Neurovascular coupling is not mediated by potassium siphoning from glial cells
Neurovascular coupling is not mediated by potassium siphoning from glial cells
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DOI：
10.1523/jneurosci.3204-06.2007
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发表时间：
2007-03-07
影响因子：
5.3
通讯作者：
Newman, Eric A.
中科院分区：
文献类型：
--
作者：
Metea, Monica R.;Kofuji, Paulo;Newman, Eric A.
神经元活动引起局部血流变化，这种反应称为神经血管耦合。一个被广泛认可的神经血管偶联假说认为，神经元活动引起的胶质细胞去极化导致K+释放到血管（K+虹吸）和血管舒张。我们现在提出两个直接测试这个胶质细胞-K+虹吸假说的神经血管耦合。通过对单个细胞施加去极化电流脉冲，从大鼠视网膜的胶质细胞中诱发钾外流。胶质细胞去极化高达100 mV，相邻小动脉的直径没有变化。我们还监测了Kir4.1基因敲除小鼠的光诱发血管反应，其中视网膜神经胶质细胞中不存在功能性Kir K+通道。Kir4.1基因敲除和野生型动物的光诱发血管舒张的幅度是相同的。相反的假设，结果表明，神经胶质细胞K+虹吸在视网膜中并没有显着的神经血管耦合。
Neuronal activity evokes localized changes in blood flow, a response termed neurovascular coupling. One widely recognized hypothesis of neurovascular coupling holds that glial cell depolarization evoked by neuronal activity leads to the release of K+ onto blood vessels (K+ siphoning) and to vessel relaxation. We now present two direct tests of this glial cell-K+ siphoning hypothesis of neurovascular coupling. Potassium efflux was evoked from glial cells in the rat retina by applying depolarizing current pulses to individual cells. Glial depolarizations as large as 100 mV produced no change in the diameter of adjacent arterioles. We also monitored light-evoked vascular responses in Kir4.1 knock-out mice, where functional Kir K+ channels are absent from retinal glial cells. The magnitude of light-evoked vasodilations was identical in Kir4.1 knock-out and wild-type animals. Contrary to the hypothesis, the results demonstrate that glial K+ siphoning in the retina does not contribute significantly to neurovascular coupling.