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Sleep/wake dependent changes in cortical glucose concentrations

机译:睡眠/苏醒依赖的皮质葡萄糖浓度变化

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摘要

Most of the energy in the brain comes from glucose and supports glutamatergic activity. The firing rate of cortical glutamatergic neurons, as well as cortical extracellular glutamate levels, increase with time spent awake and decline throughout non rapid eye movement sleep, raising the question whether glucose levels reflect behavioral state and sleep/wake history. Here chronic (2-3 days) electroencephalographic recordings in the rat cerebral cortex were coupled with fixed-potential amperometry to monitor the extracellular concentration of glucose ([gluc]) on a second-by-second basis across the spontaneous sleep-wake cycle and in response to 3 h of sleep deprivation. [Gluc] progressively increased during non rapid eye movement sleep and declined during rapid eye movement sleep, while during wake an early decline in [gluc] was followed by an increase 8-15 min after awakening. There was a significant time of day effect during the dark phase, when rats are mostly awake, with [gluc] being significantly lower during the last 3-4 h of the night relative to the first 3-4 h. Moreover, the duration of the early phase of [gluc] decline during wake was longer after prolonged wake than after consolidated sleep. Thus, the sleep/wake history may affect the levels of glucose available to the brain upon awakening. The brain overwhelmingly relies on glucose to meet its energy needs, which are higher in wake and REM sleep than in NREM sleep, but it remains unclear how the extracellular concentration of glucose [gluc] changes during sleep and wake. Using fixed-potential amperometry we find that in rat cerebral cortex [gluc] increases progressively during NREM sleep, decreases progressively during REM sleep, and initially declines (~8 min) before increasing during wake. Surprisingly, the early glucose decline upon awakening is longer after prolonged wake than after consolidated sleep, suggesting that sleep/wake history may affect brain glucose availability.
机译:大脑中的大部分能量来自葡萄糖,并支持谷氨酸能活动。皮质谷氨酸能神经元的放电速率以及皮质细胞外谷氨酸水平随着觉醒时间的增加而增加,并且在整个非快速眼动睡眠中下降,从而引发了一个疑问,即葡萄糖水平是否反映了行为状态和睡眠/唤醒历史。在此,将大鼠大脑皮层中的慢性(2-3天)脑电图记录与固定电位安培法相结合,以在整个自发性睡眠-觉醒周期中逐秒监测葡萄糖的细胞外浓度([gluc])。应对3个小时的睡眠不足。 [Gluc]在非快速眼动睡眠中会逐渐增加,在快速眼动睡眠中会下降,而在唤醒过程中[gluc]会先下降,然后在醒后增加8-15分钟。在黑夜阶段,当大鼠大部分处于清醒状态时,会有明显的一天中的时间效应,相对于最初的3-4小时,在夜晚的最后3-4小时内,葡萄糖明显降低。此外,长时间唤醒后,觉醒期间葡萄糖下降早期的持续时间比巩固睡眠后更长。因此,睡眠/唤醒历史可能会影响唤醒时大脑可用的葡萄糖水平。大脑完全依赖葡萄糖来满足其能量需求,在清醒和REM睡眠中,其能量需求要高于NREM睡眠,但是目前尚不清楚在睡眠和唤醒过程中细胞外葡萄糖的浓度如何变化。使用固定电位安培法,我们发现在大鼠的大脑皮层[gluc]在NREM睡眠过程中逐渐增加,在REM睡眠过程中逐渐减少,并且最初下降(约8分钟),然后在苏醒期间下降。出人意料的是,长时间唤醒后觉醒后早期葡萄糖下降的时间比巩固睡眠后更长,这表明睡眠/唤醒历史可能会影响脑部葡萄糖的利用率。

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