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三叉神经系统中的 CGRP 和 NO:在头痛产生中的机制和作用。

CGRP and NO in the trigeminal system: mechanisms and role in headache generation.

机构信息

Institute of Physiology & Pathophysiology, University of Erlangen-Nürnberg, Erlangen, Germany.

出版信息

Headache. 2012 Oct;52(9):1411-27. doi: 10.1111/j.1526-4610.2012.02212.x. Epub 2012 Jul 12.

Abstract

Calcitonin gene-related peptide (CGRP) and metabolic products of nitric oxide (NO) are increased in jugular venous plasma during migraine attacks and other primary headaches. Patients suffering from primary headaches are particularly sensitive to CGRP and NO donors responding with delayed headaches to an infusion of either of these substances. Accordingly, both CGRP and NO are considered as key mediators in migraine, and clinical trials have shown that inhibitors of CGRP receptors and NO synthase are effective in treating migraine. There is an implicit understanding that CGRP and NO systems interact, and here, we review the body of preclinical work on these systems focusing on the trigeminovascular system in migraine. NO derives from various cell types via 3 isoforms of NO synthase, whereas CGRP is produced from a subset of trigeminal afferents. In rodents, NO donors cause activity alterations on different levels of the trigeminal system including enhancement of CGRP release, which in turn results in arterial vasodilatation and possibly mast cell degranulation in the meninges. The activity of spinal trigeminal neurons, which is a sensitive integrative measure for trigeminal activity, is partly under the control of CGRP and NO. Both mediators facilitate nociceptive transmission, possibly via presynaptic mechanisms. These functions are supported by immunolocalization of CGRP receptor components on 3 trigeminovascular levels: cranial dura mater, trigeminal ganglion, and spinal trigeminal nucleus. Current data support a relationship of CGRP and NO actions on all levels of the trigeminovascular system and emphasize central CGRP receptors as possible therapeutic targets.

摘要

降钙素基因相关肽 (CGRP) 和一氧化氮 (NO) 的代谢产物在偏头痛发作和其他原发性头痛期间增加颈内静脉血浆中。患有原发性头痛的患者对 CGRP 和 NO 供体特别敏感,对这些物质中的任何一种输注都会导致延迟性头痛。因此,CGRP 和 NO 都被认为是偏头痛的关键介质,临床试验表明,CGRP 受体和 NO 合酶抑制剂在治疗偏头痛方面有效。人们普遍认为 CGRP 和 NO 系统相互作用,在这里,我们回顾了这些系统的临床前工作,重点是偏头痛中的三叉血管系统。NO 来源于不同的细胞类型,通过 3 种 NO 合酶同工型,而 CGRP 则由一部分三叉神经传入纤维产生。在啮齿动物中,NO 供体可引起三叉神经系统不同水平的活动改变,包括增强 CGRP 释放,这反过来又导致动脉血管扩张,并可能导致脑膜中的肥大细胞脱颗粒。脊髓三叉神经神经元的活动是三叉神经活动的敏感综合测量指标,部分受 CGRP 和 NO 的控制。这两种介质都促进伤害性传递,可能通过突触前机制。这些功能得到了 CGRP 受体成分在三叉血管系统的 3 个水平上的免疫定位的支持:颅硬膜、三叉神经节和脊髓三叉神经核。目前的数据支持 CGRP 和 NO 作用于三叉血管系统所有水平的关系,并强调了中枢 CGRP 受体作为可能的治疗靶点。

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