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在腹核中的HMGB1-RAGE轴通过调节微质激活来促进可卡因诱导的有条件位置偏好

Jian Ye¹, Shuang-Qi Gao^1,2, Zi-Cun Liu¹

¹Department of Pharmacology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Brain and behavior

|March 7, 2024

概括

神经高移动性组盒-1 (HMGB1) 通过RAGE激活微质,促进可卡因奖励记忆. 针对HMGB1-RAGE轴可能为可卡因成提供新的治疗方法.

科学领域:

神经科学是一个神经科学.
神经炎症是一种神经炎症.
成研究研究成研究

背景情况:

重复暴露于可卡因会激活微质,并从核突 (NAc) 中的神经元中释放高流动性组盒-1 (HMGB1).
HMGB1是关键的炎症调解剂,但其在可卡因成和微质激活中的作用尚不清楚.

研究的目的:

研究HMGB1介导的微质激活在可卡因奖励记忆的发展中的作用.
探索HMGB1-RAGE轴作为可卡因成的潜在治疗目标.

主要方法:

鼠被训练使用可卡因的管理和有条件的位置偏好 (CPP).
使用病毒载体操纵HMGB1表达;用米诺环素抑制微质激活.
使用特定的 (盒子A) 阻止了HMGB1-RAGE相互作用.

主要成果:

可卡因的使用增加了HMGB1信号,并在NAc中延迟了微质激活.
抑制HMGB1或微质激活减弱可卡因诱导的CPP.
阻止HMGB1-RAGE相互作用消除了可卡因奖励记忆,并抑制了可卡因诱导的微质激活.

结论:

神经HMGB1通过RAGE激活微质,在巩固可卡因奖励记忆中发挥关键作用.
HMGB1-RAGE轴代表了治疗可卡因成的新型治疗标.

关键词:

吸食可卡因成吸食可卡因成有条件的地方偏好偏好.高流动性小组框-1 高流动性小组框-1 微质细胞中的微质细胞对于高级糖化最终产品的受体.

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