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decrease basal levels of the mPOA
Kiss1
message, an effect that was not amplifi ed
by insulin administration (Fig.
20.4
) [
35
]. In fact, prolonged (72 h) fasting sup-
presses ARC kisspeptin expression and LH secretion, and prolongs the estrous
cycle in gonadal intact adult female rats [
63
]. In summary, the suppression of the
ARC kisspeptin expression by acute metabolic deprivation appears responsible for
the inhibition of pulsatile LH secretion and the subsequent prolongation of the
estrous cycle, and may be mediated by CRF-R2.
Psychological stress is often harder to defi ne than other forms of stress, although
restraint stress applied to experimental animals has long been employed as a model
for a range of emotional and behavioral disturbances and psychiatric disorders.
Clinically relevant psychological stressors stimulate the HPA axis and the sympa-
thetic nervous system, as does acute restraint. Furthermore, this stress paradigm
effectively suppresses the HPG axis, as is evident from disrupted LH pulsatility and
downregulation of ARC
Kiss1
and mPOA
Kiss1
and
Kiss1r
mRNA expression fol-
lowing restraint in adult female rats (Figs.
20.3
and
20.4
) [
35
]. However, unlike
other stressors, restraint has no effect on ARC expression of
Kiss1r
[
35
]. The
restraint-induced suppression of the LH pulse in adult female rats is blocked by
direct injections of a nonselective CRF antagonist into the locus ceruleus; however,
such treatment did not affect the hypoglycemic stress-induced suppression of LH
secretion [
64
]. icv administration of either type-specifi c (CRF-R1 or CRF-R2)
CRF-R antagonists also blocked the inhibitory effects of restraint stress on pulsa-
tile LH secretion in this animal model [
39
,
40
]. Since the ARC and mPOA expres-
sion of
Kiss1
and
Kiss1r
mRNA is robustly downregulated by icv administration of
CRF [
35
], it is logical to hypothesize that the effects of restraint stress on LH secre-
tion are downstream of the CRF-induced suppression of kisspeptin/Kiss1r
signaling.
Isolation has been widely accepted as a mild social stressor. In female mice the
stress of chronic isolation increases anxiety [
65
], undermines the regularity of
estrous cyclicity, and downregulates mPOA
Kiss1r
expression [
66
]. Adult rat
social isolates display a dysregulated CORT response, with acute stress (predator
odor) markedly exacerbating the rise in CORT compared to grouped animals—an
effect that is enhanced with age [
67
]. Individual reactivity or vulnerability to
stress can refl ect differences in dominance status among social animals. Variation
in basal glucocorticoid levels has been identifi ed to be dependent upon social rank
in numerous species. Dominant female squirrel monkeys [
68
], cynomolgus mon-
keys [
69
], and baboons [
70
] demonstrate reduced cortisol levels compared with
subordinates in the same social group, an effect that is also observed in the teleost
fi sh (
Haplochromis burtoni
) [
71
], the naked mole rat (
Heterocephalus glaber
) [
72
],
pig [
73
], and horse [
74
]. Similarly, subordinate mice [
75
] and rats [
76
] display
higher basal CORT release than their dominant counterpart. In response to stress,
however, subordinate rats displayed a signifi cantly reduced, or even completely
absent, CORT response as compared to their dominant counterparts [
76
]. This out-
come is not uncommon in other species, including primates (e.g., olive baboon) [
77
],
although this phenotype can be markedly modifi ed subject to particular stylistic
traits of social behavior in primate species [
77
]. Thus, subordination may result in
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