Neuronal activity within the brain evokes local increases in blood flow, a response termed functional hyperemia. This response ensures that active neurons receive sufficient oxygen and nutrients to maintain tissue function and health. In this review, we discuss the functions of functional hyperemia, the types of vessels that generate the response, and the signaling mechanisms that mediate neurovascular coupling, the communication between neurons and blood vessels. Neurovascular coupling signaling is mediated primarily by the vasoactive metabolites of arachidonic acid (AA), by nitric oxide, and by K⁺. While much is known about these pathways, many contentious issues remain. We highlight two controversies, the role of glial cell Ca²⁺ signaling in mediating neurovascular coupling and the importance of capillaries in generating functional hyperemia. We propose signaling pathways that resolve these controversies. In this scheme, capillary dilations are generated by Ca²⁺ increases in astrocyte endfeet, leading to production of AA metabolites. In contrast, arteriole dilations are generated by Ca²⁺ increases in neurons, resulting in production of nitric oxide and AA metabolites. Arachidonic acid from neurons also diffuses into astrocyte endfeet where it is converted into additional vasoactive metabolites. While this scheme resolves several discrepancies in the field, many unresolved challenges remain and are discussed in the final section of the review.

大脑中的神经元活动引起局部​​血流增加，这种反应称为功能性充血。这种反应可确保活跃的神经元接受足够的氧气和营养以维持组织功能和健康。在这篇综述中，我们讨论了功能性充血的功能，产生反应的血管的类型以及介导神经血管耦合，神经元与血管之间的通讯的信号传导机制。神经血管偶联信号主要由花生四烯酸（AA）的血管活性代谢产物，一氧化氮和K ⁺介导。尽管对这些途径的了解很多，但仍有许多有争议的问题。我们强调了两个争议，胶质细胞Ca ²⁺的作用介导神经血管偶联的信号传导以及毛细血管在产生功能性充血中的重要性。我们提出了解决这些争议的信号传导途径。在该方案中，星形胶质细胞尾足中Ca ^2+的增加会产生毛细血管扩张，从而导致AA代谢产物的产生。相反，神经元中Ca ^2+的增加会产生小动脉扩张，导致产生一氧化氮和AA代谢产物。来自神经元的花生四烯酸也扩散到星形胶质细胞的尾气中，并在那里转化为其他血管活性代谢产物。尽管该方案解决了该领域的一些差异，但仍有许多未解决的挑战，将在本综述的最后一部分中进行讨论。