It is almost 30 years since the prototypical triptan, sumatriptan, was licensed, revolutionizing the treatment of migraine (1). Developed to activate the serotonin 5-HT_1B and _1D receptors, the precise mechanisms and site of action of the triptans has been a hotly debated topic over the years, from an initial vascular theory to the now widely accepted neuronal theory (2). Indeed, it is now widely considered that the triptans, including sumatriptan, act to prevent the release of calcitonin gene-related peptide (CGRP) (3,4), specific modulation of which has now emerged as a standalone therapeutic option for migraine and cluster headache (5,6). Despite this increased knowledge, the exact site of action of the triptans remains elusive. While generally accepted to be acting peripherally on trigeminal nociceptive afferents, a potential central mechanism continues to be vigorously debated at most headache meetings.

中文翻译：

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舒马曲坦快速摄入大脑：血脑屏障通透性的一个持续问题。

原型曲坦类药物舒马曲坦获许可已近30年，彻底改变了偏头痛的治疗方法（1）。开发用于激活5-羟色胺5-HT _1B和_1D从最初的血管理论到现在被广泛接受的神经元理论，曲坦类药物的受体，确切的机制和作用部位一直是多年来争论不休的话题（2）。实际上，现已广泛认为曲普坦类药物（包括舒马普坦）可阻止降钙素基因相关肽（CGRP）的释放（3,4），其特定调节现已成为偏头痛和聚类的独立治疗选择。头痛（5,6）。尽管知识增加，曲普坦类药物的确切作用部位仍然难以捉摸。尽管通常认为对三叉神经痛感受传入有作用，但在大多数头痛的会议上仍在激烈地讨论潜在的中央机制。