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天体细胞末脚中的过渡性会导致脑血管收缩

Sean J Mulligan¹, Brian A MacVicar

¹Brain Research Centre, Department of Psychiatry, University of British Columbia, 2211 Wesbrook Mall, Vancouver, BC, Canada, V6T 2B5.

|September 10, 2004

概括

星球细胞通过收缩动脉小管来调节大脑血流 (CBF). 天体细胞末脚中细胞内的增加通过脂酶A2-阿拉基酸通路触发了血管收缩,揭示了新的CBF调节机制.

科学领域:

神经科学是一个神经科学.
血管生物学血管生物学
细胞生理学细胞生理学

背景情况:

大脑血流 (CBF) 的调节对大脑功能至关重要,与神经元活动有关.
星球细胞,围绕血管的质细胞,与大脑血管系统相互作用,但它们在调节血管度方面的作用尚不清楚.
血管活性神经递质通过作用于周围细胞,包括星球细胞末端,影响CBF.

研究的目的:

研究细胞内度 ([Ca2+]) 在星球细胞中调节大脑动脉小动脉直径的作用.
阐明涉及天体细胞介导的大脑血管调的信号通路.

主要方法:

利用双光子Ca2+) 解来操纵星体细胞内的细胞内水平.
作为对诱导的的波动的反应,测量了动脉直径的变化.
研究了脂酶A(2) - 阿拉基酸通路和20-基酸 (20-HETE) 在血管收缩中的参与.

主要成果:

增加[Ca2+]在天体细胞末端的脚部,由脱或诺亚上腺素触发,导致动脉收缩.
波传播到天体细胞末脚之前可观察到的血管收缩.
抑制的增加与BAPTA减弱的上腺素诱导的血管收缩.
星细胞介导的血管收缩涉及脂酶A(2) - 阿拉基酸通路和20-HETE的产生.

结论:

星球细胞通过依赖的机制积极调节脑血管度.
在天体细胞末端增加的细胞内会诱导动脉狭窄.
这种由天体细胞介导的血管收缩代表了调节大脑血流的新途径.

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