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Fig. 12.3
A model for the control of the timing of puberty in primates, in which the role of kiss-
peptin (KP,
green
) signaling is posited to be a critical component of the neural machinery essential
for generation of pulsatile GnRH (
red
) release in the hypothalamus. In this model, the GnRH pulse
generating mechanism resides in the arcuate nucleus (ARC) and the output of this signaling is
relayed to GnRH terminals in the median eminence (ME) by KP projections arising from perikarya
in the ARC. During infancy (
left panel
), ARC GnRH pulse generating activity is robust leading to
intermittent release of KP in the ME, resulting in a corresponding pattern of GnRH release into the
portal circulation. This, in turn, drives pulsatile gonadotropin (LH and FSH) secretion. In the tran-
sition from infancy to the juvenile phase of development (
middle panel
), a neurobiological brake
(central inhibition) holds the ARC GnRH pulse generating mechanism in check and pulsatile
release of KP in the ME is markedly suppressed. This leads to reduced GnRH release and to a
hypogonadotropic state in the juvenile period. Puberty is triggered when the brake is removed and
GnRH pulse generation with robust intermittent release of KP in the ME is reactivated (
right
panel
). According to this model, the mystery of primate puberty lies in the nature of the neurobio-
logical brake, i.e., the mechanism that times its application during infancy and its release at the
end of the juvenile phase of development. The thickness of the
blue
(T, testosterone) and
gold
(E, estradiol)
arrows
indicating negative feedback by the testis and ovary, respectively, refl ect the
degree of gonadal steroid inhibition exerted on LH secretion at these three stages of primate devel-
opment.
AC
anterior commissure;
AP
anterior pituitary gland;
ARC
arcuate nucleus;
OC
optic
chiasm;
ME
median eminence;
MMB
mammillary body
an increase of which is obligatory for the onset of puberty. According to this model,
kisspeptin neurons in the ARC play no regulatory role in controlling the timing of
puberty. Rather, as a component of hypothalamic GnRH pulse generation, they
subserve upstream regulatory mechanisms determining the timing of puberty onset.
In the case of primates, the upstream control system(s), which is independent of
gonadal steroids, fi rst suppress pulsatile GnRH release in infancy and, subsequently,
a reduction in this suppression reactivates pulsatility of GnRH release at the end of
juvenile development (Fig.
12.3
). In rodents, the early postnatal ontogeny of pulsa-
tile GnRH release is less clear, but later in prepubertal development, steroid- dependent
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