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Endocrine Functions of Brain Dopamine
Published in Nira Ben-Jonathan, Dopamine, 2020
GnRH neurons are unusual in that they are derived from progenitors in the epithelium of the olfactory placode [66]. During embryonic life, the nascent GnRH neurons migrate along the vomeronasal axons, across the cribiform plate and into the mediobasal hypothalamus where migration ceases and the neurons detach from their axonal guides. Mature GnRH neurons are distributed throughout the anteroventral periventricular and preoptic area of the hypothalamus. Multiple factors are involved in the embryonic migration of the GnRH neurons, ranging from transcription factors to a variety of transmembrane tyrosine kinases or G protein-coupled receptors and their ligands, to extracellular matrix proteins. Some of the factors influence the movement of the GnRH neurons indirectly, by altering the pace or targeting of the olfactory system. Loss of the GnRH neurons or their misdirection along the migration route results in failure of sexual maturation in mice and man [67].
Pubertal abnormalitiesPrecocious and delayed
Published in Joseph S. Sanfilippo, Eduardo Lara-Torre, Veronica Gomez-Lobo, Sanfilippo's Textbook of Pediatric and Adolescent GynecologySecond Edition, 2019
Isolated GnRH deficiency includes the various forms of Kallman syndrome, in addition to idiopathic hypogonadotropic hypogonadism (IHH). Kallman syndrome may involve anosmia or hyposmia, and delayed puberty due to defects in migration of GnRH neurons with the olfactory placode in fetal development.15 Genes that may be involved in IHH/KS may be X-linked as in KAL1, also known as ANOS1 (rarely affecting females) or autosomal dominant (CHD7, FGFR1) or recessive (affecting females and males). Some forms of KS may be associated with cleft palate and/or deafness (CHD7), dental anomalies or agenesis (FGFR1), or synkinesia (ANOS1). Some isolated forms of hypogonadotropic hypogonadism involve genes for GnRH (GNRHR gene) or kisspeptin or its receptor.16
Physiology of the Pituitary Gland
Published in John C Watkinson, Raymond W Clarke, Louise Jayne Clark, Adam J Donne, R James A England, Hisham M Mehanna, Gerald William McGarry, Sean Carrie, Basic Sciences Endocrine Surgery Rhinology, 2018
Mária Hérincs, Karen Young, Márta Korbonits
Secretion of GnRH is primarily regulated by 17β-oestradiol (E2) acting via oestrogen receptor alpha (ERα). However, as GnRH neurons do not express ERα, regulation of hypothalamic function by oestradiol is mediated by kisspeptin neurons, which do express this receptor and are thought to relay information regarding oestrogen levels directly to the GnRH neurons.29 In addition, the inhibitory feedback of prolactin on the gonadal axis occurs via kisspeptin, as GnRH neurons do not express prolactin receptors either, therefore rendering them insensitive to circulating prolactin levels.30 Kisspeptin and its receptor KISS-R (G-protein-coupled receptor 54, GPR54) are recently identified members of the gonadotroph axis. Kisspeptin is synthesized in several hypothalamic nuclei including the arcuate nucleus and the preoptic area. More recently, a gonadotrophin inhibitory hormone (GnIH) has been described in birds.31 The role of its mammalian counterpart RFamide-related peptide (RFRP) and its putative G-protein coupled receptor OT7T022 (also known as neuropeptide FF receptor type 1) is currently under investigation.
Serum leptin correlates in fertile and idiopathic infertile Yemeni males: a comparative cross-sectional study
Published in Systems Biology in Reproductive Medicine, 2022
Ebraheem A. Al-Nawd, Fairouz K. Alshowafi, Ahmed A. Abdullateef, Mohammad M. Abdulgabbar Noman, Rashad H. Albadani, Majed Ahmed Al-Mansoub
A significant role of leptin in male reproductive function control has been firmly established (Mintziori et al. 2020; Childs et al. 2021). Central and peripheral pathways affecting the hypothalamic-pituitary-gonadal (HBG) axis have been hypothesised, considering the wide distribution of leptin receptors throughout the body (Dutta et al. 2019; Malik et al. 2019). The mechanism by which leptin triggers gonadotropin-releasing hormone (GnRH) neurons to produce gonadotropins is still unclear because these neurons lack leptin receptors. Leptin hormone plays a significant role in male reproduction partially by stimulating the expression of Kisspeptin peptide, premammillary nucleus (PMN), cocaine-and-amphetamine-regulated transcript (CART) and pro-opiomelanocortin (POMC) that stimulate GnRH neurons. Moreover, it could partially via inhibiting the secretion of agouti-related peptide (AgRP) and Neuropeptide Y (NPY), which have an inhibitory effect on GnRH neurons (Malik et al. 2019). These mechanisms together can trigger the gonadotropin cascade and, in turn, testicular steroidogenesis and spermatogenesis. Moreover, it is believed that leptin has a direct peripheral role in spermatogenesis and endocrine function of the testes since leptin and its receptors are found in spermatozoa, seminal plasma and testes cells (Egan et al. 2017; Dutta et al. 2019; Malik et al. 2019; Sengupta et al. 2019; Khodamoradi et al. 2020; Childs et al. 2021).
The influence of estro-progestin therapy on neurohormonal activity in functional hypothalamic amenorrhea
Published in Gynecological Endocrinology, 2022
Anna Szeliga, Agnieszka Podfigurna, Gregory Bala, Blazej Meczekalski
GnRH-producing neurons were once considered the main controllers of reproductive function. By releasing GnRH in a coordinated, pulsatile manner, they are able to regulate pituitary secretion of FSH and LH. Recent studies have, however, show that GnRH neurons are not themselves the fundamental regulators of the hypothalamic-pituitary-ovarian axis. GnRH neurons themselves are actually under the control of regulatory neurons located in the arcuate nucleus of the hypothalamus, namely of kisspeptin/neurokinin B/dynorphin neurons (KNDy neurons). Due to the wide range of receptors located on their surface, GnRH neurons receive input as impulses from various regulatory systems of the hypothalamus. It is these regulatory systems that have the ability to stimulate pulsatile GnRH secretion. A key feature of KNDy neurons is their co-expression of kisspeptin (KISS1), dynorphin (Dyn), and neurokinin B (NKB) [5–7], as well as surface expression of NKB receptors (tachykinin receptor 3, NK3R), Dyn receptors, α-estrogen receptors (ERα), progesterone receptors (PR), and testosterone receptors. KISS1 receptor (KISS1R) is not expressed on KNDy neurons; instead it is located on GnRH secreting neurons, which suggests that KISS1 secreted by these neurons is not involved in autoregulation. Instead, it is a transmitter stimulating GnRH neurons [8].
Genistein affects gonadotrophin-releasing hormone secretion in GT1-7 cells via modulating kisspeptin receptor and key regulators
Published in Systems Biology in Reproductive Medicine, 2022
Jingyuan Xiong, Ye Tian, Aru Ling, Zhenmi Liu, Li Zhao, Guo Cheng
The inherent heterogeneity of the hypothalamus and the small number of GnRH neurons create technical challenges for in vivo investigation. Therefore, immortalized hypothalamic GT1-7 cells are generally used as a GnRH-expressing model to study neuronal release of GnRH (Mellon et al. 1990). Although immortalized cell lines are not equivalent to primary cell culture or explant culture of GnRH neurons, and hypothalamic KNDy neuronal network and estrogenic feedbacks cannot be mimicked in cell culture systems, GT1-7 cells retain several key characteristics of typical GnRH neurons, including the sensitivity to estrogens and GnRH secretion property, and are able to express a number of genes relevant to reproduction and energy homeostasis. Accordingly, the aim of this study was to examine whether genistein could directly influence GnRH secretion in hypothalamic neuronal GT1-7 cells, and further explore the corresponding mechanisms.