Tryptophan depletion and depressive vulnerability
Tryptophan depletion and depressive vulnerability
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DOI：
10.1016/s0006-3223(99)00095-5
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发表时间：
1999-08-15
影响因子：
10.6
通讯作者：
Delgado, PL
中科院分区：
文献类型：
--
作者：
Moreno, FA;Gelenberg, AJ;Delgado, PL
背景资料：色氨酸（TRP）的快速和短暂消耗导致大多数成功治疗并服用选择性5-羟色胺再摄取抑制剂的患者出现短暂的抑郁复发，但在无药物的有症状抑郁患者中变化不大。本研究探讨了TRP耗竭对既往重度抑郁发作（MDE）临床缓解的无药物受试者的影响。方法：12例既往MDE受试者（患者），目前处于临床缓解期且无药物至少3个月（患者），12例无轴I障碍个人或家族史的健康受试者（对照组）接受TRP耗竭。该研究以双盲对照[全浓度（102 g）和四分之一浓度（25 g）15-氨基酸饮料]交叉方式进行。在测试之前、期间和之后获得行为评级和血浆TRP水平。结果：所有受试者在两种测试饮料上都经历了血浆TRP的显著消耗，显示出显著的密切反应关系。健康对照受试者的情绪变化最小，但患者的抑郁反应更大。结论：在先前对抗抑郁药治疗和无药物的症状性抑郁患者进行的TRP耗竭研究的背景下，这些结果表明抑郁可能不是由5-HT功能异常引起的，而是由其他系统或受5-HT调节的脑区域的功能障碍引起的。生物精神病学1999;46：498-505（C）1999年生物精神病学学会。
Background: Rapid and transient depletion of tryptophan (TRP) causes a brief depressive relapse in most patients successfully treated with and taking selective serotonin reuptake inhibitors, but little change in drug-free, symptomatic depressed patients. This study investigates the effects of TRP depletion in drug-free subjects in clinical remission from a prior major depressive episode (MDE),Methods: Twelve subjects with a prior MDE, currently in clinical remission and drug-free for at least 3 months (patients), and 12 healthy subjects without personal or family history of Axis I disorder (controls), received TRP depletion. The study was conducted in a double-blind controlled [full (102-g) and quarter-strength (25 g) 15-amino acid drinks], crossover fashion. Behavioral ratings and plasma TRP levels were obtained prior to, during, and after testing,Results: All subjects experienced significant depletion of plasma TRP on both test-drinks, showing a significant close-response relation, Healthy control subjects had minimal mood changes, but patients had a depressive response of greater magnitude,Conclusions: In the context of prior TRP depletion studies with antidepressant-treated and drug-free symptomatic depressed patients, these results suggest that depression may be caused not by an abnormality of 5-HT function, but by dysfunction of other systems or brain regions modulated by 5-HT. Biol Psychiatry 1999;46:498-505 (C) 1999 Society of Biological Psychiatry.