4.5 Article

Estrogen Receptor α Gene Promoter 0/B Usage in the Rat Sexually Dimorphic Nucleus of the Preoptic Area

Journal

ENDOCRINOLOGY
Volume 151, Issue 4, Pages 1923-1928

Publisher

ENDOCRINE SOC
DOI: 10.1210/en.2009-1022

Keywords

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Funding

  1. Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research [17500215, 18390070]
  2. Ministry of Education, Culture, Sports, Science, and Technology [1686210]
  3. Grants-in-Aid for Scientific Research [22390043, 17500215, 18390070, 22500297] Funding Source: KAKEN

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The volume of the sexually dimorphic nucleus of the preoptic area (SDN-POA) is two to four times larger in male rats than in females; however, the mechanism for the establishment of sexual dimorphism and the function of this nucleus is almost unknown. Perinatal estrogen can cause sexual dimorphism via the estrogen receptor alpha (ER alpha). Recently, transgenic rats were generated that express enhanced green fluorescent protein (EGFP) under the control of the ER alpha gene promoter 0/B to tag ER alpha-positive neurons in the brain. In the present study, we examined whether this EGFP expression could be a marker for the SDN-POA in adults. EGFP-labeled cells were distributed in the core of the SDN-POA (0/B-SDN)of male and female transgenic rats, in accordance with the Nissl staining and immunoreactivity for the SDN marker, calbindin. They were also immunoreactive for ER alpha. The core was bigger in volume and contained more 0/B-SDN neurons in males than in females. The EGFP-tagged cells were packed more densely in the female core than that in males. Subcutaneous injection of 100 mu g 17 beta-estradiol to females on the day of birth, or orchidectomy of male neonates, reversed the sexually dimorphic phenotype of the volume of the 0/B-SDN, despite not affecting the cell number. We suggest that this EGFP expression in the SDN-POA could be a useful marker to clarify the sexual differentiation and function of the SDN-POA. Moreover, the ER alpha gene promoter 0/B plays a key role in the organization of the sexual differentiation of the SDN-POA. ( Endocrinology 151: 1923-1928, 2010)

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