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Tet1/DLL3/Notch1信号通路影响海马神经发生,并调节小鼠的类似抑郁的行为

Ruonan Shuang¹, Tiantian Gao², Zhongwen Sun³

¹Ningxia Medical University, Yinchuan, Ningxia, 750004, China; Chengdu University of Traditional Chinese Medicine, Chengdu, 611137, China.

European journal of pharmacology

|February 12, 2024

概括

十一转位蛋白1 (Tet1) 的下调会损害海马神经发生,并使小鼠的抑郁症行为恶化. 过度表达Tet1促进神经发生并减轻这些症状,这表明治疗点.

科学领域:

神经科学是一个神经科学.
分子生物学分子生物学
遗传学是一个遗传学.

背景情况:

十一转位蛋白1 (Tet1) 参与调节类似抑郁症的行为.
连接Tet1与抑郁症神经发生的确切机制仍未得到充分探索.

研究的目的:

研究Tet1/Delta样蛋白3 (DLL3) /Notch1途径在海马神经发生和小鼠抑郁症样行为的作用.
探索Tet1的调节机制,以应对慢性社会失败压力 (CSDS).

主要方法:

建立了一个慢性社会失败压力 (CSDS) 鼠标模型.
在海马体中过度表达了Tet1,并利用5-乙烯基-2'-脱氧氨 (EdU) 进行细胞增殖分析.
评估了 Tet1,DLL3,Notch1 和 BDNF 的蛋白质表达水平,以及细胞标记物 (EdU,DCX,Ki67).

主要成果:

CSDS显著降低了Tet1的表达,破坏了DNA甲基化/脱甲基化平衡.
降低Tet1的调节导致甲基化增加和DLL3,Notch1和BDNF的蛋白质水平降低.
在CSDS小鼠中观察到海马神经元的增殖和分化减少,较少的EDU+,DCX+和Ki67+细胞证明了这一点.
过度表达Tet1上调了DLL3和Notch1,增强了海马神经发生,并缓解了类似抑郁症的行为.

结论:

Tet1在调节海马神经发生和类似抑郁症的行为方面发挥着至关重要的作用.
1/DLL3/Notch1通路是这些效应的关键调解者.
在海马体中准Tet1/DLL3/Notch1通路为抑郁症提供了潜在的治疗策略.

关键词:

在 DLL3 中,你会看到 DLL3 文件.抑郁症抑郁症抑郁症标记1 标记1 标记第十一章没有了

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