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The role of gonadotropin‐releasing hormone neurons in polycystic ovary syndrome

2022/01/17 by Christopher R. McCartney, Rebecca E. Campbell, John C. Marshall +1
Medicine · #Hypothalamic control of reproductive hormones #Ovarian function and disorders #Reproductive Biology and Fertility

paper · pdf · doi:10.1111/jne.13093

openalex publication_date 2022/01/17 · openalex created_date 2025/10/10 · openalex updated_date 2026/07/29

Abstract

Given the critical central role of gonadotropin-releasing hormone (GnRH) neurons in fertility, it is not surprising that the GnRH neural network is implicated in the pathology of polycystic ovary syndrome (PCOS), the most common cause of anovulatory infertility. Although many symptoms of PCOS relate most proximately to ovarian dysfunction, the central reproductive neuroendocrine system ultimately drives ovarian function through its regulation of anterior pituitary gonadotropin release. The typical cyclical changes in frequency of GnRH release are often absent in women with PCOS, resulting in a persistent high-frequency drive promoting gonadotropin changes (i.e., relatively high luteinizing hormone and relatively low follicle-stimulating hormone concentrations) that contribute to ovarian hyperandrogenemia and ovulatory dysfunction. However, the specific mechanisms underpinning GnRH neuron dysfunction in PCOS remain unclear. Here, we summarize several preclinical and clinical studies that explore the causes of aberrant GnRH secretion in PCOS and the role of disordered GnRH secretion in PCOS pathophysiology.

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