Biology Reference
In-Depth Information
A similar effect of E
2
has recently been reported in guinea pigs [
30
]. It has been
argued that the kisspeptin-ir fi bers in the ARC arise from the AVPV because E
2
stimulates kisspeptin expression in that area, but not the ARC [
51
]. However, data
using dual ICC to identify efferents from ARC kisspeptin cells in rats, sheep, and
monkeys indicate that many of the kisspeptin fi bers in the ARC arise from cell bod-
ies in this area (see below). Moreover, the dissociation of effects of E
2
on kisspeptin
expression in AVPV cell bodies and ARC fi bers of adult hpg mice is not consistent
with these fi bers arising from the AVPV in this species [
50
]. If these kisspeptin
fi bers do originate from ARC cell bodies, then the increase in immunoreactivity
could be due to either (1) increased, or no change, in transport out of the cells,
coupled with a decrease in kisspeptin synthesis, or (2) simply a build-up of kiss-
peptin protein because secretion has been inhibited more than synthesis and trans-
port. Interestingly, this phenomenon is not seen in male rats [
18
] and is seen 2 days
after colchicine administration in females [
18
], so it may refl ect a chronic shift in
intracellular location of kisspeptin proteins. Regardless of the mechanisms, the
potential for changes in distribution of kisspeptin within a neuron argues for caution
in interpreting changes based on ICC analysis.
In addition to the ARC and preoptic region, there are a number of other hypotha-
lamic areas that have been shown to contain populations of kisspeptin cells in the
mammalian brain (Table
3.1
). In the monkey and human, a small number of kiss-
peptin cells, likely an extension of the ARC group, are seen in the median eminence
(monkey [
39
]) and infundibular stalk (human [
44
]). The dorsomedial nucleus of the
hypothalamus (DMH) contains a small group of kisspeptin cells, demonstrated by
ICC using specifi c antibodies, in mice, guinea pigs, sheep, and horses, but these
cells are not present in the rat or hamster (Table
3.1
). Likewise, there is species
variation in the presence of cells in the ventromedial hypothalamic (VMH) nucleus,
with cells being detected in the sheep (in some reports [
32
] but not others [
33
]) and
rats [
24
], but not in other species; as in the case of kisspeptin cells in the median
eminence [
39
], these cells may be an extension of the ARC population, in this case
laterally. Regardless, evidence of kisspeptin cells in the DMH and VMH in a num-
ber of species rests primarily on ICC data, and additional ISH data would be worth-
while to verify their presence in these species.
There are also a number of kisspeptin populations that reside outside of the classi-
cal boundaries of the hypothalamus. These include a cluster of
Kiss1
mRNA-
expressing cells in the medial nucleus of the amygdala, seen in both rats and mice
[
14
], and a small number of
Kiss1
cells in the bed nucleus of the stria terminalis
(BNST) of mice, rats, and rhesus monkeys (Table
3.1
). Like the RP3V population,
Kiss1
expression in the medial amygdala is under the stimulatory infl uence of gonadal
steroid hormones [
14
]. The localization of these populations in circuitry that mediates
pheromonal control of sexual behavior [
52
,
53
] and neuroendocrine function [
54
]
suggests that they may play a role in these functions, but this remains to be explored.
Finally, recent fi ndings suggest that kisspeptin cells may be present in wide-
spread areas of the brain outside the hypothalamus and limbic system. This evi-
dence is based on observations of transgenic mice in which
Kiss1
drives the
expression of Cre recombinase and other reporter genes [
55
]. Using such mice, Cre
Search WWH ::
Custom Search