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Effects of developmental and adult stress on hippocampal function and dendritic structure.

机译：发育和成年应激对海马功能和树突结构的影响。

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摘要

Chronic early-life stress affects a majority of the world's children and is associated with deficits in hippocampus-dependent cognitive function during adulthood. Studies in humans cannot establish with certainty whether early-life stress causes cognitive dysfunction because other influences, including differences in genes and in environment, cannot be controlled. Therefore, we created a novel mouse model of chronic early-life stress to take advantage of the power of genetically modified mice to elucidate the molecular mechanisms and roles of specific genes responsible for the consequences of early-life stress on hippocampal function and dendritic structure.;The chronic early-life stress paradigm involved altering the cage environment during the first week of life, which led to fragmentation of maternal care, in turn resulting in stress in the pups. Stress early in life was manifest in hormonal and molecular changes in the hypothalamus, and led to persistent impairment of hippocampus-dependent learning and memory in adult mice in the absence of anxiety-like or depression-like behaviors. Enrichment of the environment after the early-life stress period could not reverse the cognitive deficits provoked by the stress.;Taking advantage of genetically engineered mice expressing yellow-fluorescent protein in hippocampal neurons, we examined the neuroanatomical basis of the cognitive defects provoked by stress. Whereas we did not confirm dendritic loss after early-life stress, we found that loss of dendritic spines, even in the absence of dendritic atrophy, was associated with profound memory defects in adult mice subjected to short, multi-modal stress.;In summary, this dissertation developed mouse models for stress, and employed these models to study fundamental processes related to stress-provoked losses of hippocampus-dependent learning and memory throughout life.
机译：慢性的早期生活压力会影响世界上大多数儿童，并且与成年期海马依赖认知功能的缺陷有关。由于无法控制包括基因和环境差异在内的其他影响，因此人类研究无法确定早期应激是否会导致认知功能障碍。因此，我们创建了一个新型的慢性早期应激小鼠模型，以利用转基因小鼠的能力阐明负责早期应激对海马功能和树突结构后果的特定基因的分子机制和作用。慢性的早期生活压力范例涉及在生命的第一周内改变笼子的环境，这导致产妇护理的分散，进而导致幼崽压力。下丘脑的荷尔蒙和分子变化明显表现出生命的早期压力，并导致成年小鼠持续出现海马依赖性学习和记忆障碍，而没有焦虑样或抑郁样行为。生活早期应激阶段后的环境丰富不能逆转由应激引起的认知缺陷。；利用基因表达的小鼠在海马神经元中表达黄色荧光蛋白，我们研究了应激引起的认知缺陷的神经解剖学基础。尽管我们没有确认早年应激后的树突状丢失，但我们发现即使在没有树突状萎缩的情况下，树突棘的丢失也与遭受短时，多模式应激的成年小鼠的深层记忆缺陷有关。 ，本文开发了小鼠应激模型，并利用这些模型研究了与应激引起的海马依赖型学习和记忆丧失相关的基本过程。

著录项

  • 作者

    Rice, Courtney Jill.;

  • 作者单位

    University of California, Irvine.;

  • 授予单位 University of California, Irvine.;
  • 学科 Neurosciences.
  • 学位 Ph.D.
  • 年度 2009
  • 页码 132 p.
  • 总页数 132
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

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