Biology Reference
In-Depth Information
One technical challenge to interpreting developmental changes in RP3V kisspeptin
neurons, particularly in the rat, is that detection of kisspeptin-ir cells within this region
seems to depend upon the use of colchicine pretreatment in order to enhance detection
of immunoreactive peptide in cell bodies. In studies that have not used colchicine
pretreatment, detection of kisspeptin-ir cells in the RP3V is diffi cult [
19
,
22
,
126
-
128
].
However, kisspeptin-positive cells are readily apparent in studies that have used col-
chicine [
18
,
25
] or monitored
Kiss1
mRNA [
127
,
129
], perhaps suggesting a very
rapid secretion or turnover of the peptide in RP3V neurons of the rat. In sheep, much
like non-colchicine treated rats, kisspeptin neurons in the POA (but not those in the
ARC) were diffi cult to detect in young ewes and could not be quantifi ed during the
pubertal transition [
130
]. In contrast, RP3V kisspeptin-ir neurons in the mouse are
easily detectable without colchicine treatment. In mice and colchicine-treated rats,
RP3V kisspeptin neurons are not usually detected before about PND10 [
11
,
49
,
50
,
65
,
127
,
129
]. A pubertal increase in RP3V kisspeptin immunoreactivity and
Kiss1
mRNA expression has been reported in several studies for females of both species
[
25
,
49
-
51
,
127
]. In mice, kisspeptin-positive fi bers become evident around GnRH
neurons beginning at PND25, a time when changes in RP3V kisspeptin cell numbers
and
Kiss1
mRNA expression are increasing dramatically [
11
]. In ovariectomized,
estradiol-implanted ewes, POA
Kiss1
mRNA-containing cell numbers increased
around the time of puberty [
131
], but this change was independent of changes in LH
pulse frequency associated with puberty in this species.
In the ARC, kisspeptin-positive cells or
Kiss1
mRNA are detectable within
the fi rst few days postnatally in the female rat [
126
,
127
,
129
]. Subsequently,
kisspeptin immunoreactivity and
Kiss1
mRNA levels increase in a puberty-asso-
ciated manner [
25
,
126
,
127
]. More recently, the number of kisspeptin-positive
cells in the ARC was found to be higher in young, postpubertal ewes compared
to prepubertal animals; these changes mirrored differences in LH pulse fre-
quency [
130
]. Changes in ARC kisspeptin-ir cell numbers in ewes from that
study also paralleled an increase in the percentage of POA GnRH neurons that
exhibited close appositions of kisspeptin-immunopositive varicosities, suggest-
ing that potential changes in kisspeptin input to GnRH neurons during puberty
in that species arises from the ARC kisspeptin cells. This is further supported by
preliminary evidence that 50-70% of GnRH neurons receive close contacts
from kisspeptin fi bers that also contain dynorphin, indicating that they arise
from KNDy neurons (Lehman and Goodman, unpublished data). A role for
ovine ARC kisspeptin neurons in puberty is consistent with the positive correla-
tion between the number of
Kiss1
mRNA-containing cells in the middle ARC
and an increase in LH pulse frequency during puberty in estradiol-treated ovari-
ectomized ewes [
131
]. These data fi t well with those in primates, where
Kiss1
mRNA expression increased in female monkeys during the midpubertal phase
of development [
42
]. Interestingly, this increase in
Kiss1
mRNA expression is
paralleled by an increase in kisspeptin release in the primate median eminence
[
132
] and in the amount of kisspeptin secretion induced by a GABA receptor
antagonist [
133
]. Thus, in these species, kisspeptin input from the ARC may
play an important role in puberty onset.
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