2019
DOI: 10.1159/000503146
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17β-Estradiol Increases Arcuate KNDy Neuronal Sensitivity to Ghrelin Inhibition of the M-Current in Female Mice

Abstract: Obesity and anorexia result in dysregulation of the hypothalamic-pituitary-gonadal axis, negatively impacting reproduction. Ghrelin, secreted from the stomach, potentially mediates negative energy states and neuroendocrine control of reproduction by acting through the growth hormone secretagogue receptor (GHSR). GHSR is expressed in hypothalamic arcuate (ARC) Kisspeptin/Neurokinin B (Tac2)/Dynorphin (KNDy) neurons. Ghrelin is known to inhibit the M-current produced by KCNQ channels in other ARC neurons. In add… Show more

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Cited by 23 publications
(20 citation statements)
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“…Although the specific mechanism is unclear, we speculate that NPY and GHRL in hypothalamus may participate in development of pubertal PCOS through kisspeptin / GnRH system in view of both our previous study [ 8 ] and study of Shen et al [ 29 ] showed that the increased expression and release of kisspeptin and GnRH in hypothalamus are the key pathogenesis of pubertal PCOS. The following provides evidence for our conjecture: a, Immunofluorescence double-labeling experiment showed that GnRH neurons and kisspeptin neurons in ARC were the direct targets of NPY and GHRL in hypothalamus respectively, consistent with research of Conde et al [ 30 ] and Dhillon et al [ 31 ]; b, Kisspeptin, as the nodal regulatory centre of reproductive function, binds into kisspeptin receptor (G-protein coupled receptor-54, GPR-54) on GnRH neurons or NPY neurons and promotes GnRH and NPY secretion from hypothalamus [ 32 35 ]; c, Previous studies have shown that NPY is necessary for the pulsatility of GnRH release [ 36 ], promoting the secretion of GnRH [ 11 ]. However, GHRL is inhibitory to GnRH/LH release [ 12 ].…”
Section: Discussionsupporting
confidence: 90%
“…Although the specific mechanism is unclear, we speculate that NPY and GHRL in hypothalamus may participate in development of pubertal PCOS through kisspeptin / GnRH system in view of both our previous study [ 8 ] and study of Shen et al [ 29 ] showed that the increased expression and release of kisspeptin and GnRH in hypothalamus are the key pathogenesis of pubertal PCOS. The following provides evidence for our conjecture: a, Immunofluorescence double-labeling experiment showed that GnRH neurons and kisspeptin neurons in ARC were the direct targets of NPY and GHRL in hypothalamus respectively, consistent with research of Conde et al [ 30 ] and Dhillon et al [ 31 ]; b, Kisspeptin, as the nodal regulatory centre of reproductive function, binds into kisspeptin receptor (G-protein coupled receptor-54, GPR-54) on GnRH neurons or NPY neurons and promotes GnRH and NPY secretion from hypothalamus [ 32 35 ]; c, Previous studies have shown that NPY is necessary for the pulsatility of GnRH release [ 36 ], promoting the secretion of GnRH [ 11 ]. However, GHRL is inhibitory to GnRH/LH release [ 12 ].…”
Section: Discussionsupporting
confidence: 90%
“…Although the specific mechanism is unclear, we speculate that NPY and GHRL in hypothalamus may participate in development of pubertal PCOS through kisspeptin / GnRH system in view of our previous study showed that the increased expression and release of kisspeptin and GnRH in hypothalamus are the key pathogenesis of pubertal PCOS [7]. The following provides evidence for our conjecture: a, Immunofluorescence doublelabeling experiment showed that GnRH neurons and kisspeptin neurons in ARC were the direct targets of NPY and GHRL in hypothalamus respectively, consistent with research of Conde et al [24] and Dhillon et al [25]; b, Kisspeptin, as the nodal regulatory centre of reproductive function, binds into kisspeptin receptor (G-protein coupled receptor-54, GPR-54) on GnRH neurons or NPY neurons and promotes GnRH and NPY secretion from hypothalamus [26][27][28][29]; c, Previous studies have shown that NPY is necessary for the pulsatility of GnRH release [30], promoting the secretion of GnRH [10]. However, GHRL is inhibitory to GnRH/LH release [11].…”
Section: Discussionsupporting
confidence: 89%
“…However, the much lower abundance of Kcnq5 suggested that increased expression was unlikely to be the sole reason for the E2-enhanced M-current [ 27 ]. Other E2-driven mechanisms must regulate the M-current such as altered coupling between ghrelin receptors and KCNQ channels in ARH kisspeptin neurons [ 82 ]. However, the strategy we outlined can easily be adapted to study other KCNQ subunits to more fully explicate the M-current in future experiments.…”
Section: Discussionmentioning
confidence: 99%