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Mechanism of action of narcolepsy medications

机译：发作性睡病药物的作用机理

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The medications used to treat narcolepsy are targeted toward alleviating symptoms such as excessive sleepiness and cataplexy. The cause of this neurological sleep disorder is still not completely clear, though a destruction of hypocretin/ orexin neurons has been implicated. The destruction of these neurons is linked to inactivity of neurotransmitters including histamine, norepinephrine, acetylcholine, and serotonin, causing a disturbance in the sleep/wake cycles of narcoleptic patients. Stimulants and MAOIs have traditionally been used to counteract excessive daytime sleepiness and sleep attacks by inhibiting the breakdown of catecholamines. Newer drugs, called wake-promoting agents, have recently become first-line agents due to their better side-effect profile, efficacy, and lesser potential for abuse. These agents similarly inhibit reuptake of dopamine, but have a novel mechanism of action, as they have been found to increase neuronal activity in the tuberomamillary nucleus and in orexin neurons. Sodium oxybate, a sodium salt of gamma-hydroxybutyrate (GHB), is another class that is used to treat many symptoms of narcolepsy, and is the only U. S. Food and Drug Administration (FDA)-approved medication for cataplexy. It has a different mechanism of action than either stimulants or wake-promoting agents, as it binds to its own unique receptor. Antidepressants, like selective serotonin re-uptake inhibitors (SSRIs) and tricyclic antidepressants (TCAs), have also been used, as similar to stimulants, they inhibit reuptake of specific catecholamines. In this article, we seek to review the mechanisms behind these classes of drugs in relation to the proposed pathophysiology of narcolepsy. Appropriate clinical strategies will be discussed, including specific combinations of medications that have been shown to be effective.
机译：用于治疗发作性睡病的药物旨在缓解症状，例如过度嗜睡和瘫痪。尽管已经暗示了降钙素/食欲素神经元的破坏，但这种神经性睡眠障碍的病因仍不完全清楚。这些神经元的破坏与包括组胺，去甲肾上腺素，乙酰胆碱和5-羟色胺在内的神经递质的失活有关，从而引起了麻醉病人的睡眠/唤醒周期的紊乱。传统上，兴奋剂和MAOI通过抑制儿茶酚胺的分解来抵消白天过多的嗜睡和睡眠攻击。由于其更好的副作用，功效和更少的滥用潜力，被称为唤醒促进剂的新型药物最近已成为一线药物。这些试剂类似地抑制多巴胺的再摄取，但是具有新的作用机理，因为已经发现它们增加了结核性乳头状核和食欲素神经元中的神经元活性。羟丁酸钠是γ-羟丁酸（GHB）的钠盐，是另一类用于治疗发作性睡病症状的药物，并且是美国食品药品监督管理局（FDA）批准的唯一一种用于猝倒的药物。它具有与兴奋剂或唤醒促进剂不同的作用机制，因为它结合了自己的独特受体。抗抑郁药，如选择性5-羟色胺再摄取抑制剂（SSRIs）和三环抗抑郁药（TCA），也已被使用，与刺激剂相似，它们抑制特定儿茶酚胺的再摄取。在本文中，我们试图回顾与发作性睡病的拟议病理生理学相关的此类药物背后的机制。将讨论适当的临床策略，包括已证明有效的特定药物组合。

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