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Fig. 12.2
A confocal projection illustrating the relationship between kisspeptin neurons (
green
)
in the arcuate nucleus (ARC) and GnRH cell bodies and projections (
red
) to the median eminence
in a coronal section of the mediobasal hypothalamus of a castrated adult male rhesus monkey.
VHT
ventral hypothalamic tract;
3V
third ventricle;
ME
median eminence. Scale bar, 100
m. From
Ramaswamy S, Guerriero KA, Gibbs RB, Plant TM. Structural interactions between kisspeptin
and GnRH neurons in the mediobasal hypothalamus of the male rhesus monkey (
Macaca mulatta
)
as revealed by double immunofl uorescence and confocal microscopy. Endocrinology. 2008
149:4387-95. Reprinted with permission from The Endocrine Society
μ
is consistent with the classical fi ndings that complete surgical deafferentation of
the rat and monkey MBH does not eliminate pulsatile LH release [
78
,
79
], and
that selective lesions of the ARC in female monkeys abolishes pulsatile LH
release [
80
]. It is also consistent with the recent fi nding that selective ablation of
KNDy neurons in the rat dramatically truncates the ovariectomy-induced increase
in LH release [
81
].
A Novel View on the Role of Kisspeptin in Puberty Onset
As discussed above, the genetic evidence for the view that kisspeptin neurons are
critical for the onset of puberty is overwhelming. Together with results from com-
pelling physiological and pharmacological studies indicating that kisspeptin is
the most potent GnRH secretagogue [
82
], a dogma has emerged that the genes
encoding kisspeptin and its receptor regulate puberty, which in turn has led to the
perception that kisspeptin signaling represents the key neural substrate that controls
the timing of the onset of puberty. Here, we offer an alternative possibility. Namely,
while kisspeptin-expressing neurons in ARC are critical for puberty, this is simply
because these cells comprise an integral component of the hypothalamic GnRH
pulse generating mechanism that generates intermittent release of the decapeptide,
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