• Toshihiko Shimizu, Mamoru Shibata, and Norihiro Suzuki.
• Department of Neurology, School of Medicine, Keio University.
• Rinsho Shinkeigaku. 2011 Feb 1; 51 (2): 103-9.

AbstractCortical spreading depression (CSD) is believed to be a phenomenon underlying migraine auras. The mutations of hemiplegic migraine genes are demonstrated to cause a reduction of CSD threshold. Consistently, tonabersat, which was developed for its ability to inhibit CSD, showed a preventive effect on attacks of migraine with aura. Besides, CSD has also been reported to activate the trigemino-vascular system, which subsequently causes migraine headache. The transient receptor potential cation channel, subfamily V, member 1 (TRPV1) receptor is known as one of the nociceptive receptors, and exists in the dura mater and the trigeminal ganglion. We demonstrated that the dural TRPV1 receptor conducts pain sensation to the trigeminal nucleus caudalis via the trigeminal ganglion, which implies possible contribution of the TRPV1 receptor to migraine headache. Also our recent data have raised the possibility that the TRPV1 receptor may play a pivotal role for the chronification of migraine. Furthermore, the TRPV1 receptor regulates the release of calcitonin gene-related peptide (CGRP). CGRP has been recognized to be associated with migraine because of its potent effect for dilation of intracranial and extracranial blood vessels. Some newly developed CGRP receptor antagonists have revealed the efficaciousness for acute migraine attacks. The present review discusses the relevance of recent advance of basic migraine research to future migraine treatment.

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