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Endocrine Abstracts (2022) 86 BPW2.3 | DOI: 10.1530/endoabs.86.BPW2.3

McGill University, Montreal, Canada


Gonadotropin-releasing hormone (GnRH) plays fundamental roles in the control of reproductive physiology. Perturbations in GnRH production or secretion cause infertility or subfertility. GnRH analogs are used clinically to both promote and inhibit the reproductive axis. GnRH is produced in neurons in the hypothalamus and is released in pulses into the pituitary portal system. The hormone binds to its cell surface receptor, GnRHR, on pituitary gonadotrope cells, where it stimulates the synthesis and secretion of the gonadotropins, luteinizing hormone (LH) and follicle-stimulating hormone (FSH). LH and FSH regulate key processes in the gonads, including steroidogenesis and gametogenesis. Gonadal steroids feedback to the brain and pituitary to regulate their own synthesis through both negative and positive (in females) feedback. Steroid negative feedback inhibits GnRH secretion, slowing pulsatile GnRH release. Estrogen positive feedback may promote a surge of GnRH release (at least in some species) and amplifies the pituitary response to GnRH, leading to a surge of LH, which triggers ovulation. More than four decades ago, it was discovered that the frequency of GnRH pulses differentially impacts LH and FSH secretion. High and low GnRH pulse frequencies favor LH and FSH release, respectively. However, the mechanisms through which gonadotropes ‘decode’ pulse frequency have remained elusive. In this lecture, I will discuss our recent efforts, using genetically modified mice, to understand how GnRH differentially regulates LH and FSH synthesis and secretion. Our data may challenge the concept of the gonadotrope as a GnRH pulse frequency decoder or at least may require a change in thinking about the nature of GnRH signaling in gonadotropes.

Volume 86

Society for Endocrinology BES 2022

Harrogate, United Kingdom
14 Nov 2022 - 16 Nov 2022

Society for Endocrinology 

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