Cortical 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.