Bola R Aaron, Kiyatkin Eugene A
Behavioral Neuroscience Branch, National Institute on Drug Abuse-Intramural Research Program, National Institutes of Health, Baltimore, Maryland.
J Neurophysiol. 2018 Feb 1;119(2):499-508. doi: 10.1152/jn.00692.2017. Epub 2017 Nov 8.
As an essential part of sympathetic activation that prepares the organism for "fight or flight," peripheral norepinephrine (NE) plays an important role in regulating cardiac activity and the tone of blood vessels, increasing blood flow to the heart and the brain and decreasing blood flow to the organs not as necessary for immediate survival. To assess whether this effect is applicable to the brain, we used high-speed amperometry to measure the changes in nucleus accumbens (NAc) levels of oxygen and glucose induced by intravenous injections of NE in awake freely moving rats. We found that NE at low doses (2-18 μg/kg) induces correlative increases in NAc oxygen and glucose, suggesting local vasodilation and enhanced entry of these substances in brain tissue from the arterial blood. By using temperature recordings from the NAc, temporal muscle, and skin, we show that this central effect is associated with strong skin vasoconstriction and phasic increases in intrabrain heat production, indicative of metabolic neural activation. A tight direct correlation between NE-induced changes in metabolic activity and NAc levels of oxygen and glucose levels suggests that local cerebral vasodilation is triggered via a neurovascular coupling mechanism. Our data suggest that NE, by changing vascular tone and cardiac activity, triggers a visceral sensory signal that rapidly reaches the central nervous system via sensory nerves and induces neural activation. This neural activation leads to a chain of neurovascular events that promote entry of oxygen and glucose in brain tissue, thus preventing any possible metabolic deficit during functional activation. NEW & NOTEWORTHY Using high-speed amperometry and thermorecording in freely moving rats, we demonstrate that intravenous norepinephrine at physiological doses induces rapid correlative increases in nucleus accumbens oxygen and glucose levels coupled with increased intrabrain heat production. Although norepinephrine cannot cross the blood-brain barrier, by changing cardiac activity and vascular tone, it creates a sensory signal that reaches the central nervous system via sensory nerves, induces neural activation, and triggers a chain of neurovascular events that promotes intrabrain entry of oxygen and glucose.
作为交感神经激活的重要组成部分,它使机体做好“战斗或逃跑”的准备,外周去甲肾上腺素(NE)在调节心脏活动和血管张力、增加心脏和大脑的血流量以及减少流向对即时生存并非必需的器官的血流量方面发挥着重要作用。为了评估这种效应是否适用于大脑,我们使用高速安培法测量了清醒自由活动大鼠静脉注射NE后伏隔核(NAc)中氧气和葡萄糖水平的变化。我们发现低剂量(2 - 18μg/kg)的NE会引起NAc中氧气和葡萄糖的相关增加,这表明局部血管舒张以及这些物质从动脉血进入脑组织的量增加。通过记录NAc、颞肌和皮肤的温度,我们表明这种中枢效应与强烈的皮肤血管收缩和脑内热产生的阶段性增加有关,这表明存在代谢性神经激活。NE诱导的代谢活动变化与NAc中氧气和葡萄糖水平之间紧密的直接相关性表明,局部脑血管舒张是通过神经血管耦合机制触发的。我们的数据表明,NE通过改变血管张力和心脏活动,触发一种内脏感觉信号,该信号通过感觉神经迅速到达中枢神经系统并诱导神经激活。这种神经激活导致一系列神经血管事件,促进氧气和葡萄糖进入脑组织,从而防止功能激活期间任何可能的代谢不足。新发现及值得注意的是,在自由活动的大鼠中使用高速安培法和温度记录,我们证明生理剂量的静脉注射去甲肾上腺素会导致伏隔核中氧气和葡萄糖水平迅速相关增加,同时脑内热产生增加。尽管去甲肾上腺素不能穿过血脑屏障,但通过改变心脏活动和血管张力,它会产生一种通过感觉神经到达中枢神经系统的感觉信号,诱导神经激活,并触发一系列神经血管事件,促进氧气和葡萄糖进入脑内。