ATP release and hydrolysis contribute to rat pial arteriolar dilatation elicited by neuronal activation.

ATP release and hydrolysis contribute to rat pial arteriolar dilatation elicited by neuronal activation.
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ATP 释放和水解有助于神经元激活引起的大鼠软脑膜小动脉扩张。

DOI:
10.1113/expphysiol.2006.036863
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发表时间:
2007
影响因子:
2.7
通讯作者:
Pelligrino,DaleA
Pelligrino,DaleA
中科院分区:
医学4区
文献类型:
--
作者:
Xu,Hao-Liang;Pelligrino,DaleA

文献摘要

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由于星形胶质细胞与脑小动脉的密切解剖关系,因此被认为是信号转换器,将信息从激活的神经元传递到大脑微循环。这些转发的信号可能涉及星形胶质细胞末端释放血管活性因子。这种机制被称为“神经血管耦合”,其解剖成分(即神经元、星形胶质细胞和血管细胞)被称为“神经血管单元”。神经血管耦合的过程常常涉及上游扩张。在代谢需求增加期间,这是必要的,以便允许更多的血液到达扩张的下游血管,从而改善对激活的神经元的营养供应。如果没有它,下游扩张可能无效,使神经元处于危险之中,特别是在神经元剧烈活动(例如癫痫发作)期间。在大脑中,软脑膜小动脉代表重要的“上游”血管段。软脑膜小动脉覆盖着一层厚厚的星形胶质细胞突起,称为神经胶质细胞界限。从解剖学上讲,这本质上将软脑膜小动脉与下面的神经元隔离开来。因此,源自神经元的血管舒张信号通过间接途径到达软脑膜小动脉,主要涉及星形胶质细胞和神经胶质细胞。在这里,我们讨论了一个过程,其中嘌呤能机制在星形胶质细胞与星形胶质细胞之间的通讯以及神经胶质细胞向软脑膜小动脉信号导致血管舒张中发挥着关键的神经元活动依赖性作用。
Owing to their intimate anatomical relationship with cerebral arterioles, astrocytes have been postulated as signal transducers, transferring information from activated neurones to the cerebral microcirculation. These forwarded signals may involve the release of vasoactive factors from the end‐feet of astrocytes. This mechanism is termed ‘neurovascular coupling’ and its anatomical components (i.e. neurone, astrocyte and vascular cells) are termed the ‘neurovascular unit’. The process of neurovascular coupling often involves upstream dilatation. This is necessary during periods of increased metabolic demand, in order to permit more blood to reach dilated downstream vessels, thereby improving nutrient supply to the activated neurones. Without it, that downstream dilatation might be ineffective, placing neurones at risk, especially during episodes of intense neuronal activity, such as seizure. In the brain, pial arterioles represent important ‘upstream’ vascular segments. The pial arterioles overlie a thick layer of astrocytic processes, termed the glia limitans. This essentially isolates pial arterioles, anatomically, from the neurones below. Vasodilating signals that originate in the neurones therefore reach the pial arterioles via indirect pathways, primarily involving astrocytes and the glia limitans. Here we discuss a process whereby purinergic mechanisms play a key and neuronal activity‐dependent role in astrocyte to astrocyte communication, as well as in glia limitans to pial arteriolar signals leading to vasodilatation.