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Influence of estrogen on reproductive organization in perinatal mouse brain, with special reference to xenoestrogen

Research Project

Project/Area Number 10670032
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field General anatomy (including Histology/Embryology)
Research InstitutionTokai University

Principal Investigator

SEIKI Kanji  Dept.of Molphology, Tokai Univ. School of Med., Professor, 医学部, 教授 (40055934)

Co-Investigator(Kenkyū-buntansha) HANAMOTO Hideko  Dept.of Molphology, Tokai Univ. School of Med., Instructor, 医学部, 助手 (50156824)
Project Period (FY) 1998 – 1999
Project Status Completed (Fiscal Year 1999)
Budget Amount *help
¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1999: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1998: ¥500,000 (Direct Cost: ¥500,000)
Keywordsestriol / nicotine / estrogen receptor / neuron-specific enolase / brain reproductive organization / preoptic area / amygdala / 免疫組織化学 / 妊娠マウス / エストロゲン / 視床下部 / 生殖中枢
Research Abstract

We have set out to obtain an information of whether high E levels during pregnancy would affect the development of perinatal mouse brain, especially the sex-related area through an estrogen receptor (ER) mechanism. We also examined the influence of habitual smoking during pregnancy on perinatal brain development by ad libitum administration of a nicotine-water solution.
We have investigated the effects of administration of estriol (EィイD23ィエD2) and/or nicotine to pregnant mouse on neonatal offspring brain development, using immunohistochemical and radiobiochemical techniques.
Estriol caused significant decreases in brain weight and ER concentration after birth, whereas nicotine plus EィイD23ィエD2 brought about no changes in brain weight or ER concentration. Intensities of ER- and neuron-specific enolase (NSE)-immunostainings were both enhanced by EィイD23ィエD2 in the reproductive organization including the preoptic area (POA), anterior to middle medial basal hypothalamus (AMBH) and amygdala (AM) after birth, Nicotine alone did not enhance the ER-immunostain intensity in POA, AMBH or AM, whereas it did enhance the NSE-immunostain intensity in these brain areas. On the contrary, simultaneous administration of nicotine and EィイD23ィエD2 brought about the reverse effect of ER- and NSE-immunostain intensities.
These results indicate that estrogen treatment during the perinatal period influences, through its receptor, the development and growth of the reproductive organization in the fetal brain. The influence of nicotine needs to be further elucidated.

Report

(3 results)
  • 1999 Annual Research Report   Final Research Report Summary
  • 1998 Annual Research Report
  • Research Products

    (6 results)

All Other

All Publications (6 results)

  • [Publications] 清水勘治: "環境エストロゲンxenoextrogenの脳の初期発生過程への影響に対するニコチンの修飾作用"喫煙科学研究財団 研究年報. 679-684 (1998)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1999 Final Research Report Summary
  • [Publications] 花本秀子: "Effect of estrogen and nicotine on perinatal mouse brain development"Medical Science Research. 27. 367-373 (1999)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1999 Final Research Report Summary
  • [Publications] K.Seiki, et al.: "Effect of estrogen and nicotine on perinatal mouse brain development"Smoking Research Foundation Annual Research Report. 679-684 (1998)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1999 Final Research Report Summary
  • [Publications] H.Fujii-Hanamoto, et al.: "Effect of estrogen and nicotine on perinatal mouse brain development"Medical Science Research. 27. 367-373 (1999)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1999 Final Research Report Summary
  • [Publications] 清木 勘治: "環境エストロゲンxenoestrogenの脳の初期発生過程への影響に対するニコチンの修飾作用"喫煙科学研究財団 研究年報. 679-684 (1998)

    • Related Report
      1999 Annual Research Report
  • [Publications] 花本 秀子: "Effect of estrogen and nicotine on perinatal mouse brain development"Medical Science Research. 27. 367-373 (1999)

    • Related Report
      1999 Annual Research Report

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Published: 1998-04-01   Modified: 2016-04-21  

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