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Michelle L. Gottsch

Researcher at University of Washington

Publications -  18
Citations -  6345

Michelle L. Gottsch is an academic researcher from University of Washington. The author has contributed to research in topics: Kisspeptin & Gonadotropin-releasing hormone. The author has an hindex of 17, co-authored 18 publications receiving 5923 citations.

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A Role for Kisspeptins in the Regulation of Gonadotropin Secretion in the Mouse

TL;DR: Kisspeptins are products of the KiSS-1 gene, which bind to a G protein-coupled receptor known as GPR54, and it is concluded that kisspeptin-GPR54 signaling may be part of the hypothalamus circuitry that governs the hypothalamic secretion of GnRH.
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Activation of Gonadotropin-Releasing Hormone Neurons by Kisspeptin as a Neuroendocrine Switch for the Onset of Puberty

TL;DR: It is demonstrated that kisspeptin exerts a potent depolarizing effect on the excitability of almost all adult GnRH neurons and that the responsiveness of Gn RH neurons tokisspeptin increases over postnatal development.
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Kisspeptin Activation of Gonadotropin Releasing Hormone Neurons and Regulation of KiSS-1 mRNA in the Male Rat

TL;DR: These results demonstrate that GnRH neurons are direct targets for regulation by kisspeptins and that KiSS-1 mRNA is regulated by gonadal hormones, suggesting that Ki SS-1 neurons play an important role in the feedback regulation of gonadotropin secretion.
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Regulation of Gonadotropin-Releasing Hormone Secretion by Kisspeptin/Dynorphin/Neurokinin B Neurons in the Arcuate Nucleus of the Mouse

TL;DR: A model whereby NKB and dynorphin act autosynaptically onkisspeptin neurons in the Arc to synchronize and shape the pulsatile secretion of kisspeptin and drive the release of GnRH from fibers in the median eminence is proposed.
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Differential Regulation of KiSS-1 mRNA Expression by Sex Steroids in the Brain of the Male Mouse

TL;DR: Kisspeptins are products of the Kiss1 gene, which bind to GPR54, a G protein-coupled receptor, and the effects of T are mediated by both ERalpha and AR pathways, suggesting that both estrogen receptor (ER) and androgen receptor (AR) play a role in T-mediated regulation of KiSS-1.