How Tachykinin Peptides Control Reproductive Hormone Release and Fertility

Tachykinins (NKA, NKB, and substance P) participate in the central control of GnRH release through neuronal circuits that activate Kiss1 neurons and synchronize their activity within the arcuate nucleus. Their roles extend across the full spectrum of reproductive function: regulating the pulsatile pattern of GnRH release, determining the timing of puberty onset, and controlling the preovulatory LH surge in females. The review synthesizes evidence that tachykinins are critical for all major aspects of fertility attainment and maintenance.

This is a narrative review article summarizing recent advances in understanding tachykinin biology in reproductive neuroendocrinology, drawing from both animal studies and human data.

Understanding how tachykinins regulate fertility opens doors for new treatments for reproductive disorders. Neurokinin B is already a drug target — NK3 receptor antagonists are being developed for conditions like polycystic ovary syndrome and endometriosis. Deeper knowledge of the full tachykinin system could yield additional therapeutic opportunities.

The discovery of kisspeptin-neurokinin B-dynorphin (KNDy) neurons revolutionized reproductive neuroendocrinology. This review places tachykinins within that broader framework, highlighting how peptide-based signaling networks coordinate the precise hormonal patterns needed for fertility — an area now translating into novel drugs for reproductive health conditions.

As a review article, this paper synthesizes existing research rather than presenting new data. The authors note existing controversies and open questions in the field, including unresolved aspects of how individual tachykinins interact within the reproductive circuits.