nonprimate and primate studies that demonstrate the involvement of KP and GnIH in the metabolic regulation of reproduction.

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Lack of Functional GABA<sub>B</sub> Receptors Alters <b><i>Kiss1</i></b>, <b><i>Gnrh1 </i></b>and <b><i>Gad1</i></b> mRNA Expression in the Medial Basal Hypothalamus at Postnatal Day 4

Cited by 31 publications

References 65 publications

Multiple failures in the lutenising hormone surge generating system in GABAB1KO female mice

Multiple failures in the lutenising hormone surge generating system in GABAB1KO female mice

Local production of neurostradiol affects gonadotropin-releasing hormone (GnRH) secretion at mid-gestation inLagostomus maximus(Rodentia, Caviomorpha)

The involvement of gonadotropin inhibitory hormone and kisspeptin in the metabolic regulation of reproduction

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