Gonadotropin-releasing hormone (GnRH) secretion from GnRH neurons and its modulation by neuropeptides are essential for mammalian reproduction. Here, I review the neuropeptides that have been shown to act directly and that may also act indirectly, on GnRH neurons, the reproduction-related processes with which the neuropeptides may be associated or the physiological information they may convey, as well as their cognate receptors, signaling pathways and roles in the modulation of GnRH neuronal firing, [Ca], GnRH secretion and reproduction. The review focuses on recent research in mice, which offer the most tractable experimental system for studying mammalian GnRH neurons.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1007/s00441-018-2893-z | DOI Listing |
J Pediatr Endocrinol Metab
January 2025
Department of Paediatrics, School of Medical Sciences, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
Objectives: Kisspeptin plays a major role in the onset of puberty by stimulating the gonadotropin-releasing hormone (GnRH) neurons. The aim of this study was to investigate whether GnRH inhibits kisspeptin secretion via a negative feedback mechanism and potential associations between kisspeptin levels and other hormones of importance for pubertal onset.
Methods: Thirteen girls with suspected central precocious puberty underwent a GnRH stimulation test twice in a randomized, placebo-controlled manner.
J Endocr Soc
January 2025
Cellular and Molecular Endocrinology Laboratory LIM/25, Division of Endocrinology and Metabolism, Clinicas Hospital, School of Medicine, University of Sao Paulo, 01246-903 Sao Paulo, Brazil.
Human puberty is a dynamic biological process determined by the increase in the pulsatile secretion of GnRH triggered by distinct factors not fully understood. Current knowledge reveals fine tuning between an increase in stimulatory factors and a decrease in inhibitory factors, where genetic and epigenetic factors have been indicated as key players in the regulation of puberty onset by distinct lines of evidence. Central precocious puberty (CPP) results from the premature reactivation of pulsatile secretion of GnRH.
View Article and Find Full Text PDFAndrology
January 2025
Section of Endocrinology and Investigative Medicine, Imperial College London, London, UK.
The hypothalamic-pituitary-gonadal axis is regulated by the gonadotropin-releasing hormone pulse generator in the hypothalamus. This is comprised of neurons that secrete kisspeptin in a pulsatile manner to stimulate the release of GnRH, and, in turn, downstream gonadotropins from the pituitary gland, and subsequently sex steroids and gametogenesis from the gonads. Many reproductive disorders in both males and females are characterized by hypothalamic dysfunction, including functional disorders (such as age-related hypogonadism, obesity-related secondary hypogonadism, hyperprolactinemia, functional hypothalamic amenorrhea and polycystic ovary syndrome), structural pathologies (such as craniopharyngiomas or radiation or surgery-related hypothalamic dysfunction), and pubertal disorders (constitutional delay of growth and puberty and congenital hypogonadotropic hypogonadism).
View Article and Find Full Text PDFBMC Genomics
January 2025
MOE Key Laboratory of Marine Genetics and Breeding, College of Marine Life Sciences / Key Laboratory of Tropical Aquatic Germplasm of Hainan Province, Sanya Oceanographic Institution, Ocean University of China, Qingdao / Sanya, China.
Background: The golden pompano (Trachinotus ovatus) is an economically significant warm-water aquaculture species in China. The time required for sexual maturity of T. ovatus is relatively long.
View Article and Find Full Text PDFJCEM Case Rep
January 2025
Department of Endocrinology and Metabolism, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan.
Congenital hypogonadotropic hypogonadism (CHH) can cause delayed secondary sexual characteristics and contribute to juvenile osteoporosis, with multiple causative genes having been reported. We treated a 27-year-old man diagnosed with central hypogonadism, presenting with delayed secondary sexual characteristics and juvenile osteoporosis, using bone resorption inhibitors and testosterone therapy. Genetic testing revealed missense variants both in the fibroblast growth factor receptor 1 () and gonadotropin-releasing hormone receptor () genes, a combination that has not been previously reported.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!