Adult Neurogenesis & Alcohol-Induced Learning Deficits
成人神经发生
基本信息
- 批准号:7140473
- 负责人:
- 金额:$ 20.86万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2005
- 资助国家:美国
- 起止时间:2005-07-18 至 2007-06-30
- 项目状态:已结题
- 来源:
- 关键词:behavioral /social science research tagconfocal scanning microscopydevelopmental disease /disorderdevelopmental neurobiologydisease /disorder modelearly experienceembryo /fetus toxicologyethanolfetal alcohol syndromehippocampusimmunocytochemistrylaboratory mouselearning disorderslongitudinal animal studymature animalneurogenesispolymerase chain reaction
项目摘要
DESCRIPTION (provided by applicant): The denate gyrus of the hippocampus is an area where new neurons continue to be generated throughout adult life. Although the role of adult hippocampal neurogenesis is still debated, accumulating evidence suggests that it is involved in the acquisition of certain forms of hippocampal-dependent learning. Based on those findings, we have begun to explore the relationship between learning deficits and neurogenesis in adult offspring of prenatal ethanol exposed rodents. For these studies, we have utilized a mouse model of fetal alcohol exposure (FAE) that is based on free-choice and represents a moderate alcohol access model of FAE. Adult offspring of FAE mice display learning deficits similar to that of the FAE rat, but the FAE mouse model is not confounded by potential diet and pair feeding effects. Preliminary data presented in this proposal demonstrate that FAE does not impair basal neurogenesis under standard housing conditions, but abolishes the neurogenic response to enriched environment. Studies outlined in this exploratory R21 proposal are designed to determine a) whether FAE also impairs the neurogenic response to hippocampal-dependent learning, and b) whether mitigation of the neurogenic response to behavioral challenge is due to intrinsic defects of FAE progenitors and/or due to microenvironmental changes within the neurogenic niche of the adult SGZ. Our preliminary studies are among the first to demonstrate that prenatal exposures can result in persistent defects in adult hippocampal neurogenesis. Since learning disabilities are among the most prevalent and pervasive fetal alcohol-related defects in children, further studies to understand the basis of these deficits in animal models of prenatal ethanol exposure seems warranted.
描述(由申请人提供):海马体的齿状回是一个在整个成年生活中不断产生新神经元的区域。尽管成人海马神经发生的作用仍有争议,但越来越多的证据表明,它与海马依赖学习的某些形式的习得有关。基于这些发现,我们已经开始探索在产前乙醇暴露的啮齿动物成年后代中学习缺陷和神经发生之间的关系。在这些研究中,我们使用了胎儿酒精暴露(FAE)的小鼠模型,该模型基于自由选择,代表了FAE的中度酒精获取模型。FAE小鼠的成年后代表现出与FAE大鼠相似的学习缺陷,但FAE小鼠模型不受潜在的饮食和配对喂养效应的影响。本研究提出的初步数据表明,FAE在标准住房条件下不会损害基础神经发生,但会消除对富集环境的神经发生反应。本探索性R21提案中概述的研究旨在确定a) FAE是否也会损害海马依赖性学习的神经源性反应,以及b)对行为挑战的神经源性反应的减轻是否由于FAE祖细胞的内在缺陷和/或由于成人SGZ神经源性生态位的微环境变化。我们的初步研究是首次证明产前暴露可导致成人海马神经发生持续缺陷的研究之一。由于学习障碍是儿童中最普遍和普遍的胎儿酒精相关缺陷之一,因此在产前乙醇暴露的动物模型中进一步研究了解这些缺陷的基础似乎是有必要的。
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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Lee Anna Cunningham其他文献
Lee Anna Cunningham的其他文献
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{{ truncateString('Lee Anna Cunningham', 18)}}的其他基金
Network mechanisms of impaired adult hippocampal neurogenesis in a mouse model of prenatal alcohol exposure
产前酒精暴露小鼠模型中成年海马神经发生受损的网络机制
- 批准号:
9887882 - 财政年份:2020
- 资助金额:
$ 20.86万 - 项目类别:
Network mechanisms of impaired adult hippocampal neurogenesis in a mouse model of prenatal alcohol exposure
产前酒精暴露小鼠模型中成年海马神经发生受损的网络机制
- 批准号:
10455050 - 财政年份:2020
- 资助金额:
$ 20.86万 - 项目类别:
Network mechanisms of impaired adult hippocampal neurogenesis in a mouse model of prenatal alcohol exposure
产前酒精暴露小鼠模型中成年海马神经发生受损的网络机制
- 批准号:
10670849 - 财政年份:2020
- 资助金额:
$ 20.86万 - 项目类别:
Network mechanisms of impaired adult hippocampal neurogenesis in a mouse model of prenatal alcohol exposure
产前酒精暴露小鼠模型中成年海马神经发生受损的网络机制
- 批准号:
10229363 - 财政年份:2020
- 资助金额:
$ 20.86万 - 项目类别:
Adult Neurogenesis & Alcohol-Induced Learning Deficits
成人神经发生
- 批准号:
6968661 - 财政年份:2005
- 资助金额:
$ 20.86万 - 项目类别:
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