Published in the journal Nature Communications, the research explains the role played by a protein called kisspeptin. It was already known to be critical to fertility, but the Otago researchers showed kisspeptin acted in the brain.
''We've known that kisspeptin was important, but we didn't know where it was acting. Was it acting in the ovaries? Was it acting in the pituitary? Was it acting in the brain?
''We even know exactly which cells it's working in in the brain,'' Prof Herbison said.
The discovery could allow the development of contraceptive drugs to act directly on the part of the brain controlling fertility.
It was unclear whether it would still need to be taken daily, but it would be an important alternative to the hormone oral contraceptive pill. The findings were likely to have a more immediate impact in the field of infertility research.
Kisspeptin was already being experimented with ''rather gingerly'' to trigger the reproduction system, and also to improve IVF treatment.
The overseas researchers conducting the studies would be greatly assisted by the explanation of how kisspeptin acted.
''Our new understanding of the exact mechanism by which [the protein] kisspeptin acts as a master controller of reproduction is an exciting breakthrough which opens up avenues for tackling what is often a very heart-breaking health issue.
''Through detailing this mechanism, we now have a key chemical switch to which drugs can be precisely targeted,'' Prof Herbison said.
The team discovered the cellular location of signalling between kisspeptin and its receptor, Gpr54, and demonstrated it occurred in a small population of nerve cells in the brain called gonadotropin-releasing hormone (GnRH) neurons.
The researchers studied mice that lacked Gpr54 receptors in only their GnRH neurons, and found they did not undergo puberty and were infertile. The mice could be restored to normal fertility by inserting the Gpr54 gene into just the GnRH neurons.
Targeting kisspeptin could also be useful for treating diseases such as prostate cancer which were influenced by sex steroid hormone levels in the blood.
The research was assisted by collaboration with the laboratory of Gunther Schutz at Heidelberg University, Germany, where one of the mouse models was generated.
The work was funded by the Health Research Council of New Zealand, and the former Ministry of Science and Innovation.
''We are delighted to have published this work in one of the top scientific journals, and also to be able to maintain the leading role of New Zealand researchers in understanding fertility control,'' Prof Herbison said.
