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mediated though CCKA receptors located on peripheral vagal endings [
53
], which
signal through the NTS in the brainstem to the oxytocin neurons in the hypothala-
mus [
28
]. Recently, another gastric peptide hormone, secretin, has also been shown
to increase the activity and secretion of oxytocin neurons. This effect appears to also
be mediated by the noradrenergic pathway, because intracerebroventricular (icv)
injection of the
1 adrenergic antagonist, benoxathian, blocked the increase in
fi ring rate of oxytocin (and vasopressin) neurons [
54
]. Hence, visceral inputs to
oxytocin neurons (including those active in parturition and lactation) converge on
the noradrenergic inputs via the vagus nerve.
The SON and PVN also receive prominent inputs from several forebrain areas,
including areas in the anteroventral region of the third ventricle (AV3V): the subfor-
nical organ (SFO), the organum vasculosum of the lamina terminalis (OVLT) and
the median preoptic nucleus (MnPO) [
45
]. The SFO and OVLT are located outside
the blood brain barrier and so peripheral stimuli can stimulate oxytocin secretion by
acting on AV3V inputs. These projections from the AV3V are best characterised as
mediating osmoregulation, and lesions of this region reduces oxytocin secretion and
consequently impairs sodium excretion, but does not affect the milk-ejection refl ex
or parturition [
55
]. In addition to the above afferent inputs that have been exten-
sively studied, the SON and PVN also receive numerous afferent inputs that have
been less well characterised and whose physiological function is not well-
established. These inputs include (but are not limited to): arcuate nucleus, bed
nucleus of the stria terminalis, diagonal band of Broca, raphe nuclei, tuberomam-
millary nucleus and suprachiasmatic nucleus.
Up to this point, we have provided a brief background of the oxytocin system and
its importance in pregnancy, parturition and lactation. There is remarkable plasticity
in the activity of oxytocin neurons that emerges at the end of pregnancy to facilitate
delivery of the offspring and delivery of milk to the offspring. This emergent behav-
iour requires afferent input for its expression, and so any afferent input that exhibits
plasticity over the course of pregnancy is a likely candidate to be involved in the
processes that underpin this change in behaviour at a cellular level. Our recent
results suggest that kisspeptin might be an important newly discovered player in the
regulation of oxytocin neurons in pregnancy and lactation. The remainder of this
chapter focuses on how kisspeptin affects the oxytocin neurons and highlights new
data that indicates that central kisspeptin regulation of oxytocin neurons emerges
towards the end of pregnancy.
α
Circulating Kisspeptin Concentrations in Pregnancy
and Lactation
Investigations of kisspeptin regulation of fertility have focussed on central interac-
tions with GnRH neurons [
56
]. However, our initial interest was in the effects of
circulating kisspeptin on oxytocin neurons because IV kisspeptin administration
increases plasma oxytocin levels in non-pregnant female rats [
1
], and the plasma
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