Barr L C, Heninger G R, Goodman W, Charney D S, Price L H
Clinical Neuroscience Research Unit, Abraham Ribicoff Research Facilities, Connecticut Mental Health Center, Department of Psychiatry, Yale University School of Medicine, New Haven, USA.
Biol Psychiatry. 1997 May 1;41(9):949-54. doi: 10.1016/S0006-3223(96)00224-7.
Short-term reduction in plasma tryptophan (tryptophan depletion) produces a relapse of depressive symptoms in 60% of previously depressed patients recently recovered with serotonin reuptake inhibitor treatment. Tryptophan depletion does not consistently increase depressive symptoms in unmedicated depressed patients or in depressed patients whose symptoms are remitted with a norepinephrine reuptake inhibitor. These data suggest that serotonin reuptake inhibitor treatment itself may confer vulnerability to the development of depressive symptoms during tryptophan depletion. In order to further investigate this possibility, six healthy individuals underwent double-blind placebo-controlled tryptophan depletion before and following six weeks of treatment with fluoxetine 20 mg/day. No increased vulnerability to the mood-lowering effects of tryptophan depletion occurred as a result of fluoxetine treatment. Additionally, fluoxetine treatment itself was not associated with changes in mood or quality of life in these healthy volunteers. These data indicate that serotonin reuptake inhibitor treatment alone does not produce the depressive effects of tryptophan depletion that are observed in serotonin reuptake inhibitor-treated depressed and obsessive compulsive disorder patients.
短期降低血浆色氨酸水平（色氨酸耗竭）会使60%近期通过5-羟色胺再摄取抑制剂治疗而康复的既往抑郁症患者出现抑郁症状复发。色氨酸耗竭并不会持续增加未接受药物治疗的抑郁症患者或症状通过去甲肾上腺素再摄取抑制剂得以缓解的抑郁症患者的抑郁症状。这些数据表明，5-羟色胺再摄取抑制剂治疗本身可能会使人在色氨酸耗竭期间易出现抑郁症状。为了进一步研究这种可能性，6名健康个体在接受20毫克/天氟西汀治疗6周前后，接受了双盲安慰剂对照的色氨酸耗竭试验。氟西汀治疗并未导致对色氨酸耗竭降低情绪作用的易感性增加。此外，氟西汀治疗本身与这些健康志愿者的情绪或生活质量变化无关。这些数据表明，单独的5-羟色胺再摄取抑制剂治疗不会产生在接受5-羟色胺再摄取抑制剂治疗的抑郁症和强迫症患者中所观察到的色氨酸耗竭的抑郁效应。
