TRPV1 in migraine pathophysiology

被引：98

作者：

Meents, Jannis E. ^{[1
]}

Neeb, Lars ^{[1
]}

Reuter, Uwe ^{[1
]}

机构：

[1] Charite, Dept Neurol, D-10117 Berlin, Germany

来源：

TRENDS IN MOLECULAR MEDICINE | 2010年 / 16卷 / 04期

关键词：

NERVE GROWTH-FACTOR; GENE-RELATED PEPTIDE; VANILLOID RECEPTOR TRPV1; PRIMARY SENSORY NEURONS; KINASE-C-EPSILON; CAPSAICIN RECEPTOR; SUBSTANCE-P; DURA-MATER; TRIGEMINOVASCULAR SYSTEM; PROSTAGLANDIN E-2;

D O I：

10.1016/j.molmed.2010.02.004

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Migraine is among the most prevalent headache disorders and results from dysfunctions within the trigeminovascular system (TVS). The inflammatory processes that have been suggested to occur in the cascade of events resulting in migraine sensitise trigeminal nociceptors, possibly causing hyperalgesia and allodynia. Trigeminal nociceptors express the heat- and capsaicin-gated channel TRPV1, which seems to play a significant role in the development of peripheral and central sensitisation and of hyperalgesia and allodynia. Here, we review the molecular mechanisms leading to the sensitisation of TRPV1 and attempt to link them to migraine-relevant pathophysiological processes. We argue that antagonising TRPV1 sensitisation is a promising approach and should receive more attention in future research as well as in the development of anti-migraine drugs.

引用

页码：153 / 159

页数：7

共 108 条

[1] Vanilloid type 1 receptors (VR1) on trigeminal sensory nerve fibres play a minor role in neurogenic dural vasodilatation, and are involved in capsaicin-induced dural dilation [J].