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压力的表观遗传控制和环境丰富对焦虑和前额叶皮层BDNF表达的相互作用

Nívea Karla de Gusmão Taveiros Silva¹, Gabriel Araújo Costa¹, Marina Gomes de Almeida¹

¹Pharmacology Department, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.

Neuropharmacology

|October 25, 2025

概括

环境丰富 (EE) 并没有阻止慢性不可预测的轻度压力 (CMS) 在小鼠中引起类似焦虑的行为. 然而,用5-aza-2'-deoxycytidine (5-azaC) 抑制DNA甲基化可以减轻这些由压力引起的行为变化.

科学领域:

神经科学是一个神经科学.
精神病学是一个精神病学.
表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.

背景情况:

慢性压力会导致抑郁和焦虑障碍,因为它会破坏来自大脑的神经营养因子 (BDNF) 的信号传递,并促进前额叶皮层 (PFC) 的表观遗传变化.
环境丰富 (EE) 可能通过其对BDNF表达和表观遗传调节的影响来调节与压力相关的精神病理的脆弱性.

研究的目的:

为了研究下值慢性不可预测的轻度压力 (CMS) 对以前安置在环境丰富 (EE) 的小鼠的影响.
为了检查类似焦虑的行为,皮质水平,PFC Bdnf表达,BDNF蛋白水平和DNA甲基化概况.
探索DNA甲基化机制在调解CMS对EE养小鼠的影响中的作用.

主要方法:

在暴露于下值慢性不可预测的轻度应激 (CMS) 之前,小鼠被安置在标准或环境丰富 (EE) 条件下.
评估了类似焦虑的行为,以及血皮质水平,PFC中的Bdnf mRNA表达,BDNF蛋白水平和DNA甲基化概况.
用DNA甲基化抑制剂5-aza-2-deoxycytidine (5-azaC) 来研究表观遗传调解.

主要成果:

在被EE安置的小鼠中,CMS导致了类似焦虑的行为,这种效应被5-azaC的使用减弱了,这表明表观遗传的参与.
单独使用EE就会增加皮质,但当EE与CMS结合使用时,这种情况会被抑制.
在PFC中,EE紧随其后的是CMS下调的特定BdnfmRNA外原体,在外原体IX的DNA甲基化中没有检测到任何变化. 在EE的小鼠中,5-azaC降低了BDNF.

结论:

低于值的CMS可以在曾经接触过EE的小鼠中诱导类似焦虑的行为,这表明EE并不能给予完全的保护.
表观遗传机制,特别是DNA甲基化,在介导CMS在EE养小鼠的行为和分子效应方面发挥着作用.
EE和CMS之间的相互作用涉及BDNF表达和皮质水平的复杂调节,这对与压力相关的精神病理有影响.

关键词:

5-Aza-2′-deoxycytidine的使用情况在Bdnf的外表上.慢性轻度压力慢性轻度压力通过DNA甲基化.恢复力恢复力

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