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在小鼠模型中,OPRM1 (mu-opioid受体基因) A112G多态性对双氧化和可卡因自我管理行为的影响
Yong Zhang1, Matthew Randesi1, Julie A Blendy2
1Laboratory of the Biology of Addictive Diseases, the Rockefeller University, New York, NY 10065, United States.
Neuroscience
|January 11, 2024
概括
穆阿片类受体 (OPRM1) 基因的遗传变异影响了氧化和可卡因的联合摄入. 这项研究表明,特定的OPRM1基因变异增加了两种药物的自我管理,并改变了奖励途径基因表达.
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:
- 同时使用片受体 (MOP-r) 激动剂,如氧化和可卡因正在增加,导致更多的过量死亡.
- 在OPRM1基因 (MOP-r基因) 中的功能单核酸多态 (SNPs) 在使个体倾向于双重阿片类药物和精神兴奋剂摄入中的作用仍然不清楚.
- 双重自我管理 (SA) 的MOP-r激动剂和可卡因尚未被广泛研究,特别是关于神经生物学变化.
研究的目的:
- 调查OPRM1基因SNP A118G对氧化SA以及随后的双氧化和可卡因SA的影响.
- 为了将SA行为和神经生物学变化与A118G功能遗传变异 (A/G和G/G基因型) 的小鼠与野生类型 (A/A) 的小鼠进行比较.
- 为了检查与奖励相关的基因表达在背上条纹体的变化后的双重药物SA.
主要方法:
- 具有A/G,G/G和A/A基因型的雄性和雌性小鼠在10天内自行服用氧化.
- 在接受氧化SA后,小鼠接受了10天的双重SA,在氧化后接受了可卡因.
- 在SA.后分析了24个奖励相关基因的背上条纹mRNA水平.
主要成果:
- 与A/A小鼠相比,具有A/G和G/G基因型的小鼠表现出明显更大的氧化SA.
- 在A/G和G/G小鼠中,双SA阶段也显示可卡因摄入量增加.
- 氧化和可卡因的SA改变了背上条纹体中的Pdyn,Fkbp5,Oprk1和Oprm1的mRNA水平.
结论:
- 在OPRM1基因的功能遗传变异显著影响双重阿片类药物和可卡因SA.
- 这种遗传变异导致状体的奖励通路内的基因表达发生改变.
- 这些发现突出了OPRM1基因型在对氧化和可卡因联合使用的敏感性中的作用.
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