OBJECTIVE Cerebral arterial networks match blood flow delivery with neural activity. Neurovascular response begins with a stimulus and a focal change in vessel diameter, which by themselves is inconsequential to blood flow magnitude, until they spread and alter the contractile status of neighboring arterial segments. We sought to define the mechanisms underlying integrated vascular behavior and considered the role of intercellular electrical signaling in this phenomenon. Approach and Results: Electron microscopic and histochemical analysis revealed the structural coupling of cerebrovascular cells and the expression of gap junctional subunits at the cell interfaces, enabling intercellular signaling among vascular cells. Indeed, robust vasomotor conduction was detected in human and mice cerebral arteries after focal vessel stimulation: a response attributed to endothelial gap junctional communication, as its genetic alteration attenuated this behavior. Conducted responses were observed to ascend from the penetrating arterioles, influencing the contractile status of cortical surface vessels, in a simulated model of cerebral arterial network. Ascending responses recognized in vivo after whisker stimulation were significantly attenuated in mice with altered endothelial gap junctional signaling confirming that gap junctional communication drives integrated vessel responses. The diminishment in vascular communication also impaired the critical ability of the cerebral vasculature to maintain blood flow homeostasis and hence tissue viability after stroke. CONCLUSIONS Our findings highlight the integral role of intercellular electrical signaling in transcribing focal stimuli into coordinated changes in cerebrovascular contractile activity and expose, a hitherto unknown mechanism for flow regulation after stroke.

中文翻译：

---

在脑血管挑战期间，细胞间传导可优化动脉网络功能并保持血流稳态。

目的脑动脉网络将血流输送与神经活动相匹配。神经血管反应始于血管直径的刺激和局灶性改变，其本身与血流量无关紧要，直到它们扩散并改变邻近动脉节段的收缩状态为止。我们试图定义潜在的整合血管行为的机制，并考虑了这种现象中细胞间电信号传导的作用。方法和结果：电子显微镜和组织化学分析揭示了脑血管细胞的结构偶联以及细胞界面间隙连接亚基的表达，从而使血管细胞之间能够进行细胞间信号传导。实际上，在局灶性血管刺激后，在人和小鼠的脑动脉中检测到了强大的血管舒缩传导：归因于内皮间隙连接通讯的反应，因为其遗传改变减弱了这种行为。在脑动脉网络的模拟模型中，观察到传导反应从穿透的小动脉上升，影响皮层表面血管的收缩状态。晶须刺激后体内识别出的上升反应在具有改变的内皮间隙连接信号的小鼠中被显着减弱，这证实了间隙连接通信驱动了整合的血管反应。血管通讯的减少也损害了脑血管维持血流动态平衡的关键能力，从而损害了中风后组织的生存能力。