Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 102, Issue 12, Pages 4608-4612Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0500752102
Keywords
developmental neurobiology; neuroendocrinology; sexual differentiation
Categories
Funding
- NIMH NIH HHS [K02 MH001349, R01 MH57759, R01 MH057759, F31 MH070092, F31MH70092, K02 MH01349] Funding Source: Medline
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Sex differences in brain and behavior are ubiquitous in sexually reproducing species. One cause of sexual dimorphisms is developmental differences in circulating concentrations of gonadal steroids. Neonatal testes produce androgens; thus, males are exposed to both testosterone and estradiol, whereas females are not exposed to high concentrations of either hormone until puberty. Classically, the development of neural sex differences is initiated by estradiol, which activates two processes in male neonates; masculinization, the development of male-type behaviors, and defeminization, the loss of the ability to display female-type behaviors. Here, we test the hypothesis that defeminization is regulated by estrogen receptor beta (ER beta). Adult male ER beta knockout and WT mice were gonadectomized, treated with female priming hormones, and tested for receptive behavior. Indicative of incomplete defeminization, male ER beta knockout mice showed significantly higher levels of female receptivity as compared with WT littermates. Testes-intact males did not differ in any aspects of their male sexual behavior, regardless of genotype. In olfactory preference tests, males of both genotypes showed equivalent preferences for female-soiled bedding. Based on these results, we hypothesize that ER beta is involved in defeminization of brain and behavior. This aspect of ER beta function may lead to developments in our understanding of neural-based sexually dimorphic human behaviors.
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