在小鼠心房中,从交感神经末端释放神经递质的脂质依赖调节
Julia G Odnoshivkina1, Guzel V Sibgatullina2, Alexey M Petrov3
1Laboratory of Biophysics of Synaptic Processes, Kazan Institute of Biochemistry and Biophysics, Federal Research Center "Kazan Scientific Center of RAS", 2/31 Lobachevsky Street, Box 30, Kazan 420111, Russia; Kazan State Medical University, 49 Butlerova Street, Kazan 420012, Russia.
Biochimica et biophysica acta. Biomembranes
|July 2, 2023
概括
心脏中预突触神经递质的释放受到膜脂质的调节. 胆固醇的氧化增强了释放,而斯芬戈米林的水解抑制了再吸收,影响了心脏调节.
科学领域:
- 神经科学是一个神经科学.
- 心脏病学 心脏病学
- 细胞生物学 细胞生物学
背景情况:
- 交感神经递质释放调节心脏功能.
- 预突触机制,包括再吸收,对于控制神经递质水平至关重要.
研究的目的:
- 为了研究血的血脂在调节神经递质释放和重新吸收在心脏的交感神经终端的作用.
- 阐明胆固醇和基米林的修饰如何影响突触前活动.
主要方法:
- 使用假光神经递质FFN511.11在小鼠心房组织中监测预突触外细胞活动.
- 利用高 (K+) 脱极化诱导神经递质释放.
- 使用reserpine来抑制神经递质的吸收.
- 用胆固醇氧化酶和基胺酶修改心房膜,以评估脂质效应.
- 评估这些修改对FFN511释放和储强化的影响.
主要成果:
- 高K+脱极化诱导FFN511释放,由储增强,表明重新吸收.
- 在耗尽容易释放的池之后,Reserpine的强化被废除了.
- 血胆固醇的氧化增加了FFN511的释放,并强化了保留素的作用.
- 斯芬戈米林水解增强了FFN511的释放速度,但阻断了储的强化.
- 当酶访问回收突触囊泡时,酶效应被抑制,而不是等离子体lemma.
结论:
- 一个快速的神经递质再吸收机制,依赖于囊泡外细胞分裂,发生在交感神经活动.
- 血中的脂质成分,特别是胆固醇和髓,可以动态调节这种再吸收过程.
- 血细胞脂质的修改,而不是囊泡脂质,显著改变引起的神经递质释放,影响心脏调节.
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