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首页> 外文期刊>Journal of psychopharmacology >Does 5-HT restrain panic? A tryptophan depletion study in panic disorder patients recovered on paroxetine (reprinted from vol 16, pg 5, 2002)
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Does 5-HT restrain panic? A tryptophan depletion study in panic disorder patients recovered on paroxetine (reprinted from vol 16, pg 5, 2002)

机译：5-HT抑制恐慌吗？在帕罗西汀上康复的恐慌症患者的色氨酸耗竭研究（转载自第16卷，第5页，2002年）

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The neurobiological basis of panic disorder has not been clearly established, although a role for serotonin (5-HT) has been postulated. It is clear that drugs which increase 5-HT neurotransmission are effective in treating the condition but how they do so remains a point of debate. The aim of this study was to determine if lowering brain serotonin activity using the technique of tryptophan depletion provoked a short-term relapse of panic symptoms in patients with panic disorder who had responded to drug treatment. Fourteen patients with panic disorder who had responded to treatment with the selective serotonin reuptake inhibitor (SSRI) paroxetine received a tryptophan-free amino acid drink on one occasion and a control drink on the other in a double-blind crossover design. In addition, they received an infusion of flumazenil (used as a pharmacological challenge) and placebo on each day. The tryptophan depleted drink produced an 87% reduction in plasma tryptophan concentration. Flumazenil produced a panic attack (defined by changes in the panic inventory) in seven out of 14 patients when tryptophan depleted and one out of 14 on the control day (p < 0.02). Three patients also experienced temporary depressive symptoms when tryptophan depleted, with no mood changes being seen on the control days. We conclude that rapid lowering of brain serotonin function can allow the precipitation of panic symptoms in response to flumazenil in panic disorder patients who have responded to treatment with an SSRI. This implies that in panic disorder increased 5-HT availability is important in maintaining the response to SSRIs.
机译：尽管已假定5-羟色胺（5-HT）的作用，但尚未明确建立惊恐障碍的神经生物学基础。显然，增加5-HT神经传递的药物对于治疗该病是有效的，但如何治疗仍是争论的焦点。这项研究的目的是确定使用色氨酸耗竭技术降低脑部5-羟色胺活性是否会导致对药物治疗有反应的恐慌症患者的恐慌症状短期复发。对选择性5-羟色胺再摄取抑制剂（SSRI）帕罗西汀治疗有反应的14例恐慌症患者在双盲交叉设计中，一次分别接受了不含色氨酸的氨基酸饮料，而另一次接受了对照饮料。另外，他们每天接受氟马西尼（用作药理学挑战）和安慰剂的输注。色氨酸消耗的饮料可使血浆色氨酸浓度降低87％。当色氨酸耗尽时，氟马西尼在14位患者中有7位产生了惊恐发作（由惊慌库存的变化定义），而在对照日则有14位患者产生了惊恐发作（p <0.02）。色氨酸耗尽时，三名患者也出现了暂时性的抑郁症状，在对照日未见情绪变化。我们得出的结论是，在对SSRI治疗有反应的恐慌症患者中，脑部5-羟色胺功能的快速降低可使恐慌症状的沉淀减轻。这意味着在恐慌症中，增加的5-HT利用率对于维持对SSRI的反应至关重要。

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