Molecular Research on Environmental Influence on Neuroplasticity and Neurogenesis

环境对神经可塑性和神经发生影响的分子研究

基本信息

批准号：
13470195
负责人：
KANBA Shigenobu
金额：
$ 9.28万
依托单位：
University of Yamanashi (2003)山梨医科大学 (2001-2002)
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (B)
财政年份：
2001
资助国家：
日本
起止时间：
2001 至 2003
项目状态：
已结题

项目摘要

Stress vulnerability is in part caused by long term influence from environment. Poor early environment is known to cause trait of anxiety and impaired cognitive function afterward. However, the precise mechanism is unknown. We decided to investigate the mechanism underlying long term influence by environment on brain development.We have carried our below stated research.1) By using twin methods, we determined contribution of genes and environments to development of personality. We found about 30-40% of our personality is determined by genes. Non-shared environment has strong contribution as compared to shared environment.2)Serotonin transporter gene is known to be associated with the trait of anxiety. We investigated association between the polymorphism of the gene and binding potential of transporter in vivo human brain that is measured by PET.3)We studied neurochemical functions of stress related chemicals such as nitric oxide, brain estrogen, prolactin releasing peptide, orexine, amyloid P component.We focused hippocampal functions in stress response and tried to answer to some questions below.1)How does environment stress impairs hippocampal functions including neurogenesis at molecular levels?2)How does Interferon that is know to cause depression clinically damage hippocampus?By understanding these mechanisms, what can we do to repair these aspects of pathology?

应激脆弱性部分是由环境的长期影响造成的。众所周知，不良的早期环境会导致随后的焦虑和认知功能受损。然而，确切的机制尚不清楚。我们决定调查环境对大脑发育的长期影响的机制。我们进行了以下研究。1）通过使用孪生方法，我们确定了基因和环境对人格发展的贡献。我们发现我们的性格大约有30-40%是由基因决定的。与共享环境相比，非共享环境有很强的贡献。2）已知5-羟色胺转运蛋白基因与焦虑特征相关。我们研究了该基因的多态性与通过 PET 测量的人脑体内转运蛋白结合电位之间的关联。3）我们研究了应激相关化学物质的神经化学功能，如一氧化氮、脑雌激素、催乳素释放肽、食欲素、淀粉样蛋白 P我们关注应激反应中的海马功能，并试图回答以下一些问题。1）环境压力如何在分子水平上损害包括神经发生在内的海马功能？2）干扰素是如何知道的导致抑郁症在临床上损害海马体？通过了解这些机制，我们能做些什么来修复这些方面的病理呢？