二氧化碳增加时脑血流调节中的神经血管耦联。
Neurovascular coupling during hypercapnia in cerebral blood flow regulation.
机构信息
Hotchkiss Brain Institute, Department of Physiology and Pharmacology, Cumming School of Medicine, University of Calgary, Calgary, AB, T2N 4N1, Canada.
出版信息
Nat Commun. 2024 Sep 2;15(1):7636. doi: 10.1038/s41467-024-50165-8.
Abstract
Neuronal activity consumes cellular energy and generates carbon dioxide (CO). To counter this metabolic challenge, synaptic signalling communicates with nearby microvasculature to increase local blood flow. Is this process solely based on feedforward synaptic signalling, or is the generated CO also involved? This question was addressed in mice in a new Nature Communications publication by Tournissac and colleagues where they showed that neurovascular coupling is not affected by exogenous CO or its associated acidification.
摘要
神经元活动消耗细胞能量并产生二氧化碳（CO）。为了应对这一代谢挑战，突触信号与附近的微血管通讯以增加局部血流。这个过程仅仅基于前馈突触信号，还是生成的 CO 也参与其中？在《自然通讯》杂志上发表的一项新研究中，Tournissac 及其同事在小鼠中解决了这个问题，他们表明神经血管耦合不受外源性 CO 或其相关酸化的影响。
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