抗阵挛药物的药理学。

M R Pranzatelli
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引用次数: 0

摘要

肌阵挛的分子机制尚不清楚。用于对症治疗肌阵挛的药物被开发用于其他适应症,如癫痫。抗阵挛药物不是一个单一的化合物家族,而是构成了一组异质性的药物,它们在神经递质代谢途径的不同部位起作用,或者作为受体激动剂或拮抗剂。对于一些药物,尽管有许多已知的作用,但抗阵挛作用的机制尚不清楚。肌阵挛受多种神经递质系统的影响,与肌阵挛最相关的神经递质是γ -氨基丁酸(GABA)、谷氨酸、甘氨酸和血清素。本文综述了作用于神经递质的药物的药理学,这些神经递质是已知的或潜在的抗阵挛药物。分子生物学和药物开发的持续进步有利于传统药物治疗难以治愈的疾病的药物治疗。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The pharmacology of antimyoclonic drugs.

The molecular mechanisms of myoclonus are unknown. Drugs used in the symptomatic treatment of myoclonus were developed for other indications, such as epilepsy. Antimyoclonic drugs are not a single family of compounds but rather constitute a heterogeneous group of agents that act at various sites along the metabolic pathway of neurotransmitters or as receptor agonists or antagonists. For some drugs, the mechanism of antimyoclonic action is obscure despite many known actions. Myoclonus is affected by manipulation of more than one neurotransmitter system, and the neurotransmitters most linked to myoclonus are gamma-aminobutyric acid (GABA), glutamate, glycine, and serotonin. This is a review of the pharmacology of drugs acting on those neurotransmitters that are known or potential antimyoclonic drugs. A time of continuing advances in molecular biology and drug development is propitious for the pharmacotherapy of disorders that historically have been so refractory to conventional drug treatment.

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