慢性酒精诱导的长期工作记忆缺陷与前额叶皮层中改变的组分素H3K9二甲基化有关
Mael De Clerck1, Martin Manguin1, Nadia Henkous1
1INCIA, CNRS-UMR5287, Bâtiment Bordeaux Biologie Santé, Bordeaux, France.
Frontiers in behavioral neuroscience
|March 18, 2024
概括
慢性戒酒会导致持久的空间工作记忆缺陷,与前额叶皮层中减少的素H3氨酸9二甲基化 (H3K9me2) 有关. 巴克洛芬治疗通过恢复H3K9me2水平来逆转这些损伤.
科学领域:
- 神经科学是一个神经科学.
- 表观遗传学 在表观遗传学中,表观遗传学是指表观遗传学.
- 行为科学 行为科学
背景情况:
- 长期暴露于酒精导致持续的神经适应.
- 表观遗传修饰,特别是基因组修饰,在这些长期变化中起着至关重要的作用.
- 了解这些表观遗传变化对于解决酒精使用障碍后果至关重要.
研究的目的:
- 调查慢性酒精暴露对空间工作记忆 (WM) 的长期影响.
- 为了检查前额叶皮层 (PFC) 内素H3 lysine 9二甲基化 (H3K9me2) 的相关变化.
- 评估GABAB激动剂巴克洛芬在戒断期间对WM和H3K9me2水平的影响.
主要方法:
- 雄性C57BL/6小鼠经历了慢性乙醇暴露,随后进行了为期3周的戒断期.
- 用自发交替T迷宫测试来评估空间WM.
- 通过免疫组织化学分析大脑区域的基因组修饰 (H3K9me2,H3K9ac);在戒断期间服用巴克洛芬.
主要成果:
- 戒酒导致WM损伤,PFC中的H3K9me2降低,伴随着H3K9ac.ac.增加.
- 巴克洛芬治疗使WM性能正常化,并恢复了PFC中的H3K9me2和H3K9ac水平.
- 戒酒导致H3K9me2和H3K9ac的区域特异性变化,PFC H3K9me2水平与WM表现正相关.
结论:
- 戒酒后持续的WM缺陷与PFC H3K9me2.2的长期下降有关.
- 在PFC中的H3K9me2是慢性酒精暴露后维持空间工作记忆的关键表观遗传标记.
- 向G9a基因组甲基转移酶可能为酒精戒断引起的认知障碍提供治疗潜力.
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