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首页> 外文期刊>Nature >Calcium transients in astrocyte endfeet cause cerebrovascular constrictions
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Calcium transients in astrocyte endfeet cause cerebrovascular constrictions

机译：星形胶质细胞末端的钙瞬变引起脑血管收缩

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摘要

Cerebral blood flow (CBF) is coupled to neuronal activity and is imaged in vivo to map brain activation(1). CBF is also modified by afferent projection fibres that release vasoactive neurotransmitters(2,3) in the perivascular region, principally on the astrocyte endfeet(4,5) that outline cerebral blood vessels(6). However, the role of astrocytes in the regulation of cerebrovascular tone remains uncertain. Here we determine the impact of intracellular Ca2+ concentrations ([Ca2+](i)) in astrocytes on the diameter of small arterioles by using two-photon Ca2+ uncaging(7,8) to increase [Ca2+](i). Vascular constrictions occurred when Ca2+ waves evoked by uncaging propagated into the astrocyte endfeet and caused large increases in [Ca2+](i). The vasoactive neurotransmitter noradrenaline(2,3) increased [Ca2+](i) in the astrocyte endfeet, the peak of which preceded the onset of arteriole constriction. Depressing increases in astrocyte [Ca2+](i) with BAPTA inhibited the vascular constrictions in noradrenaline. We find that constrictions induced in the cerebrovasculature by increased [Ca2+](i) in astrocyte endfeet are generated through the phospholipase A(2)-arachidonic acid pathway and 20-hydroxyeicosatetraenoic acid production. Vasoconstriction by astrocytes is a previously unknown mechanism for the regulation of CBF.
机译：脑血流（CBF）与神经元活动耦合，并在体内成像以绘制大脑激活图（1）。 CBF还可以通过传入的投射纤维进行修饰，这些投射纤维可以在血管周围区域释放血管活性神经递质（2,3），主要是在勾勒出大脑血管的星形胶质细胞末端（4,5）上（6）。然而，星形胶质细胞在调节脑血管张力中的作用仍不确定。在这里，我们通过使用两光子Ca2 +解笼（7,8）增加[Ca2 +]（i），确定星形胶质细胞中细胞内Ca2 +浓度（[Ca2 +]（i））对小动脉直径的影响。当通过解开引起的Ca2 +波传播到星形胶质细胞的末端时，会引起血管收缩，并导致[Ca2 +]（i）大量增加。星形胶质细胞末端的血管活性神经递质去甲肾上腺素（2,3）增加[Ca2 +]（i），其峰值先于小动脉收缩发作。 BAPTA抑制星形胶质细胞[Ca2 +]（i）的增加会抑制去甲肾上腺素的血管收缩。我们发现星形胶质细胞末端增加[Ca2 +]（i）在脑血管系统中引起的收缩是通过磷脂酶A（2）-花生四烯酸途径和20-羟基二十碳四烯酸生产而产生的。星形胶质细胞的血管收缩是调节CBF的先前未知的机制。

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