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18-21 of pregnancy, icv kisspeptin-10 caused an immediate, robust increase in oxy-
tocin neuron fi ring rate following the injection. Unlike the response to peripheral
kisspeptin-10, the increase in fi ring rate seen with central administration appeared
substantially different between neurons, with some neurons showing a return to
basal fi ring within 10 min, while others showed a sustained shift to a higher fi ring
rate that lasted tens of minutes, somewhat reminiscent of the initial observations of
kisspeptin excitation of GnRH neurons in vitro [
65
]. The most remarkable aspect of
this response to icv kisspeptin-10 is that it only becomes apparent during
pregnancy.
We have no knowledge of the functional consequences of the emergence of this
sensitivity of oxytocin neurons to central kisspeptin during pregnancy, but it is
tempting to speculate that it might be involved in driving, or facilitating, bursting
behaviour of oxytocin neurons during parturition. Consistent with this speculation,
the excitation of oxytocin neurons seen in response to icv kisspeptin-10 in late-
pregnant rats was also evident in the one oxytocin neuron that we have recorded
from a lactating rat, the only other time in a mammal's life that oxytocin neurons are
known to exhibit high-frequency co-ordinated bursts of action potentials to release
a bolus of oxytocin into the bloodstream.
Not only do we not know the function of central kisspeptin excitation of oxytocin
neurons in late pregnancy, we also do not know the mechanisms that underpin the
emergence of this excitation. One possibility is an increased accessibility of kiss-
peptin to Kiss1r that leads to the excitation of oxytocin neurons by icv kisspeptin.
In addition, there might be up-regulation of Kiss1r expression in oxytocin neurons
(or their afferent inputs), the laying down of a new kisspeptin projection to oxytocin
neurons, and/or the up-regulation of kisspeptin expression in an existing projection
to oxytocin neurons. These possibilities are a focus of current work in our
laboratory.
Conclusion
Kisspeptin and its receptor, Kiss1r (in rodents), have been described as an essential
gatekeeper of reproductive function [
72
]. Our recent work has expanded our knowl-
edge of the critical role that kisspeptin plays in reproductive function via excitation
of oxytocin neurons. During pregnancy and lactation, dynamic and transient changes
occur within the oxytocin system. The synthesis, dendritic release and peripheral
secretion are all modifi ed in order to facilitate and synchronise the function of oxy-
tocin neurons in labour, birth and lactation, as well as in maternal behaviour. We
have shown that circulating kisspeptin excites oxytocin neurons throughout life,
which might become important when the placenta secretes kisspeptin during preg-
nancy. Possibly of more importance for successful reproduction, we have also
shown that the excitation of oxytocin neurons by central administration of kiss-
peptin appears to be dramatically changed over the course of pregnancy, emerging
only in late pregnancy. The mechanisms behind this change have yet to be established
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