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ERα in Tac2 Neurons Regulates Puberty Onset in Female Mice

Megan L Greenwald-Yarnell1, Courtney Marsh1, Margaret B Allison1

  • 1Neuroscience Graduate Program (M.L.G.-Y., S.M.M., M.G.M.); Division of Metabolism, Endocrinology and Diabetes (M.L.G.-Y., M.B.A., C.M.P., C.K., A.M., S.M.M., M.G.M.), Department of Internal Medicine; and Departments of Obstetrics and Gynecology (C.M., C.F.E., S.M.M.) and Molecular and Integrative Physiology (M.B.A., R.C., C.F.E., S.M.M., M.G.M.), University of Michigan, Ann Arbor, Michigan 48109.

Endocrinology
|February 11, 2016
PubMed

Insights

Estrogen receptor alpha in kisspeptin neurons restrains reproductive onset. Ablating this receptor in Tac2 neurons triggers precocious puberty and estrogen excess, highlighting its role in controlling pubertal timing.

Area of Science:

  • Neuroendocrinology
  • Reproductive Biology
  • Molecular Endocrinology

Background:

  • Estrogen action on kisspeptin (Kiss1) neurons is implicated in reproductive regulation.
  • The specific roles of estrogen receptor alpha (ERα) in different Kiss1 neuronal populations remain unclear.

Purpose of the Study:

  • To investigate the function of ERα in kisspeptin neurons, particularly in arcuate nucleus KNDy (Kiss1, neurokinin B, dynorphin) neurons versus rostral hypothalamic Kiss1 neurons.
  • To determine if ERα in Tac2-expressing neurons restrains reproductive onset and function.

Main Methods:

  • Generated Tac2(Cre) and Kiss1(Cre) knock-in mice crossed with Esr1(flox) mice to create ERα(Tac2)KO and ERα(Kiss1)KO models.
  • Analyzed Kiss1 expression in the arcuate nucleus and rostral hypothalamus.
  • Assessed reproductive parameters including vaginal opening, vaginal cornification, gonadotropin levels, and uterine hypertrophy.

Main Results:

  • Deletion of ERα in Tac2 neurons (ERα(Tac2)KO) and all Kiss1 neurons (ERα(Kiss1)KO) elevated arcuate nucleus Kiss1 expression.
  • ERα in rostral Kiss1 neurons is crucial for controlling Kiss1 expression in that region.
  • Both ERα(Kiss1)KO and ERα(Tac2)KO females exhibited precocious puberty and signs of estrogen excess.

Conclusions:

  • Estrogen receptor alpha in Tac2-expressing neurons is essential for restraining pubertal onset.
  • Deletion of ERα in these neurons leads to hypergonadotropic hyperestrogenism and precocious puberty.
  • These findings demonstrate a critical role for ERα in Tac2 neurons in regulating the timing of puberty and hypothalamic reproductive drive.

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