Low-dose tryptophan depletion in recovered depressed patients induces changes in cognitive processing without depressive symptoms
Low-dose tryptophan depletion in recovered depressed patients induces changes in cognitive processing without depressive symptoms
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DOI：
10.1016/j.biopsych.2004.11.016
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发表时间：
2005-03-01
影响因子：
10.6
通讯作者：
Harmer, CJ
中科院分区：
文献类型：
--
作者：
Hayward, G;Goodwin, GM;Harmer, CJ
背景：急性色氨酸耗竭可导致恢复的抑郁症患者抑郁症状短暂重现。神经化学机制被认为是脑血清素神经传递的损害，但其影响的神经心理学机制尚不清楚。方法：为了评估低剂量色氨酸耗损能否在不引起情绪变化的情况下梳理出易感受试者对底物耗损敏感的心理机制，采用被试间随机设计。康复的抑郁症患者（n = 24）和健康的志愿者（n = 24）在禁食期间分别服用不含色氨酸或含有31.2克和33.2克氨基酸的对照混合物。摄食前、摄食后5小时进行客观、主观情绪评定；在后一个时间点，还评估了认知和情绪处理。结果：低剂量色氨酸缺失对情绪无影响。然而，情绪和认知加工的显著变化发生在康复的抑郁组，而在健康志愿者中发生的程度较小。在恢复的病人身上所看到的效果表明急性抑郁症中所见的损伤又回来了。结论：我们的数据表明，低剂量色氨酸耗损可以在不引起抑郁症状的情况下，对抑郁症易感人群和健康志愿者中脑血清素急性减少的认知相关性进行研究。
Background: Acute tryptophan depletion can induce a transient reappearance of depressive symptoms in recovered depressed patients. The neurochemical mechanism is thought to be impairment of brain serotonin neurotransmission, but the neuropsychologic mechanisms underlying the effect are unclear.Methods: To assess whether low-dose tryptophan depletion can tease out the psychological mechanisms sensitive to substrate depletion in vulnerable subjects without inducing mood changes, a between-subjects randomized design was used. Recovered depressed patients (n = 24) and healthy volunteers (n = 24) were administered while fasting either a tryptophan-free or a control mixture, containing 31.2 and 33.2 g of amino acids, respectively. Objective and subjective ratings of mood were made before and 5 hours after ingestion; at the latter time point, cognitive and emotional processing were also assessed.Results: Low-dose tryptophan depletion did not affect mood. Significant changes in emotional and cognitive processing occurred in the recovered depressed group, however, and to a lesser extent in the healthy volunteers. The profile of effects seen in the recovered patients suggested a return of the impairments seen in acute depression.Conclusions: Our data suggest that low-dose tryptophan depletion permits investigation of the cognitive correlates of acute reductions in brain serotonin in populations vulnerable to depression and in healthy volunteers, without causing depressive symptoms.