Initiation and completion of female reproductive maturation in the absence of kisspeptin/GPR54 signaling
Résumé
Puberty onset is initiated in the brain by activating gonadotropin-releasing hormone (GnRH) neurosecretion. Different permissive signals must be integrated for the initiation of reproductive maturation, however the neural circuits controlling timely awakening of the reproductive axis are not understood. The identification of the neuropeptide kisspeptin as a potent activator of GnRH neuronal activity suggests that kisspeptin-releasing neurons might coordinate puberty onset. To test this hypothesis we generated mice specifically lacking kisspeptin cells. Unexpectedly, puberty onset in females was unaffected by kisspeptin neuron ablation. Furthermore, the animals were fertile, albeit had smaller ovaries. Consistent with this, female mice lacking neurons that express the kisspeptin receptor GPR54 were also fertile. Acute ablation of kisspeptin neurons in adult animals inhibited fertility suggesting compensation for the loss of kisspeptin neurons early during development. Our data demonstrate that the initiation and completion of reproductive maturation can take place in the absence of kisspeptin/GPR54 signaling.
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