PERSONAL DE APOYO
SOAJE Marta
artículos
Título:
Role of Oxytocin on Prolactin Secretion During Late Pregnancy
Autor/es:
VILLEGAS-GABUTTI, CARLOS M.; PENNACCHIO, GISELA; VIVAS, LAURA; JAHN GA; SOAJE, MARTA
Revista:
NEUROENDOCRINOLOGY
Editorial:
KARGER
Referencias:
Año: 2018 vol. 106 p. 324 - 334
ISSN:
0028-3835
Resumen:
AbstractBackgrounds/Aims: Oxytocin is involved in PRL release acting directly on anterior pituitary lactotrophs. Our aim is to determine whether oxytocin mediates the stimulatory action of mifepristone and naloxone on PRL secretion during late pregnancy acting as a releasing factor (PRF) in the presence of a low dopaminergic tone. Methods: by RIA, circulating and pituitary oxytocin and PRL levels were measured in rats previously treated with mifepristone and naloxone. Pituitary oxytocin receptors expression in mifepristone treated rats was evaluated by RT-PCR and activation of oxytocinergic neurons was measured by analyzing the number of double immunoreactive neurons for Fos and oxytocin (Fos-OT-ir) in two PVN divisions (PaLM and PaMM) and in SON in mifepristone and naloxone treated rats. Results: elevated serum oxytocin levels and a fall of pituitary oxytocin content were observed 10 min after naloxone administration both in vehicle and mifepristone treated rats. The increase of serum PRL levels induced by naloxone in mifepristone treated rats was prevented by previous administration of an oxytocin receptor antagonist. Mifepristone increased pituitary oxytocin receptors expression. The number of Fos-OT-ir neurons in the PaMM and SON increased in mifepristone and naloxone treated rats. Conclusions: These findings suggest that PRL secretion induced by naloxone in mifepristone treated rats involves a previous increase in serum oxytocin levels. These results together with the activation of hypothalamic oxytocinergic neurons and the higher expression of pituitary oxytocin receptors support the hypothesis that oxytocin may act as a PRF during late pregnancy, when the inhibitory action of progesterone is blocked.