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NOS 中间神经元在脑血管调节生理学中的复杂贡献。

The complex contribution of NOS interneurons in the physiology of cerebrovascular regulation.

机构信息

Department of Pharmacology, Université de Montréal Montreal, QC, Canada.

出版信息

Front Neural Circuits. 2012 Aug 9;6:51. doi: 10.3389/fncir.2012.00051. eCollection 2012.

DOI:10.3389/fncir.2012.00051
PMID:22907993
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3414732/
Abstract

Following the discovery of the vasorelaxant properties of nitric oxide (NO) by Furchgott and Ignarro, the finding by Bredt and coll. of a constitutively expressed NO synthase in neurons (nNOS) led to the presumption that neuronal NO may control cerebrovascular functions. Consequently, numerous studies have sought to determine whether neuraly-derived NO is involved in the regulation of cerebral blood flow (CBF). Anatomically, axons, dendrites, or somata of NO neurons have been found to contact the basement membrane of blood vessels or perivascular astrocytes in all segments of the cortical microcirculation. Functionally, various experimental approaches support a role of neuronal NO in the maintenance of resting CBF as well as in the vascular response to neuronal activity. Since decades, it has been assumed that neuronal NO simply diffuses to the local blood vessels and produce vasodilation through a cGMP-PKG dependent mechanism. However, NO is not the sole mediator of vasodilation in the cerebral microcirculation and is known to interact with a myriad of signaling pathways also involved in vascular control. In addition, cerebrovascular regulation is the result of a complex orchestration between all components of the neurovascular unit (i.e., neuronal, glial, and vascular cells) also known to produce NO. In this review article, the role of NO interneuron in the regulation of cortical microcirculation will be discussed in the context of the neurovascular unit.

摘要

继 Furchgott 和 Ignarro 发现一氧化氮(NO)具有血管舒张特性之后,Bredt 及其同事发现神经元中存在一种组成型表达的一氧化氮合酶(nNOS),这使得人们推测神经元 NO 可能控制脑血管功能。因此,许多研究试图确定神经源性 NO 是否参与调节脑血流量(CBF)。从解剖学上看,NO 神经元的轴突、树突或体都被发现与皮质微循环的所有节段的血管基底膜或血管周围星形胶质细胞接触。从功能上看,各种实验方法支持神经元 NO 在维持静息 CBF 以及在神经元活动引起的血管反应中的作用。几十年来,人们一直认为神经元 NO 可以简单地扩散到局部血管,并通过 cGMP-PKG 依赖性机制引起血管舒张。然而,NO 并不是脑微循环中血管舒张的唯一介质,并且已知它与许多也参与血管控制的信号通路相互作用。此外,脑血管调节是神经血管单元(即神经元、神经胶质和血管细胞)所有组成部分之间复杂协调的结果,这些细胞也被认为可以产生 NO。在这篇综述文章中,将从神经血管单元的角度讨论 NO 中间神经元在调节皮质微循环中的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5504/3414732/8599444a9b64/fncir-06-00051-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5504/3414732/0dcf329d47ae/fncir-06-00051-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5504/3414732/4d49a613d61e/fncir-06-00051-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5504/3414732/8599444a9b64/fncir-06-00051-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5504/3414732/0dcf329d47ae/fncir-06-00051-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5504/3414732/4d49a613d61e/fncir-06-00051-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5504/3414732/8599444a9b64/fncir-06-00051-g0003.jpg

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