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Neonatal testosterone suppresses a neuroendocrine pulse generator required for reproduction

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  • Jean-Marc Israel

    (INSERM, U862, Neurocentre Magendie
    Université de Bordeaux)

  • Jean-Marie Cabelguen

    (INSERM, U862, Neurocentre Magendie
    Université de Bordeaux)

  • Gwendal Le Masson

    (INSERM, U862, Neurocentre Magendie
    Université de Bordeaux)

  • Stéphane H. Oliet

    (INSERM, U862, Neurocentre Magendie
    Université de Bordeaux)

  • Philippe Ciofi

    (INSERM, U862, Neurocentre Magendie
    Université de Bordeaux)

Abstract

The pituitary gland releases hormones in a pulsatile fashion guaranteeing signalling efficiency. The determinants of pulsatility are poorly circumscribed. Here we show in magnocellular hypothalamo-neurohypophyseal oxytocin (OT) neurons that the bursting activity underlying the neurohormonal pulses necessary for parturition and the milk-ejection reflex is entirely driven by a female-specific central pattern generator (CPG). Surprisingly, this CPG is active in both male and female neonates, but is inactivated in males after the first week of life. CPG activity can be restored in males by orchidectomy or silenced in females by exogenous testosterone. This steroid effect is aromatase and caspase dependent, and is mediated via oestrogen receptor-α. This indicates the apoptosis of the CPG network during hypothalamic sexual differentiation, explaining why OT neurons do not burst in adult males. This supports the view that stereotypic neuroendocrine pulsatility is governed by CPGs, some of which are subjected to gender-specific perinatal programming.

Suggested Citation

  • Jean-Marc Israel & Jean-Marie Cabelguen & Gwendal Le Masson & Stéphane H. Oliet & Philippe Ciofi, 2014. "Neonatal testosterone suppresses a neuroendocrine pulse generator required for reproduction," Nature Communications, Nature, vol. 5(1), pages 1-10, May.
  • Handle: RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms4285
    DOI: 10.1038/ncomms4285
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