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ERa in Tac2 Neurons Regulates Puberty Onset in Female Mice.

Authors	Greenwald-Yarnell ML, Marsh C, Allison MB, Patterson CM, Kasper C, MacKenzie A, Cravo R, Elias CF, Moenter SM, Myers MG
Submitted By	Submitted Externally on 1/10/2022
Status	Published
Journal	Endocrinology
Year	2016
Date Published	4/1/2016
Volume : Pages	157 : 1555 - 65
PubMed Reference	26862996
Abstract	A variety of data suggest that estrogen action on kisspeptin (Kiss1)-containing arcuate nucleus neurons (which coexpress Kiss1, neurokinin B (the product of Tac2) and dynorphin (KNDy) neurons restrains reproductive onset and function, but roles for estrogen action in these Kiss1 neurons relative to a distinct population of rostral hypothalamic Kiss1 neurons (which does not express Tac2 or dynorphin) have not been directly tested. To test the role for estrogen receptor (ER)a in KNDy cells, we thus generated Tac2(Cre) and Kiss1(Cre) knock-in mice and bred them onto the Esr1(flox) background to ablate ERa specifically in Tac2-expressing cells (ERa(Tac2)KO mice) or all Kiss1 cells (ERa(Kiss1)KO mice), respectively. Most ERa-expressing Tac2 neurons represent KNDy cells. Arcuate nucleus Kiss1 expression was elevated in ERa(Tac2)KO and ERa(Kiss1)KO females independent of gonadal hormones, whereas rostral hypothalamic Kiss1 expression was normal in ERa(Tac2)KO but decreased in ERa(Kiss1)KO females; this suggests that ERa in rostral Kiss1 cells is crucial for control of Kiss1 expression in these cells. Both ERa(Kiss1)KO and ERa(Tac2)KO females displayed early vaginal opening, early and persistent vaginal cornification, increased gonadotropins, uterine hypertrophy, and other evidence of estrogen excess. Thus, deletion of ERa in Tac2 neurons suffices to drive precocious gonadal hyperstimulation, demonstrating that ERa in Tac2 neurons typically restrains pubertal onset and hypothalamic reproductive drive.

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