Department of Biology and Biotechnology "Lazzaro Spallanzani", Laboratory of General Physiology, University of Pavia, Pavia, Italy.
Department of Brain and Behavioral Sciences, University if Pavia, Pavia, Italy.
Int J Biochem Cell Biol. 2021 Jun;135:105983. doi: 10.1016/j.biocel.2021.105983. Epub 2021 Apr 21.
Neurovascular coupling (NVC) represents the mechanisms whereby an increase in neuronal activity (NA) may lead to local vasodilation and increase in regional cerebral blood flow (CBF). It has long been thought that neurons and astrocytes generate the vasoactive mediators regulating local changes in CBF, whereas cerebrovascular endothelial cells are not able to directly sense NA. Unexpectedly, recent evidence demonstrated that brain microvascular endothelial cells may sense NA through inward-rectifier K (K2.1) channels and may detect synaptic activity via N-methyl-d-aspartate (NMDA) receptors (NMDARs). In the present perspective, therefore, we discuss the hypothesis that endothelial K2.1 channels and NMDARs play a key role in NVC and in CBF regulation, which is crucial to unravel the cellular and molecular underpinnings of blood oxygen level-dependent signals.
神经血管耦合（NVC）代表了神经元活动（NA）增加可能导致局部血管扩张和局部脑血流（CBF）增加的机制。长期以来，人们一直认为神经元和星形胶质细胞产生调节局部 CBF 变化的血管活性介质，而脑血管内皮细胞不能直接感知 NA。出乎意料的是，最近的证据表明，脑微血管内皮细胞可能通过内向整流钾（K2.1）通道感知 NA，并通过 N-甲基-D-天冬氨酸（NMDA）受体（NMDARs）检测突触活动。因此，在本观点中，我们讨论了内皮 K2.1 通道和 NMDAR 在 NVC 和 CBF 调节中起关键作用的假说，这对于揭示血氧水平依赖信号的细胞和分子基础至关重要。
