分子信号预测皮质脊髓轴突生长状态和肌肉反应可塑性,由神经调节诱导
Neela Zareen1, Halley Yung1, Walter Kaczetow2
1Department of Molecular, Cellular, and Biomedical Sciences, Center for Discovery and Innovation, City University of New York School of Medicine, New York, NY 10031.
电机皮层刺激,特别是间歇性爆刺激 (iTBS),在脊髓损伤 (SCI) 后促进神经可塑性和轴突生长. 通过激活关键分子通路,iTBS显示出增强运动功能的恢复的前景.
科学领域:
- 神经科学是一个神经科学.
- 生物医学工程 生物医学工程
- 再生医学是一种再生医学.
背景情况:
- 电机皮层刺激可以诱导可塑性并改善受伤后的运动功能.
- 了解这种可塑性背后的分子机制对于开发有效疗法至关重要.
- 识别持久可塑性的生物标志物可以指导治疗优化.
研究的目的:
- 研究由电神经调节诱导的结构和生理可塑性的分子机制.
- 在运动皮层刺激后识别耐用可塑性的分子预测因子 (生物标志物).
- 为了比较重复多脉冲刺激 (rMPS) 和间歇性甲爆刺激 (iTBS) 在促进皮质脊髓管 (CST) 发芽和运动唤起潜力 (MEP) 塑性方面的疗效.
主要方法:
- 应用了两种神经调节协议 (rMPS和iTBS),持续时间和随访时间各不相同.
- 评估了皮质脊髓管 (CST) 发芽和运动唤起潜力 (MEP) 的可塑性.
- 分析了包括mTOR,PTEN和Stat3在内的分子信号通路.
- 神经调节是在椎脊髓损伤 (SCI) 的背景下进行的.
主要成果:
- 间歇性爆刺激 (iTBS) 诱导了短期刺激后的CST发芽,而iTBS和重复多脉冲刺激 (rMPS) 诱导了长期刺激后的发芽.
- 在有效的神经调节条件下,mTOR信号的激活和PTEN蛋白的失活预测了轴突的生长.
- 长期的iTBS在产生持续的LTP-like增强30天后,通过Stat3信号的介导,对欧洲议会议员具有独特的有效性.
- 在SCI之后,iTBS促进了Stat3激活,与rMPS不同,这表明运动恢复的潜力更大.
结论:
- 不同的分子生物标志物存在于结构 (轴突生长) 和生理 (MEP可塑性) 神经调节诱导的可塑性.
- 运动皮层外周神经调节诱导了支持轴突生长的分子变化,特别是在SCI后.
- 间歇性甲突破刺激 (iTBS) 似乎更适合SCI修复,因为它能够通过不同的分子途径促进CST生长和MEP可塑性.
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