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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Compensatory network changes in the dentate gyms restore long-term potentiation following ablation of neurogenesis in young-adult mice
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Compensatory network changes in the dentate gyms restore long-term potentiation following ablation of neurogenesis in young-adult mice

机译:齿状体育馆中的补偿性网络变化可消除成年小鼠神经发生消融后的长期增效作用

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摘要

It is now well established that neurogenesis in the rodent sub-granular zone of the hippocampal dentate gyms continues throughout adulthood. Neuroblasts born in the dentate subgranular zone migrate into the granule cell layer, where they differentiate into neurons known as dentate granule cells. Suppression of neurogenesis by irradiation or genetic ablation has been shown to disrupt synaptic plasticity in the dentate gyrus and impair some forms of hippocampus-dependent learning and memory. Using a recently developed transgenic mouse model for suppressing neurogenesis, we sought to determine the long-term impact of ablating neurogenesis on synaptic plasticity in young-adult mice. Consistent with previous reports, we found that ablation of neurogenesis resulted in significant deficits in dentate gyrus long-term potentiation (LTP) when examined at a time proximal to the ablation. However, the observed deficits in LTP were not permanent. LTP in the dentate gyrus was restored within 6 wk and this recovery occurred in the complete absence of neurogenesis. The recovery in LTP was accompanied by prominent changes within the dentate gyrus, including an increase in the survival rate of newborn cells that were proliferating just before the ablation and a reduction in inhibitory input to the granule cells of the dentate gyrus. These findings suggest that prolonged suppression of neurogenesis in young-adult mice results in wide-ranging compensatory changes in the structure and dynamics of the dentate gyrus that function to restore plasticity.
机译:现在已经确定,在整个成年期,海马齿状体育馆的啮齿类动物亚颗粒区的神经发生一直持续。在齿状亚细颗粒区出生的成神经细胞迁移到颗粒细胞层,在那里它们分化成称为齿状颗粒细胞的神经元。通过辐射或遗传消融抑制神经发生可破坏齿状回中的突触可塑性,并损害某些形式的海马依赖性学习和记忆。使用最近开发的转基因小鼠模型来抑制神经发生,我们试图确定消融神经发生对年轻成年小鼠突触可塑性的长期影响。与以前的报告一致,我们发现在消融的近端时间进行检查时,神经发生的消融导致齿状回长期增强(LTP)的明显缺陷。但是,观察到的LTP缺陷不是永久性的。齿状回中的LTP在6周内恢复,并且这种恢复发生在完全没有神经发生的情况下。 LTP的恢复伴随着齿状回内部的显着变化,包括刚消融前增殖的新生细胞的存活率增加,以及对齿状回的颗粒细胞的抑制性输入减少。这些发现表明,长期抑制年轻成年小鼠的神经发生会导致齿状回的结构和动力学发生广泛的补偿性变化,从而恢复可塑性。

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  • 作者单位

    Department of Neurology, University of Michigan Medical School, Ann Arbor, Ml 48109,Neuroscience Graduate Program, University of Michigan Medical School, Ann Arbor, Ml 48109;

    Molecular and Behavioral Neuroscience Institute, University of Michigan Medical School, Ann Arbor, Ml 48109;

    Department of Neurology, University of Michigan Medical School, Ann Arbor, Ml 48109;

    Neuroscience Graduate Program, University of Michigan Medical School, Ann Arbor, Ml 48109,Molecular and Behavioral Neuroscience Institute, University of Michigan Medical School, Ann Arbor, Ml 48109;

    Department of Neurology, University of Michigan Medical School, Ann Arbor, Ml 48109,Neuroscience Graduate Program, University of Michigan Medical School, Ann Arbor, Ml 48109,VA Ann Arbor Healthcare System, Ann Arbor, Ml 48105;

    Neuroscience Graduate Program, University of Michigan Medical School, Ann Arbor, Ml 48109,Molecular and Behavioral Neuroscience Institute, University of Michigan Medical School, Ann Arbor, Ml 48109,Department of Molecular andIntegrative Physiology, University of Michigan Medical School, Ann Arbor, Ml 48109;

  • 收录信息 美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

    adult neurogenesis; thymidine kinase; metaplasticity; miniature inhibitory postsynaptic currents;

    机译:成人神经发生;胸苷激酶;可塑性;微型抑制突触后电流;

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