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in this species, but kisspeptin cells do not express melatonin receptor 1A (the signaling
form of the receptor) in the ovine brain [
77
]. Because the time frame of the action of
melatonin (several days or even weeks) compared to the immediate effects of
kisspeptin on GnRH secretion, it seems most likely that some other cell type trans-
duces the melatonin signal to the ARC kisspeptin cells. Recent evidence for a circa-
dian-based molecular mechanism within the pars tuberalis of the pituitary couples the
variations of the melatonin signal with the variations of thyroid hormones within
the hypothalamus [
78
]. Given that most of the kisspeptin cells of the ARC express the
thyroid hormone receptor [
79
], it is possible that there may be some involvement of
melatonin to modulate thyroid hormone secretion, which, in turn, impacts upon kiss-
peptin function, to govern seasonal changes in breeding patterns.
Kisspeptin and Gonadotropin Inhibitory Hormone
as Key Reciprocal Regulators in Seasonal Breeding
Gonadotropin inhibitory hormone (GnIH), also called RFRP-3, is a neuropeptide
produced in cells of the dorsomedial nucleus/paraventricular nucleus of the hypo-
thalamus in mammals. GnIH was originally isolated from the quail brain [
80
] and is
associated with seasonality in birds [
81
]. In the ewe, GnIH gene expression and
protein production are higher during the nonbreeding season than in the breeding
season [
30
], and terminal projections from GnIH cells to GnRH neurons increase
during the nonbreeding season [
30
]. Using an antagonist (RF9) to the GnIH recep-
tor, Caraty et al. [
82
] were able to demonstrate release of LH, indicating that endog-
enous GnIH must act to restrain GnRH/LH secretion. The response to the antagonist
was higher in the nonbreeding season than the breeding season, perhaps for the
same reason that responses to kisspeptin are greater at this time (see above). These
recent fi ndings suggest that kisspeptin and GnIH act in concert to control seasonal
cycles of breeding in mammals such as sheep. It should be noted however, that this
antagonist may act through the putative GnIH receptor (also known as NPFF1) or
NPFF2 receptors, having cardiovascular effects [
83
], and may also interact with
other, as yet unidentifi ed receptors. In the sheep, GnIH exerts dual effects on the
GnRH neurons, as well as on pituitary gonadotropes. The effect on the gonado-
tropes is by means of projections of the GnIH neurons to the external zone of the
median eminence [
84
] and secretion into the hypophyseal portal blood [
85
]. Portal
blood levels of GnIH are higher in the anestrous season, indicating a role in the sup-
pression of pituitary function in this reproductive state. There is virtually no projection
of GnIH neurons to the external zone of the median eminence in the hamster [
86
],
so pituitary action may not be relevant in these animals.
In hamsters, the level of GnIH expression has also been found to respond to sea-
son, but with results different to those seen in sheep. In particular, studies in Syrian
and Siberian hamsters surprisingly showed increased levels of GnIH expression and
numbers of immunoreactive cells under long-day (stimulatory) photoperiod [
87
],
with no change being observed in Wistar rats (which are not seasonal breeders).
Castration had no effect on GnIH gene expression during long days, and testosterone
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