Neonatal testosterone suppresses a neuroendocrine pulse generator required for reproduction

Jean-Marc Israel, Jean-Marie Cabelguen, Gwendal Le Masson, Stéphane H. Oliet, Philippe Ciofi
Nat Commun. 2014-02-11; 5(1):
DOI: 10.1038/ncomms4285

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1. Nat Commun. 2014;5:3285. doi: 10.1038/ncomms4285.

Neonatal testosterone suppresses a neuroendocrine pulse generator required for
reproduction.

Israel JM(1), Cabelguen JM(1), Le Masson G(1), Oliet SH(1), Ciofi P(1).

Author information:
(1)1] INSERM, U862, Neurocentre Magendie, F-33077 Bordeaux, France [2] Université
de Bordeaux, F-33077 Bordeaux, France.

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.

DOI: 10.1038/ncomms4285
PMID: 24518793 [Indexed for MEDLINE]

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