Ask about this productRelated genes to: GnRHR antibody
- Gene:
- GNRHR NIH gene
- Name:
- gonadotropin releasing hormone receptor
- Previous symbol:
- GRHR
- Synonyms:
- LHRHR
- Chromosome:
- 4q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-01-15
- Date modifiied:
- 2016-10-05
Related products to: GnRHR antibody
Related articles to: GnRHR antibody
- A mid-adolescent boy presented with pubertal delay and micropenis. His sister had amenorrhoea. Laboratory evaluation confirmed hypogonadotropic hypogonadism. Brain MRI showed normal pituitary and hypothalamus, though the olfactory bulbs assessment was limited by artefacts. Testosterone therapy enabled the development of secondary sexual characteristics. Subsequent genetic testing identified compound heterozygous pathogenic variants in the gonadotropin-releasing hormone receptor gene, establishing the molecular basis of isolated hypogonadotropic hypogonadism (IHH). Identifying a genetic cause allowed proper counselling regarding prognosis, fertility induction and familial risk. Management focuses on completing sexual maturation, fertility induction and genetic counselling. This case emphasises that mid-adolescents with absent sexual characteristics apart from pubic hair should be evaluated for hypogonadotropic hypogonadism. Early recognition and prompt investigation support timely pubertal induction, fertility preservation and genetic counselling, improving long-term outcomes. Furthermore, this report highlights the pivotal role of genetic testing in guiding the diagnosis and long-term treatment management in patients with IHH. - Source: PubMed
Publication date: 2026/06/01
Lucas Miguelda Bernarda Rodrigues InêsRosmaninho-Salgado JoanaMirante Alice - Gonadotropins are glycoprotein hormones that are often secreted from the gonadotrope cells of the pituitary gland. These hormones play an essential role in growth, reproduction and sexual function. - Source: PubMed
Kheiri FarshidFaghani MostafaBerenjegani Mohammad MohammadiGouran Somayeh TirbakhshDomakani Matin Rahimi - Zearalenone (ZEA) is a potent estrogenic mycotoxin known to disrupt reproductive functions, but its precise central neuroendocrine mechanisms remain unclear. This study investigated the effects of ZEA on the hypothalamic-pituitary Kiss1/GPR54 signaling pathway in weaned gilts. A total of 32 gilts were randomly assigned to four dietary treatments contained with 0, 0.15, 1.5, or 3.0 mg/kg ZEA for a 32-day feeding trial. Histopathology, immunohistochemistry, and mRNA/protein expression analyses of GPR30, Kiss1, GPR54, GnRH, and GnRHR in the hypothalamus and pituitary gland were conducted. ZEA exposure induced significant histological damage in both tissues. In the hypothalamus, Kiss1, GPR54, GnRH, and GnRHR exhibited a non-linear response, increasing at moderate doses and decreasing at 3.0 mg/kg ZEA, whereas GPR30 expression was continuously upregulated. In the pituitary gland, GnRHR showed a similar non-linear pattern. Furthermore, high-dose ZEA down-regulated pituitary Kiss1 and GPR54 while up-regulating GnRH and GPR30 expressions. In conclusion, ZEA induces reproductive neuroendocrine toxicity through a complex, dose-dependent modulation of the Kiss1/GPR54 signaling axis. The persistent upregulation of GPR30 suggests it acts as a crucial mediator in disrupting this endocrine feedback loop within the hypothalamus and pituitary gland. - Source: PubMed
Publication date: 2026/04/22
Yuan ZixueZhou MinLuan YueKong LeiYang WeirenJiang Shuzhen - Several reproductive issues in both men and women are caused by changes in the pulsatile secretion of luteinizing hormone (LH) and follicle-stimulating hormone (FSH). For males to sustain spermatogenesis and Leydig cell function, and for females to ensure orderly folliculogenesis, ovulation, and ovarian steroidogenesis, precise coordination of LH and FSH secretion is necessary. Pituitary responsiveness, the frequency or amplitude of gonadotropin-releasing hormone pulses, or the dysregulation of feedback signals mediated by sex steroids and inhibins all disrupt the balance between LH and FSH secretion. Oligozoospermia, luteal-phase abnormalities, anovulation, or complete spermatogenic failure are possible clinical signs of these alterations. In addition to functional neuroendocrine disturbances, emerging genetic and epigenetic evidence, including pathogenic variants in genes such as gonadotropin-releasing hormone receptor, kisspeptin, kisspeptin receptor, luteinizing hormone beta subunit, follicle-stimulating hormone beta subunit, follicle-stimulating hormone receptor, and luteinizing hormone/choriogonadotropin receptor, has highlighted the role of inherited and acquired molecular defects in disrupting gonadotropin regulation. This narrative review synthesizes contemporary mechanistic, clinical, translational, and genetic evidence elucidating how dysregulated secretion of LH and FSH contributes to reproductive dysfunction. The molecular processes that regulate gonadotropin synthesis and release, as well as neuroendocrine regulation, gene-level determinants of hypothalamic-pituitary-gonadal (HPG) axis dysfunction, and the clinical phenotypes that result from their disruption, are all given special attention. We conclude with a discussion of new treatment strategies that target local intragonadal regulators to enhance gametogenic capacity, modulate gonadotropin signaling, or restore physiological gonadotropin-releasing hormone (GnRH) pulsatility, with consideration of how genetic insights may inform personalized therapeutic approaches. - Source: PubMed
Publication date: 2026/03/31
Zikopoulos AthanasiosMoustakli EfthaliaPotiris AnastasiosParaschos Vasilis SebastianKatopodis PeriklisMachairoudias PavlosAntsaklis PanagiotisKathopoulis NikolaosAnagnostaki IsminiStavros Sofoklis - Depression is a common comorbidity of chronic pain. Gonadotropin-releasing hormone (GnRH) and its receptor (GnRHR) expressed in the central nervous system are involved in non-reproductive functions. Herein, we aimed to elucidate the role and mechanism of action of GnRH in pain-related depression like behaviour in a mouse model. And we found that both GnRH and GnRHR were down-regulated in the anterior cingulate cortex of mice that were subjected to chronic pain-induced depression with complete Freund's adjuvant. Specifically, either systemic treatment with GnRH agonists or GnRH overexpression in the anterior cingulate cortex effectively ameliorated the chronic pain-induced depression-like behaviour via GnRHR signalling. Moreover, GnRHR co-localized with both excitatory and inhibitory neurons, and GnRH agonists or overexpressed GnRH rescued the complete Freund's adjuvant-stimulated imbalance of excitatory-inhibitory neurons in the anterior cingulate cortex. Chemogenetic activation of anterior cingulate cortex neurons reversed GnRH agonist-induced improvement in depression-like behaviour in complete Freund's adjuvant-treated mice. Furthermore, this specific role of GnRH was dependent on the activation of protein kinase C and Erb-B2 receptor tyrosine kinase 4 signalling pathway. Therefore, our findings indicate that GnRH/GnRHR is involved in the development of chronic pain-related depression, which may through rebalancing the excitatory-inhibitory neurons via the activation of protein kinase C/Erb-B2 receptor tyrosine kinase 4 pathway. Thus, GnRH could be a potential target for the treatment of chronic pain-related depression. - Source: PubMed
Publication date: 2026/04/16
Huang YanmeiChen YunfengLiu XueqinXu YangChen LingCao WenyuZhong Xiaolin