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highlighted because intravenous (IV) administration of kisspeptin-10 increased
plasma levels of oxytocin in non-pregnant female rats [
1
]. However, this result was
quickly overshadowed by the discovery of the role of Kiss1r/KISS1R and kiss-
peptin neurons in fertility through actions on GnRH neurons.
In 2011, the possibility of an important role for kisspeptin in the regulation of the
oxytocin system was again brought to light by our fi nding that intravenous kisspeptin-
10 increases the fi ring rate of oxytocin-secreting neurons [
2
]. Here, we will give an
overview of that work and our more recent fi ndings that suggest that central kiss-
peptin excitation of oxytocin neurons emerges over the course of pregnancy, which
might have important implications for successful delivery of the offspring at birth
and successful delivery of milk during lactation.
Pregnancy and Lactation
Reproduction is the process by which new offspring are produced and is a funda-
mental process of life. The hypothalamic-pituitary-gonadal axis, including the
kisspeptin neurons, is a critical part of reproduction, but fertility is only the fi rst step
in successful reproduction. Reproduction also requires successful pregnancy, partu-
rition and, in mammals, lactation. In all mammals, there are complex interactions of
neural, endocrine and behavioural processes that enable a female to successfully
meet the challenge of pregnancy and lactation. Elucidating these different mecha-
nisms and pathways is important for understanding the transient physiological states
of pregnancy and lactation. The mechanisms that are recruited during these states
refl ect profound changes in brain neurochemistry and morphology, and this includes
the oxytocin system.
The hormone oxytocin has recently come to prominence as an important modu-
lator of various behaviours, including social recognition, pair bonding, anxiety and
maternal behaviours [
3
]. However, oxytocin is best known for its role in parturition
and lactation [
4
]. The word oxytocin comes from the Greek 'quick birth', and oxy-
tocin facilitates mammalian reproduction through uterine contractions during labour
(parturition) and milk ejection in response to suckling during lactation [
5
].
Circulating oxytocin concentrations rise progressively over the course of pregnancy
[
6
,
7
], but only induce uterine contraction when specifi c oxytocin receptors (OTRs)
are up-regulated in the uterus immediately prior to birth [
8
,
9
]. The contracting
uterus provides positive feedback to induce further oxytocin secretion ('the Ferguson
refl ex', Fig.
10.1
) [
10
].
Oxytocin is the strongest uterotonic substance known and is widely used to
induce labour in humans, yet oxytocin-defi cient mice successfully complete parturi-
tion [
11
]. This suggests that oxytocin secretion is not essential for birth. However,
the importance of oxytocin for the initiation and maintenance of labour, and for
delivery, remains controversial. Oxytocin plays a vital role in timing of delivery,
because oxytocin-defi cient mice give birth at random times following a circadian
clock reset [
12
]. Furthermore, OTR antagonists administered prior to labour delay
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