Glial Cell Calcium Signaling Mediates Capillary Regulation of Blood Flow in the Retina

被引:117
作者
Biesecker, Kyle R. [1 ]
Srienc, Anja I. [1 ]
Shimoda, Angela M. [1 ]
Agarwal, Amit [2 ]
Bergles, Dwight E. [2 ]
Kofuji, Paulo [1 ]
Newman, Eric A. [1 ]
机构
[1] Univ Minnesota Twin Cities, Dept Neurosci, 6-145 Jackson Hall,321 Church St SE, Minneapolis, MN 55455 USA
[2] Johns Hopkins Univ, Sch Med, Solomon H Snyder Dept Neurosci, Baltimore, MD 21205 USA
关键词
blood flow; calcium signaling; capillary; glia; neurovascular coupling; retina; NITRIC-OXIDE SYNTHASE; CORTEX IN-VIVO; FUNCTIONAL HYPEREMIA; ALZHEIMERS-DISEASE; NEURONAL-ACTIVITY; VASCULAR NETWORK; NORMAL BRAIN; PERICYTES; MOUSE; RESPONSES;
D O I
10.1523/JNEUROSCI.1782-16.2016
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The brain is critically dependent on the regulation of blood flow to nourish active neurons. One widely held hypothesis of blood flow regulation holds that active neurons stimulate Ca2+ increases in glial cells, triggering glial release of vasodilating agents. This hypothesis has been challenged, as arteriole dilation can occur in the absence of glial Ca2+ signaling. We address this controversy by imaging glial Ca2+ signaling and vessel dilation in the mouse retina. We find that sensory stimulation results in Ca2+ increases in the glial endfeet contacting capillaries, but not arterioles, and that capillary dilations often follow spontaneous Ca2+ signaling. In IP3R2(-/-) mice, where glial Ca2+ signaling is reduced, light-evoked capillary, but not arteriole, dilation is abolished. The results show that, independent of arterioles, capillaries actively dilate and regulate blood flow. Furthermore, the results demonstrate that glial Ca2+ signaling regulates capillary but not arteriole blood flow.
引用
收藏
页码:9435 / 9445
页数:11
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