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Fig. 18.6
The activation of GnRH after kisspeptin administration is time dependent. The
percentage of GnRH-ir cells expressing FOS after vehicle, 2 nmol, or 4 nmol kisspeptin adminis-
tration at zietgerber time (ZT) 1 or ZT 11 in OVX hamsters. Mean (±SEM) percentage of POA
GnRH-ir cells expressing FOS after kisspeptin administration at ZT 1 or ZT 11. From Williams
WP, 3rd, Jarjisian SG, Mikkelsen JD, Kriegsfeld LJ. Circadian control of kisspeptin and a gated
GnRH response mediate the preovulatory luteinizing hormone surge. Endocrinology.
2011;152(2):595-606. Epub 2010/12/31. Reprinted with permission from The Endocrine Society
sensitivity to upstream signaling. Alternatively, it is possible that the master clock
in the SCN communicates timing information to GnRH cells that do not maintain
the capacity for endogenous rhythmicity. Given that SCN-derived VIPergic cells
project monosynaptically to GnRH neurons, this cell phenotype represents an ideal
candidate to communicate such timing information. Finally, a combination of both
mechanisms may underlie such daily changes in GnRH cell sensitivity, with
VIPergic SCN communication synchronizing independent GnRH cellular oscilla-
tors to coordinate the timing in their responsiveness to upstream signaling.
Clock Genes and Kisspeptin Control of Ovulation
The same clock genes that drive circadian rhythms at the cellular level in the SCN
are also expressed throughout other brain regions and peripheral tissues. GnRH
cells express clock genes, both in vitro [
112
,
113
] and in vivo [
114
,
115
]. Mice with
a mutation in the essential circadian clock gene,
Clock
, display abnormal estrous
cycles and abnormal LH surge induction in response AVP administration [
6
], sug-
gesting an important role for clock genes (potentially in GnRH cells) in normal
estrous cycling and ovulation. Studies in which the rescue of
Clock
is restricted to
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