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A Hyperandrogenic Mouse Model to Study Polycystic Ovary Syndrome
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Investigating GABA Neuron-Specific Androgen Receptor Knockout in two Hyperandrogenic Models of PCOS.

Irene E Sucquart1, Chris Coyle2, Valentina Rodriguez Paris1,3

  • 1Fertility & Research Centre, School of Clinical Medicine, University of New South Wales Sydney, Randwick, NSW 2031, Australia.

Endocrinology
|May 24, 2024
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Summary

Androgen signaling in GABA neurons is not essential for developing PCOS-like reproductive and metabolic issues. However, it is crucial for the prenatal androgen excess-induced changes in brain connections to GnRH neurons.

Keywords:
DHTGABAandrogen receptormicepolycystic ovary syndrome

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Area of Science:

  • Neuroendocrinology
  • Reproductive Biology
  • Metabolic Disorders

Background:

  • Androgen excess is central to polycystic ovary syndrome (PCOS), a leading cause of anovulatory infertility.
  • Hyperandrogenism during development or chronically is linked to PCOS reproductive and metabolic dysfunction.
  • GABAergic neurons are implicated as potential androgen targets in PCOS pathogenesis.

Purpose of the Study:

  • To investigate the role of androgen signaling in GABAergic neurons in PCOS development.
  • To test if GABAergic androgen receptor signaling is critical for PCOS pathogenesis in mouse models.

Main Methods:

  • Generated GABA-specific androgen receptor knockout (GABARKO) mice using cre-lox technology.
  • Exposed GABARKO and wild-type (WT) mice to prenatal androgen excess (PNA) or peripubertal androgen excess (PPA).
  • Phenotyped mice for reproductive and metabolic traits; assessed GABAergic input to GnRH neurons in PNA mice.

Main Results:

  • Chronic PPA-induced reproductive and metabolic dysfunction was similar in GABARKO and WT mice.
  • Prenatal androgen excess (PNA) caused acyclicity in both GABARKO and WT mice, with no significant impact on ovarian morphology or LH secretion.
  • PNA increased GABAergic synapses to GnRH neurons in WT mice, but this plasticity was abolished in GABARKO mice.

Conclusions:

  • Direct androgen signaling in GABA neurons is not essential for developing PCOS-like traits in these androgenized models.
  • Developmental programming of GnRH neuron innervation by prenatal androgen excess depends on androgen signaling within GABA neurons.