Lopez-Rodriguez Faustino, Kim Joseph, Poland Russell E
Department of Psychiatry and Biobehavioral Sciences, Brain Research Institute, UCLA School of Medicine, Los Angeles, CA 90024, USA.
Neuropsychopharmacology. 2004 Jun;29(6):1105-11. doi: 10.1038/sj.npp.1300406.
Sleep deprivation can exert antidepressant effects in humans in less than 24 h, making it the fastest acting antidepressant treatment. However, it is rarely used clinically because the effect disappears once the subject goes back to sleep. An understanding of the neurobiological mechanisms underlying the antidepressant effect of sleep deprivation should help to develop new rapidly acting antidepressant strategies. In the present report, an animal model of depression (the forced-swim test) was used to determine whether the effects of total sleep deprivation parallel those obtained with antidepressant drugs. Using the disk-over-water method, rats deprived of sleep for 24 h exhibited increased swimming behavior when compared to cage control rats, mimicking the effects of serotonergic antidepressants. After 48 h, sleep-deprived rats exhibited increased swimming when compared to both cage control and stimulus control rats, demonstrating that the effect is due to sleep deprivation per se, and not to extraneous factors inherent in the sleep deprivation protocol (such as stress and movement). We believe that this paradigm can be used to study the neurobiological mechanisms of rapid antidepressant effects induced by sleep deprivation.
睡眠剥夺可在不到24小时内对人类产生抗抑郁作用，使其成为起效最快的抗抑郁治疗方法。然而，它在临床上很少使用，因为一旦受试者重新入睡，效果就会消失。了解睡眠剥夺抗抑郁作用的神经生物学机制应有助于开发新的快速起效的抗抑郁策略。在本报告中，使用一种抑郁动物模型（强迫游泳试验）来确定完全睡眠剥夺的效果是否与抗抑郁药物的效果相似。采用水上圆盘法，与笼养对照大鼠相比，睡眠剥夺24小时的大鼠游泳行为增加，这与血清素能抗抑郁药的效果相似。48小时后，与笼养对照大鼠和刺激对照大鼠相比，睡眠剥夺大鼠的游泳行为均增加，表明这种效果是由睡眠剥夺本身引起的，而不是睡眠剥夺方案中固有的外部因素（如压力和运动）。我们认为，这种范式可用于研究睡眠剥夺诱导的快速抗抑郁作用的神经生物学机制。
