大脑中转录因子deltaFosB的表达控制了对可卡因的敏感性
M B Kelz1, J Chen, W A Carlezon
1Laboratory of Molecular Psychiatry and Yale Center for Genes and Behavior, Yale University School of Medicine, New Haven, Connecticut 06508, USA.
Nature
|September 28, 1999
概括
长期暴露于可卡因持续增加大脑中的deltaFosB.
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
- 成研究 研究成研究
背景情况:
- 急性可卡因暴露暂时诱导核中Fos蛋白.
- 长期暴露于可卡因会导致核中持续的deltaFosB表达.
- deltaFosB涉及与慢性药物使用相关的神经可塑性.
研究的目的:
- 调查deltaFosB在调解慢性可卡因暴露的影响中的作用.
- 为了确定deltaFosB诱导是否增强对可卡因奖励和运动运动效应的敏感性.
主要方法:
- 利用转基因小鼠在特定的核中诱导deltaFosB表达.
- 用可卡因评估行为反应和分子变化.
主要成果:
- 诱导的deltaFosB表达增加了对可卡因奖励和运动激活效应的反应.
- 德尔塔B介导的效应部分是由于AMPA谷氨酸受体亚单元GluR2表达的增加.
- 在核中持续的deltaFosB积累与持续的行为变化相关.
结论:
- 德尔塔B在提高对可卡因的敏感性方面发挥着至关重要的作用.
- 由deltaFosB改变的基因表达可能会导致可卡因成的发展.
- 这种转录因子是潜在的成治疗标.
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