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自愿跑步增强的突触可塑性、学习和记忆是由 C57BL 小鼠中的 Notch1 信号通路介导的。

Voluntary running-enhanced synaptic plasticity, learning and memory are mediated by Notch1 signal pathway in C57BL mice.

机构信息

College of Medicine, State Key Laboratory of Medicinal Chemical Biology, Key Laboratory of Bioactive Materials for Ministry of Education, Nankai University, Tianjin, 300071, China.

College of Life Sciences, Nankai University, Tianjin, 300071, China.

出版信息

Brain Struct Funct. 2018 Mar;223(2):749-767. doi: 10.1007/s00429-017-1521-0. Epub 2017 Sep 20.

DOI:10.1007/s00429-017-1521-0
PMID:28932899
Abstract

It is well known that voluntary running can enhance synaptic plasticity and improve learning and memory abilities. The Notch1 receptor is also reported to be associated with these processes, but its role in running-induced alterations is unclear. In this study, we aimed to investigate whether the Notch1 signalling pathway was involved in voluntary running-induced enhancement of synaptic plasticity, learning and memory. Notch1 heterozygous deficient (Notch1) mice and wildtype (WT) C57BL littermates were randomly divided into runner group and non-runner group. Mice were given free access to running wheels for 14 days in both the Notch1 runner group and the WT runner group. Our results demonstrate that Notch1 knockdown impairs the performance in the novel object recognition (NOR) test and Morris water maze test and decreases the synaptic plasticity. Voluntary running improves spatial learning and memory abilities, promotes synaptic plasticity and increases expressions of postsynaptic proteins in WT mice but not in Notch1 mice. Our results suggest that Notch1 plays a vital role in spatial learning and memory, synaptic plasticity under normal physiological conditions and voluntary running conditions. These findings will set the groundwork and fill in some gaps for understanding the role of Notch1 signalling in voluntary running-induced phenomena.

摘要

众所周知,自愿跑步可以增强突触可塑性,提高学习和记忆能力。 Notch1 受体也与这些过程有关,但它在跑步引起的变化中的作用尚不清楚。在这项研究中,我们旨在研究 Notch1 信号通路是否参与了自愿跑步引起的突触可塑性、学习和记忆的增强。 Notch1 杂合缺失(Notch1)小鼠和野生型(WT)C57BL 同窝仔鼠被随机分为跑步组和非跑步组。 Notch1 跑步组和 WT 跑步组的小鼠均被给予自由使用跑步轮 14 天。我们的结果表明,Notch1 敲低会损害新物体识别(NOR)测试和 Morris 水迷宫测试的表现,并降低突触可塑性。自愿跑步可改善空间学习和记忆能力,促进突触可塑性,并增加 WT 小鼠而非 Notch1 小鼠的突触后蛋白表达。我们的结果表明,Notch1 在正常生理条件下和自愿跑步条件下对空间学习和记忆、突触可塑性起着至关重要的作用。这些发现将为理解 Notch1 信号在自愿跑步引起的现象中的作用奠定基础并填补一些空白。

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