Beyond the GnRH Axis: Kisspeptin Regulation of the Oxytocin System in Pregnancy and Lactation - Kisspeptin Signaling in Reproductive Biology - page 198

Fig. 10.1 A schematic representation of oxytocin regulation of parturition. Oxytocin cells fi re
in bursts similar to those seen during lactation but which are superimposed upon a higher base-
line activity ( left hand side ). This pattern of activity results in pulsatile secretion of oxytocin
from the posterior pituitary gland which acts on myometrial oxytocin receptors to induce uterine
contractions and cause fetal expulsion. The uterine contractions feedback to the supraoptic
nucleus (SON) via the nucleus tractus solitarii (NTS) in the brainstem ( right hand side ) to fur-
ther enhance oxytocin cell activity and thus maintain parturition. Each burst of activity precedes
the birth of a pup
the onset of delivery, and when given early in delivery, they increase the time
between the deliveries of each pup [ 13 ]. Additionally, selective oxytocin agonists
given centrally accelerate birth, as well as the onset of maternal behaviour [ 14 , 15 ].
This suggests that, at least in rats, oxytocin is important for the initiation and the
maintenance of parturition [ 13 ].
While it might be controversial as to whether oxytocin plays an indispensable
role in parturition, the critical role that oxytocin plays in milk let-down during lacta-
tion is not disputed. The release of milk is mediated by secretion of oxytocin from
the posterior pituitary gland, and oxytocin's action at OTR in the mammary gland
induces a rise in intra-mammary pressure and release of milk: an oxytocin-mediated
refl ex upon suckling [ 16 ]. The oxytocin knockout mice fail to deliver milk to their