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Brain masculinization requires androgen receptor function.

Takashi Sato1, Takahiro Matsumoto, Hirotaka Kawano

  • 1Institute of Molecular and Cellular Biosciences, University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo 113-0032, Japan.

Proceedings of the National Academy of Sciences of the United States of America
|January 30, 2004
PubMed
Summary

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This summary is machine-generated.

Perinatal testosterone masculinizes the male brain via estrogen signaling, but androgen receptor (AR) function is also crucial for male behaviors. AR inactivation in mice impaired male behaviors, highlighting AR

Area of Science:

  • Neuroendocrinology
  • Developmental Neuroscience
  • Behavioral Endocrinology

Background:

  • Testosterone during perinatal development is crucial for masculinizing the male brain and establishing adult male-typical behaviors.
  • Testosterone's effects in the brain are mediated by its conversion to estrogen and subsequent estrogen receptor (ER)-mediated signaling.
  • The specific role of the androgen receptor (AR) in this perinatal brain masculinization process remains incompletely understood due to testosterone's conversion to estrogen.

Purpose of the Study:

  • To investigate the necessity of androgen receptor (AR) signaling in perinatal brain masculinization and the subsequent expression of male-typical behaviors.
  • To differentiate the roles of AR-dependent and estrogen receptor (ER)-dependent pathways in mediating androgen effects on behavior.
  • To elucidate the contribution of AR signaling to the development of sexual and aggressive behaviors in male mice.

Related Experiment Videos

Main Methods:

  • Generation of mice with a null mutation in the androgen receptor (AR) using the Cre-loxP system.
  • Behavioral analysis of AR-null mutant mice (AR(L-/Y) males and AR(L-/L-) females) to assess sexual and aggressive behaviors.
  • Pharmacological manipulation using nonaromatizable androgen (5alpha-dihydrotestosterone, DHT) and 17beta-estradiol to evaluate the rescue of behavioral deficits.

Main Results:

  • AR-null male mice (AR(L-/Y)) exhibited a complete loss of male-typical sexual and aggressive behaviors.
  • Female AR-null mice (AR(L-/L-)) displayed normal female sexual behaviors.
  • Treatment with DHT partially restored aggressive behaviors but not sexual behaviors in AR(L-/Y) males.
  • Perinatal DHT treatment in females induced masculinization, but this effect was abolished by concurrent AR inactivation.
  • Impaired male behaviors in ERalpha(-/-) mice were rescued by DHT treatment, suggesting distinct pathways.

Conclusions:

  • Perinatal brain masculinization fundamentally requires androgen receptor (AR) function.
  • The expression of adult male-typical behaviors is mediated by a combination of both AR-dependent and AR-independent androgen signaling pathways.
  • Estrogen receptor (ER) signaling is critical for some aspects of male behavior, but AR signaling is essential for the initial masculinization process.