The contribution of astrocytes to the regulation of cerebral blood flow.
The contribution of astrocytes to the regulation of cerebral blood flow.
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DOI：
10.3389/fnins.2014.00103
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发表时间：
2014
影响因子：
4.3
通讯作者：
Howarth C
中科院分区：
文献类型：
--
作者：
Howarth C
为了维持正常的脑功能，脑血流量（CBF）与神经元代谢需求相匹配至关重要。因此，血流增加到神经元更活跃的区域（称为功能性充血的反应）。神经元活化、胶质细胞活性、脑能量代谢和脑血管系统之间的紧密关系（称为神经代谢和神经血管耦合）是功能性MRI（fMRI）信号的基础，但尚未完全了解。随着功能成像技术，特别是BOLD功能磁共振成像技术的广泛应用，它们的实用性取决于我们准确可靠地解释结果的能力。越来越多的数据表明，星形胶质细胞可以充当“桥梁”，将神经活动水平的信息传递给血管，以协调氧气和葡萄糖的输送与组织的能量需求。人们普遍认为，星形胶质细胞的血管活性物质的钙依赖性释放导致小动脉扩张和伴随神经元活动的血流量增加。然而，负责星形胶质细胞和血管之间这种通信的信号分子尚未得到明确的证实。事实上，对于活动诱导的星形胶质细胞钙离子变化是否足够广泛和快速以引起这种功能性充血反应存在争议。在这篇综述中，我将总结的证据已经令人信服地证明，星形胶质细胞能够改变脑小动脉的直径。我将讨论刺激诱导的星形胶质细胞钙瞬变的发生率、存在和时间，并描述支持和反对星形胶质细胞钙依赖性血管活性物质形成和释放的证据。我还将审查星形胶质细胞诱发的小动脉直径变化的替代机制，并考虑在这一令人兴奋的研究领域仍有待回答的问题。
In order to maintain normal brain function, it is critical that cerebral blood flow (CBF) is matched to neuronal metabolic needs. Accordingly, blood flow is increased to areas where neurons are more active (a response termed functional hyperemia). The tight relationships between neuronal activation, glial cell activity, cerebral energy metabolism, and the cerebral vasculature, known as neurometabolic and neurovascular coupling, underpin functional MRI (fMRI) signals but are incompletely understood. As functional imaging techniques, particularly BOLD fMRI, become more widely used, their utility hinges on our ability to accurately and reliably interpret the findings. A growing body of data demonstrates that astrocytes can serve as a “bridge,” relaying information on the level of neural activity to blood vessels in order to coordinate oxygen and glucose delivery with the energy demands of the tissue. It is widely assumed that calcium-dependent release of vasoactive substances by astrocytes results in arteriole dilation and the increased blood flow which accompanies neuronal activity. However, the signaling molecules responsible for this communication between astrocytes and blood vessels are yet to be definitively confirmed. Indeed, there is controversy over whether activity-induced changes in astrocyte calcium are widespread and fast enough to elicit such functional hyperemia responses. In this review, I will summarize the evidence which has convincingly demonstrated that astrocytes are able to modify the diameter of cerebral arterioles. I will discuss the prevalence, presence, and timing of stimulus-induced astrocyte calcium transients and describe the evidence for and against the role of calcium-dependent formation and release of vasoactive substances by astrocytes. I will also review alternative mechanisms of astrocyte-evoked changes in arteriole diameter and consider the questions which remain to be answered in this exciting area of research.
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DOI：
10.1073/pnas.95.26.15741
发表时间：
1998-12-22
影响因子：
11.1
作者：
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影响因子：
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影响因子：
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作者：
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