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多巴胺载体淘汰老鼠显示表观遗传变化,以应对可卡因暴露

Samara Vilca^1,2, Claes Wahlestedt^1,2, Sari Izenwasser¹

¹Department of Psychiatry and Behavioral Sciences, Miller School of Medicine, University of Miami, Miami, FL 33136, USA.

|July 29, 2023

概括

向表观遗传调节剂氨酸脱甲基酶6B (KDM6B) 和含原蛋白4 (BRD4) 可能为可卡因使用障碍 (CUD) 提供新的治疗方法. 这些对可卡因反应的表观遗传变化取决于性别,这表明了量身定制的治疗策略.

科学领域:

神经科学是一个神经科学.
药理学药理学是指药理学的学科.
遗传学是一个遗传学.

背景情况:

可卡因使用障碍 (CUD) 缺乏有效的治疗方法,需要新的治疗策略.
表观遗传机制正在成为CUD药物治疗的有希望的标.
多巴胺载体 (DAT) 转基因大鼠作为CUD易感性研究的新型模型.

研究的目的:

研究慢性可卡因暴露对表观遗传调节器KDM6B和BRD4.4的影响.
检查前额皮层 (PFC) 内这些表观遗传标记的性别和基因型依赖的变化.
探索针对KDM6B和BRD4进行CUD治疗的潜力.

主要方法:

慢性使用可卡因 (10毫克/公斤8天) 给DAT转基因大鼠 (野生型,异合体和淘汰赛).
在前额皮层 (PFC) 中分析KDM6B和BRD4表达.
通过不同基因型和性别对表观遗传标记表达的比较.

主要成果:

可卡因改变了KDM6B和BRD4的表达方式,取决于性别和基因型.
在使用可卡因后,HET雄性大鼠的KDM6B和BRD4表达减少,而HET雌性大鼠的表达增加.
科伊大鼠表现出BRD4表达的增加,科伊雌性也表现出KDM6B表达的显著增加,在雌性中观察到的效果更大.

结论:

表观遗传调节器KDM6B和BRD4与对可卡因的神经生物学反应有关.
对KDM6B和BRD4表达的性别特异性改变表明,这些标在性别依赖的成机制中起着作用.
针对KDM6B和/或BRD4可能是一个可行的治疗途径,以性别特定的方式治疗CUD相关的行为.

关键词:

这就是BRD4D.这一数据,就是这就是KDM6B.这是可卡因,可卡因.表观遗传学是指表观遗传学.淘汰赛淘汰赛是一个淘汰赛.

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