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Fig. 11.4 Schematic of the development of sexually dimorphic AVPV/PeN Kiss1 neurons. Males
secrete elevated testosterone (T) at birth, while newborn females secrete negligible levels of sex
steroids. Postnatal T converted to estradiol infl uences the development of neural circuits, leading
to their masculinization in adulthood. AVPV/PeN Kiss1 neurons are more abundant in adult
females than males. It is currently unknown how the perinatal sex steroid milieu organizes the
sexual differentiation of Kiss1 neurons, although the AVPV as a whole is differentiated through
Bax -dependent apoptotic mechanisms. However, the sexual differentiation of Kiss1 neurons is
likely not due to Bax -dependent apoptosis [ 40 ], though other apoptotic mechanisms have not been
ruled out. Current data indicate that the Kiss1 gene may be more transcriptionally active in females,
pointing to epigenetic alterations as a putative mechanism
detectable kisspeptin-ir cells in the AVPV/PeN on or before PND 10 [ 28 , 64 ].
Currently, kisspeptin protein levels have not been directly compared between sexes
from PND 11 through PND 21, but the sex difference in kisspeptin-ir cell number
was readily apparent in mice on PND 25 [ 28 ] and in rats on PND 21 [ 64 ].
Possible Mechanisms of Steroid-Mediated Sexual
Differentiation of AVPV/PeN Kiss1 Neurons
Sexual differentiation of the AVPV/Pen Kiss1 system is dependent on the postnatal sex
steroid milieu, but it is unclear exactly how E 2 (aromatized from T) directs this devel-
opmental process. Several sex steroid-dependent mechanisms, such as differential neu-
rogenesis, migration, epigenetics, and apoptosis, have been implicated in the sexual
differentiation and development of other neuronal populations (Fig. 11.4 ) [ 32 , 72 - 74 ].
E 2 , for example, can promote neurogenesis in the olfactory bulb and dentate gyrus of
the adult rat hippocampus, leading to more newly formed neurons in females [ 32 ].
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