在慢性压力模型中,电通过微质重编程促进了BDNF依赖的神经发生
Lijuan Zhang1,2,3,4, Ting Wei1, Xuan Liu1
1Acupuncture and Tuina School, Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan, China.
电针 (EA) 通过将微质转化为亲神经的状态来缓解抑郁症. 这一过程通过PKA/MeCP2/BDNF途径增强脑衍生神经营养因子 (BDNF) 信号传递,促进海马神经发生和突触可塑性.
科学领域:
- 神经科学是一个神经科学.
- 整合和补充医学是整合和补充医学.
- 分子生物学分子生物学
背景情况:
- 异常的微质激活和受损的成年海马神经发生因应于抑郁症.
- 电针 (EA) 显示出临床抗抑郁作用,但其涉及微质和神经发生的机制尚不清楚.
研究的目的:
- 研究EA如何调节微质活动并促进海马神经发生.
- 阐明涉及EA抗抑郁作用的分子通路,包括BDNF信号传递.
主要方法:
- 小鼠经历了慢性不可预测的轻度压力 (CUMS),并接受EA,伊米普拉或车载治疗.
- 行为测试 (糖糖偏好,强迫游泳,尾部悬浮,开放场地,高空加迷宫) 评估了抑郁和焦虑.
- 免疫光学,戈尔吉染色,西部斑点和qRT-PCR分析了微质表型,神经发生和BDNF信号传递.
- 功能丧失实验使用微质切除 (PLX5622) 和TrkB阻断 (ANA-12).
主要成果:
- EA显著减少了CUMS诱导的焦虑抑郁行为.
- 在海马体中,EA诱导了微质表型向亲神经原性状态的转变.
- 微质切除取消了EA的治疗作用,证实了它们的必要性.
- 通过PKA激活和MeCP2-介导的转录释放,EA通过上调BDNF信号来增强海马神经发生.
结论:
- 通过促进微质转化为亲神经原性表型,EA 发挥抗抑郁作用.
- PKA/MeCP2/BDNF通路调解EA增强海马神经发生和突触可塑性.
- 向微质细胞和BDNF信号传递代表了抑郁症的潜在治疗策略.
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