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通过Bdnf-e2-通过TrkB激活表达神经元来调节腹感 - - 在中腔下丘脑中表达神经元
Pengcheng Chu1,2, Wei Guo1, He You1,2
1School of Pharmaceutical Sciences, IDG/McGovern Institute for Brain Research, Tsinghua University, Beijing 100084, China.
Biomolecules
|May 27, 2023
概括
大脑衍生神经营养因子 (BDNF) 促进剂e2对于调节能量平衡至关重要. 通过VMH和TrkB途径影响和能量摄入,破坏小鼠中的这种促进剂会导致肥胖.
科学领域:
- 神经科学是一个神经科学.
- 代谢调节 代谢调节 代谢调节 代谢调节
- 分子生物学分子生物学
背景情况:
- 大脑衍生神经营养因子 (BDNF) 在大脑中扮演着不同的角色,由各种促进者调节.
- 在控制能量平衡和新陈代谢方面,BDNF促进剂的具体作用尚未完全理解.
研究的目的:
- 研究特定BDNF促进体在调节能量平衡中的作用.
- 确定关键的BDNF促进体和参与控制肥胖的脑区域.
主要方法:
- 使用了带有破坏BDNF促进体 (e1,e2,e4,e6) 的转基因小鼠.
- 评估了代谢表型,包括肥胖,发热,过和腹.
- 研究了BDNF转录表达在中腹下丘脑 (VMH).
- 在VMH神经元中使用遗传操纵 (再表达,TrkB删除) 和化学遗传学.
- 将TrkB激动性抗体注射到VMH中.
主要成果:
- 破坏BDNF促进剂e1和e2,但不是e4或e6,导致小鼠肥胖.
- 破坏BDNF促进体e2导致过和减少腹感,主要与VMH表达有关.
- 在VMH中恢复BDNF e2转录或激活VMH神经元改善了肥胖和过.
- 在VMH神经元中的TrkB受体信号传递对于调节能量摄入和腹感至关重要.
结论:
- 在VMH神经元中的BDNF促进体e2转录对于调节能量摄入和腹感至关重要.
- BDNF e2-VMH-TrkB 途径是能量平衡和肥胖的一个关键调节器.
- 针对这种途径为代谢障碍提供了潜在的治疗策略.
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