Reproduction in mammals is dependent on the function of specific neurons that secrete GnRH. These neurons send projections to the hypothalamus, which serves as an interface between the neural and peripheral endocrine systems. Here gonadotropin releasing hormone (GnRH) is released into the pituitary portal blood vessels for delivery to the anterior pituitary to elicit the secretion of luteinizing hormone (LH) and folliclestimulating hormone (FSH).
Alterations in the development of this system or in the secretion of GnRH are associated with a number of reproductive disorders including hypogonadotropic hypogonadism, hypothalamic amenorrhoea, hyperprolactinemia and polycystic ovary syndrome (PCOS).
PCOS is a common complex endocrinopathy that occurs in up to 10% of women. A hallmark of PCOS is increased LH concentrations and LH:FSH ratios. Among the heterogeneity of symptoms in PCOS women, it is still not clear why the GnRH-induced LH level is altered.
Researchers demonstrate that a significant subset of GnRH neurons both in mice and humans express the Anti-Mu¨llerian hormone (AMH) receptor, and that AMH potently activates the GnRH neuron firing in mice.
Combining in vivo and in vitro experiments, authors show that AMH increases GnRH-dependent LH pulsatility and secretion, supporting a central action of AMH on GnRH neurons.
Increased LH pulsatility is an important pathophysiological feature in many cases of polycystic ovary syndrome (PCOS), the most common cause of female infertility, in which circulating AMH levels are also often elevated. However, the origin of this dysregulation remains unknown.
These findings raise the intriguing hypothesis that AMH-dependent regulation of GnRH release could be involved in the pathophysiology of fertility and could hold therapeutic potential for treating PCOS.