Neumeister A, Turner E H, Matthews J R, Postolache T T, Barnett R L, Rauh M, Vetticad R G, Kasper S, Rosenthal N E
National Institute of Mental Health, Clinical Psychobiology Branch, Bethesda, MD, USA.
Arch Gen Psychiatry. 1998 Jun;55(6):524-30. doi: 10.1001/archpsyc.55.6.524.
Although hypotheses about the therapeutic mechanism of action of light therapy have focused on serotonergic mechanisms, the potential role, if any, of catecholaminergic pathways has not been fully explored.
Sixteen patients with seasonal affective disorder who had responded to a standard regimen of daily 10000-lux light therapy were enrolled in a double-blind, placebo-controlled, randomized crossover study. We compared the effects of tryptophan depletion with catecholamine depletion and sham depletion. Ingestion of a tryptophan-free amino acid beverage plus amino acid capsules was used to deplete tryptophan. Administration of the tyrosine hydroxylase inhibitor alpha-methyl-paratyrosine was used to deplete catecholamines. Diphenhydramine hydrochloride was used as an active placebo during sham depletion. The effects of these interventions were evaluated with measures of depression, plasma tryptophan levels, and plasma catecholamine metabolites.
Tryptophan depletion significantly decreased plasma total and free tryptophan levels. Catecholamine depletion significantly decreased plasma 3-methoxy-4-hydroxyphenylethyleneglycol and homovanillic acid levels. Both tryptophan depletion and catecholamine depletion, compared with sham depletion, induced a robust increase (P<.001, repeated-measures analysis of variance) in depressive symptoms as measured with the Hamilton Depression Rating Scale, Seasonal Affective Disorder Version.
The beneficial effects of light therapy in the treatment of seasonal affective disorder are reversed by both tryptophan depletion and catecholamine depletion. These findings confirm previous work showing that serotonin plays an important role in the mechanism of action of light therapy and provide new evidence that brain catecholaminergic systems may also be involved.
尽管关于光疗法治疗作用机制的假说主要集中在血清素能机制上，但儿茶酚胺能通路的潜在作用（如果有的话）尚未得到充分研究。
16名对每日10000勒克斯标准光疗法方案有反应的季节性情感障碍患者参加了一项双盲、安慰剂对照、随机交叉研究。我们比较了色氨酸耗竭、儿茶酚胺耗竭和假耗竭的效果。摄入不含色氨酸的氨基酸饮料加氨基酸胶囊用于耗竭色氨酸。给予酪氨酸羟化酶抑制剂α-甲基-对酪氨酸用于耗竭儿茶酚胺。盐酸苯海拉明在假耗竭期间用作活性安慰剂。通过抑郁测量、血浆色氨酸水平和血浆儿茶酚胺代谢物来评估这些干预措施的效果。
色氨酸耗竭显著降低了血浆总色氨酸和游离色氨酸水平。儿茶酚胺耗竭显著降低了血浆3-甲氧基-4-羟基苯乙二醇和高香草酸水平。与假耗竭相比，色氨酸耗竭和儿茶酚胺耗竭均导致汉密尔顿抑郁量表（季节性情感障碍版）测量的抑郁症状显著增加（P<.001，重复测量方差分析）。
色氨酸耗竭和儿茶酚胺耗竭均可逆转光疗法治疗季节性情感障碍的有益效果。这些发现证实了先前的研究工作，即血清素在光疗法的作用机制中起重要作用，并提供了新的证据表明脑儿茶酚胺能系统也可能参与其中。
