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首页> 美国卫生研究院文献>The Journal of Neuroscience >Sleep Deprivation Decreases Binding of 11CRaclopride to Dopamine D2/D3 Receptors in the Human Brain
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Sleep Deprivation Decreases Binding of 11CRaclopride to Dopamine D2/D3 Receptors in the Human Brain

机译：睡眠剥夺减少11C雷氯必利与人脑中多巴胺D2 / D3受体的结合。

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Sleep deprivation can markedly impair human performance contributing to accidents and poor productivity. The mechanisms underlying this impairment are not well understood, but brain dopamine systems have been implicated. Here, we test whether one night of sleep deprivation changes dopamine brain activity. We studied 15 healthy subjects using positron emission tomography and [11C]raclopride (dopamine D2/D3 receptor radioligand) and [11C]cocaine (dopamine transporter radioligand). Subjects were tested twice: after one night of rested sleep and after one night of sleep deprivation. The specific binding of [11C]raclopride in the striatum and thalamus were significantly reduced after sleep deprivation and the magnitude of this reduction correlated with increases in fatigue (tiredness and sleepiness) and with deterioration in cognitive performance (visual attention and working memory). In contrast, sleep deprivation did not affect the specific binding of [11C]cocaine in the striatum. Because [11C]raclopride competes with endogenous dopamine for binding to D2/D3 receptors, we interpret the decreases in binding to reflect dopamine increases with sleep deprivation. However, we cannot rule out the possibility that decreased [11C]raclopride binding reflects decreases in receptor levels or affinity. Sleep deprivation did not affect dopamine transporters (target for most wake-promoting medications) and thus dopamine increases are likely to reflect increases in dopamine cell firing and/or release rather than decreases in dopamine reuptake. Because dopamine-enhancing drugs increase wakefulness, we postulate that dopamine increases after sleep deprivation is a mechanism by which the brain maintains arousal as the drive to sleep increases but one that is insufficient to counteract behavioral and cognitive impairment.
机译：睡眠不足会明显损害人的行为，从而导致事故和生产力下降。尚不清楚这种损伤的潜在机制，但是已经牵涉到大脑多巴胺系统。在这里，我们测试一夜睡眠剥夺是否会改变多巴胺的大脑活动。我们使用正电子发射断层扫描和[ 11 C]雷洛必利（多巴胺D2 / D3受体放射性配体）和[ 11 C]可卡因（多巴胺转运体放射性配体）研究了15位健康受试者。对受试者进行两次测试：休息一晚后和睡眠剥夺一晚后。剥夺睡眠后，[ 11 C]雷氯必利在纹状体和丘脑中的特异性结合显着降低，且这种降低的程度与疲劳（疲倦和嗜睡）的增加以及认知能力的下降有关（视觉注意力和工作记忆）。相反，睡眠剥夺并不影响纹状体中[ 11 C]可卡因的特异性结合。因为[ 11 C]雷氯必利与内源性多巴胺竞争与D2 / D3受体的结合，因此我们解释了结合力的降低，反映了多巴胺随睡眠剥夺而增加。但是，我们不能排除[ 11 C]雷氯必利结合减少反映受体水平或亲和力降低的可能性。睡眠剥夺并没有影响多巴胺转运蛋白（大多数促唤醒药物的靶点），因此多巴胺的增加很可能反映了多巴胺细胞释放和/或释放的增加，而不是多巴胺再摄取的减少。由于增强多巴胺的药物可提高清醒度，因此我们假设睡眠剥夺后多巴胺增加是一种机制，通过这种机制，大脑随着睡眠驱动力的增加而保持唤醒状态，但这种机制不足以抵消行为和认知障碍。

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