高血压通过增强内胆固醇附带连接来增加交感神经元活动
Minghua Li1, Michelle Sorensen1, Morgan A Johnson1
1Department of Chemical Physiology and Biochemistry, Oregon Health and Science University, Portland, OR, USA.
高血压通过增强的胆固醇附带传播增加星状质中的交感神经元活动,从而导致心血管疾病. 这种外围神经可塑性驱动同情性过度活动,独立于中枢神经系统信号.
科学领域:
- 神经科学是一个神经科学.
- 心血管生物学 心血管生物学
- 身体生理学 身体生理学
背景情况:
- 自主调节失调和交感性多动性在高血压 (HT) 和心血管疾病中很常见.
- 虽然中枢神经系统 (CNS) 影响交感激活,但外围神经可塑性也可能有所贡献.
- 在持续的多动性中,后质交感神经元的作用尚不清楚.
研究的目的:
- 调查假设,星状质神经元 (SG) 的重塑和增加胆固醇附带传输有助于HT的交感性过活性的假设.
- 在受控和高血压条件下检查孤立的SG中交感神经元的活动.
主要方法:
- 用全细胞补丁记录来评估孤立SG中的交感神经元活动.
- 在小鼠中,通过外周血管新素II输液诱导高血压.
- 在noradrenergic神经元中的胆固醇传播被基因破坏以评估其作用.
主要成果:
- 高血压小鼠在SG交感神经元中表现出高的自发活动和突触传输,独立于中枢神经系统输入.
- 干扰胆固醇传输减少了基底神经元活动,并阻止了HT诱导的增强.
- 在心脏和棕色脂肪组织投射神经元中观察到由附带传播驱动的活性增加.
结论:
- 高血压刺激了SG中胆固醇附带连接的脉内网络中的活性增加.
- 这种外围机制有助于心血管疾病中持续的同情性过度活跃.
- 这些发现强调了外围神经可塑性在与高血压相关的自主功能障碍中发挥的新角色.
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