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中枢神经系统动脉中的洞穴介导神经血管合
Brian W Chow1, Vicente Nuñez1, Luke Kaplan1
1Department of Neurobiology, Harvard Medical School, Boston, MA, USA.
Nature
|February 21, 2020
概括
动脉内皮细胞通过丰富的洞穴,独立于ENOS-NO信号传递的途径,积极调解神经血管合. 这一发现揭示了一种调节大脑血流的新机制.
科学领域:
- 神经科学
- 血管生物学
- 细胞机制
背景情况:
- 神经血管的合与大脑的能量需求和血液流动相匹配,
- 神经血管合障碍与神经退行性疾病有关,但其机制尚不清楚.
- 传统模型假定神经元或星细胞衍生因素通过光滑肌肉细胞直接扩大动脉.
研究的目的:
- 研究神经血管合的细胞和分子机制.
- 确定动脉内皮细胞 (aEC) 在中介神经血管合中的作用.
- 阐明涉及的具体途径,特别是洞穴和eNOS-NO途径的贡献.
主要方法:
- 在胡须刺激过程中,同时对神经活动和血管动态进行双光子显微镜检测.
- 在aECs中消除洞穴和/或消去内皮NO合成酶 (eNOS) 的急性遗传干扰.
- 在基因操作后评估神经血管合功能.
主要成果:
- 动脉内皮细胞 (aEC) 与其他中枢神经系统内皮细胞不同,具有丰富的洞穴.
- 特别是在aECs中消除洞穴会损害神经血管合,同时节省邻近的光滑肌肉细胞.
- 在aEC中,洞穴介导途径在很大程度上独立于eNOS-NO途径.
- 洞穴和eNOS的联合切除完全消除了神经血管合,这表明洞穴通路的重要作用.
结论:
- 动脉内皮细胞 (aECs) 在神经血管合中发挥着积极的关键作用.
- 在aEC中,一种新的洞穴依赖性途径是调节大脑血流的主要贡献者.
- 这种途径积极地将来自中枢神经系统的信号传递给平滑肌肉细胞以进行血管扩张.
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