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Fig. 20.1
Effects of neonatal lipopolysaccharide (LPS, 50 μg/kg ip) or saline control given at
postnatal day (pnd) 3-5 on kisspeptin (
Kiss1
) mRNA expression in the medial preoptic area
(mPOA) (
a
) and arcuate nucleus (ARC) (
c
) and on kisspeptin receptor (
Kiss1r
) mRNA expression
in the mPOA (
b
) and ARC (
d
) in female rats at pnd 14, pnd 32, (the day of vaginal opening (dVO)),
and at 11 weeks of age (Adult).
Kiss1
and
Kiss1r
mRNA levels were measured in brain micro-
punch samples from the mPOA or ARC using real-time reverse transcriptase-polymerase chain
reaction. Quantifi cation for
Kiss1
,
Kiss1r,
and 28S rRNA was carried out on all samples; the values
are expressed as a ratio of
Kiss1
mRNA and 28S rRNA, or
Kiss1r
mRNA and 28S rRNA
(mean ± SEM). *
P
< 0.05 vs. the respective treatment group at different time points;
#
P
< 0.05 vs.
saline control at same time point;
n
= 5-9 per group (from Knox AM, Li XF, Kinsey-Jones JS,
Wilkinson ES, Wu XQ, Cheng YS, et al. Neonatal lipopolysaccharide exposure delays puberty and
alters hypothalamic Kiss1 and Kiss1r mRNA expression in the female rat. J Neuroendocrinol.
2009 Aug;21(8):683-9. Reprinted with permission from John Wiley & Sons)
LPS delays puberty and disrupts estrous cyclicity, concordant with downregulation
of
Kiss1
, but not
Kiss1r
, mRNA expression in the medial preoptic area (mPOA)
(Fig.
20.1
) [
18
,
34
]. This decrease in
Kiss1
expression could provide a mechanism
for the observed delay of puberty. By contrast, the lack of effect of neonatal LPS
treatment on
Kiss1
or
Kiss1r
expression in the ARC would indicate that kisspeptin/
Kiss1r signaling in this brain region is not an obvious contributing factor to pubertal
delay. Interestingly, the postponement of LPS treatment from postnatal days 3 and
5 to postnatal days 7 and 9 failed to delay puberty, suggesting there is a discrete
developmental time window that is sensitive to immunological challenge [
18
].
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