Schreiber W, Opper C, Dickhaus B, Heiser P, Wesemann W, Krieg J C
Department of Psychiatry and Psychotherapy, Philipps-University, Marburg, Germany.
J Psychiatr Res. 1997 May-Jun;31(3):323-31. doi: 10.1016/s0022-3956(96)00062-3.
Sleep deprivation (SD) is an effective, however short-lived, method of treatment of depression. Preliminary findings suggest that the antidepressive effect of sleep deprivation is mediated by serotoninergic (5-HT) mechanisms. We therefore assessed serotoninergic activity before and after total SD (TSD) as well as after the following night sleep by investigating platelet LSD-binding, MAO B-activity, and 5-HT-content as well as plasma norepinephnne (NE) in 10 healthy men (age: 27.4 +/- 2.8 years). Blood samples were drawn on three consecutive days at 0700, 1300 and 1900 h, respectively. After TSD, a significant increase of LSD-binding KD and Bmax as well as of MAO-B KM and plasma NE could be observed, which, however, vanished after consecutive night sleep. Our findings favour an increased serotoninergic transmission after TSD and thus support the hypothesis, that sleep deprivation exerts its antidepressant effects by pro-serotoninergic mechanisms.
睡眠剥夺（SD）是一种治疗抑郁症的有效但短期的方法。初步研究结果表明，睡眠剥夺的抗抑郁作用是由血清素能（5-HT）机制介导的。因此，我们通过研究10名健康男性（年龄：27.4±2.8岁）的血小板LSD结合、单胺氧化酶B（MAO B）活性、5-HT含量以及血浆去甲肾上腺素（NE），评估了完全睡眠剥夺（TSD）前后以及随后一晚睡眠后的血清素能活性。分别在连续三天的07:00、13:00和19:00采集血样。TSD后，可观察到LSD结合解离常数（KD）和最大结合容量（Bmax）以及MAO-B米氏常数（KM）和血浆NE显著增加，然而，连续一晚睡眠后这些增加消失了。我们的研究结果支持TSD后血清素能传递增加的观点，从而支持了睡眠剥夺通过促进血清素能机制发挥抗抑郁作用的假说。
