Laboratory of General Physiology, Department of Biology and Biotechnology "L. Spallanzani", University of Pavia, 27100 Pavia, Italy.
Department of Biomedicine, School of Medicine, Benemérita Universidad Autónoma de Puebla, Puebla 72410, Mexico.
Int J Mol Sci. 2024 Aug 21;25(16):9071. doi: 10.3390/ijms25169071.
Nitric oxide (NO) is a highly versatile gasotransmitter that has first been shown to regulate cardiovascular function and then to exert tight control over a much broader range of processes, including neurotransmitter release, neuronal excitability, and synaptic plasticity. Endothelial NO synthase (eNOS) is usually far from the mind of synaptic neurophysiologists, who have focused most of their attention on neuronal NO synthase (nNOS) as the primary source of NO at the neurovascular unit (NVU). Nevertheless, the available evidence suggests that eNOS could also contribute to generating the burst of NO that, serving as volume intercellular messenger, is produced in response to neuronal activity in the brain parenchyma. Herein, we review the role of eNOS in both the regulation of cerebral blood flow and of synaptic plasticity and discuss the mechanisms by which cerebrovascular endothelial cells may transduce synaptic inputs into a NO signal. We further suggest that eNOS could play a critical role in vascular-to-neuronal communication by integrating signals converging onto cerebrovascular endothelial cells from both the streaming blood and active neurons.
一氧化氮（NO）是一种多功能气体递质，最初被证明可以调节心血管功能，然后对更广泛的过程进行严格控制，包括神经递质释放、神经元兴奋性和突触可塑性。内皮型一氧化氮合酶（eNOS）通常与突触神经生理学家的思维相去甚远，他们将大部分注意力集中在神经元型一氧化氮合酶（nNOS）上，将其视为神经血管单元（NVU）中 NO 的主要来源。然而，现有证据表明，eNOS 也可能有助于产生 NO 爆发，作为容积细胞间信使，NO 是对脑实质神经元活动的反应产生的。本文综述了 eNOS 在调节脑血流和突触可塑性中的作用，并讨论了脑血管内皮细胞将突触输入转导为 NO 信号的机制。我们进一步提出，eNOS 可以通过整合来自血流和活性神经元的信号，在血管到神经元的通讯中发挥关键作用。
