The study shows that adding anti‑Müllerian hormone (AMH) to hypothalamic cells boosts the production of GnRH (the hormone that tells the pituitary to release reproductive hormones) but does not change the amount of kisspeptin (Kiss‑1) made by those cells. In fact, AMH can block the increase in Kiss‑1 that normally happens when you add kisspeptin‑10. This suggests AMH can influence the reproductive hormone cascade by promoting GnRH while dampening kisspeptin‑driven signals.

<b>Purpose:</b> Anti-M&#xfc;llerian hormone (AMH) is one of the local factors involved in follicle development. In addition, AMH and its receptor are broadly expressed throughout the body. In this study, we examined how AMH modifies gene expression of Kiss-1 and GnRH.<b>Materials and methods:</b> mHypoA-50 and mHypoA-55 cells were originated from the hypothalamic anteroventral periventricular nucleus (AVPV) and arcuate nucleus (ARC), respectively, and these cells are known as Kiss-1 (which encodes kisspeptin) expressing cell models. These cells also express gonadotropin-releasing hormone (GnRH) genes. Our experiments were performed useing these cell models.<b>Results:</b> Both mHypoA-50 and mHypoA-55 hypothalamic cells expressed AMH and AMH receptor type 2 (AMHR2). Exogenous AMH failed to alter the expression levels of the Kiss-1 gene in both cell models but significantly increased GnRH gene expression by 1.73&#x2009;&#xb1;&#x2009;0.2-fold at 100&#x2009;pM in mHypoA-50 AVPV cells and by 1.74&#x2009;&#xb1;&#x2009;0.17-fold at 1&#x2009;nM in mHypoA-55 ARC cells. AMH also augmented GnRH protein expression in both cell models. Similar to the phenomenon observed in the hypothalamic cell lines, 100&#x2009;pM AMH significantly increased GnRH, but not Kiss-1, mRNA expression in primary cultures of fetal rat brain cells. Kisspeptin-10 (KP10) increased Kiss-1 gene expression in mHypoA-55 ARC cells but this was blocked by AMH. AMH did not alter the expression of the kisspeptin receptor (Kiss1R) or that of neurokinin B or dynorphin A in mHypoA-55 ARC cells.<b>Conclusions:</b> It was demonstrated that AMH participates in hypothalamic-pituitary-gonadal axis control by stimulating GnRH expression. In addition, AMH might be a potent repressor of Kiss-1 gene expression induced by KP10.