睡眠剥夺具有快速抗抑郁作用，通过对慢性轻度不可预见性应激(CMUS)抑郁模型大鼠进行72小时快眼动睡眠剥夺（REMSD），观察REMSD对不同脑区腺苷和5-HT系统的影响，结果显示海马腺苷A1受体可能通过调节5-HT系统而发挥抗抑郁，CMUS使腺苷A1受体在海马的表达升高，睡眠剥夺后海马腺苷A1受体表达下调，抑制5-HT释放的作用减弱，引起5-HT的释放增多，睡眠剥夺后海马和前皮质PKA、pCREB水平升高，而腺苷A1受体被拮抗时可阻断此效应。表明腺苷及其受体参与了睡眠剥夺快速抗抑郁效应的机制，海马腺苷A1受体起了主导作用，海马腺苷A1受体可能是通过PLC、MAPK等多条信号通路影响CREB的磷酸化水平，发挥抗抑郁效应,为快速治疗抑郁症的策略提供新思路和理论依据。

As depression is one of the mental disorders with high burden and high incidence, the study on the fast antidepressant mechanisms has important significance. Sleep deprivation has affirmative rapid antidepressant effect. To testify the effects of adenosine and its receptors in the fast antidepressant mechanism of sleep deprivation, we studied the influences of rapid-eye-movement sleep deprivation(REMSD) on adenosine and serotonin and their receptors in different regions of brain in rats treated with chronic mild unpredicted stresses(CMUS), with the methods of neurobehavioral, HPLC and molecular biological techniques (in situ hybridization, RT-PCR, immunohistochemistry, Western-blot, et al), in order to clarify the fast antidepressant mechanism of sleep deprivation, to understand more about the pathophysiology of depression, and to provide new evidences for rapid therapy of depression. In the present study, we found that the level of adenosine in hippocampus and hypothalamus decreased after CMUS, and then decreased more significantly during REMSD. CMUS can increase the expression of adenosine A1 receptor in hippocampus, while the expression of adenosine A2a receptor also increased in hippocampus, frontal cortex and corpus striatum. Sleep deprivation can come back the expression of adenosine A1 receptor in hippoc

睡眠剥夺具有快速抗抑郁作用，通过对慢性轻度不可预见性应激(CMUS)抑郁模型大鼠进行72小时快眼动睡眠剥夺（REMSD），观察REMSD对不同脑区腺苷和5-HT系统的影响，结果显示海马腺苷A1受体可能通过调节5-HT系统而发挥抗抑郁，CMUS使腺苷A1受体在海马的表达升高，睡眠剥夺后海马腺苷A1受体表达下调，抑制5-HT释放的作用减弱，引起5-HT的释放增多，睡眠剥夺后海马和前皮质PKA、pCREB水平升高，而腺苷A1受体被拮抗时可阻断此效应。表明腺苷及其受体参与了睡眠剥夺快速抗抑郁效应的机制，海马腺苷A1受体起了主导作用，海马腺苷A1受体可能是通过PLC、MAPK等多条信号通路影响CREB的磷酸化水平，发挥抗抑郁效应,为快速治疗抑郁症的策略提供新思路和理论依据。