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Kiss1  neurons of the arcuate (ARC) nucleus form an interconnected network of cells that communicate via neurokinin B (encoded by  Tac2 ) and its receptor (encoded by  Tacr3 ) and play key roles in the control of the reproductive axis through sex hormone-regulated synthesis and release of kisspeptin peptides (Kp, encoded by  Kiss1 ). The aim of this study was to determine whether the  Kiss1  cell population of the ARC already displays sexually dimorphic features at embryonic age E16.5 in mice. At this time of development,  Kiss1 -GFP- and Kp-immunoreactive cell bodies were restricted to the ARC and not found in the pre-optic area (POA). The  Kiss1 -GFP cell population was identical in size between sexes but had significantly lower  Kiss1 ,  Tac2 , and  Tacr3  mRNA levels and lower Kp-ir fiber density in the POA in male compared to female fetuses. Receptors for androgen ( Ar ) and estrogen ( Esr1 ,  Esr2 ,  Gpr30 ) and the  Cyp19a1  gene (encoding the estradiol-producing enzyme aromatase) transcripts were also detected in fetal ARC  Kiss1 -GFP cells with significant sex differences for  Ar  (higher in males) and  Esr1  (higher in females). Functional studies on primary cultures of sorted fetal  Kiss1 -GFP cells revealed a significant negative effect of estradiol treatment on neurite outgrowth on the fourth day of culture in the female group specifically. We conclude that the ARC  Kiss1  cell population is already sexually differentiated at E16.5 and that its morphogenetic development may be particularly vulnerable to estradiol exposure at this early developmental time.

Sexually dimorphic gene expression and neurite sensitivity to estradiol in fetal arcuate Kiss1 cells