Calcitonin gene related peptide (CGRP) has been proposed to contribute to pain 
transmission and inflammation and for these reasons to the mechanism of 
migraine. CGRP is, in fact, expressed in and released from a subset of polymodal 
primary sensory neurons of the trigeminal ganglion. Release of CGRP in the 
dorsal spinal cord has been associated to nociceptive transmission, and release 
from perivascular nerve endings causes neurogenic vasodilatation. CGRP levels 
increase in the cranial circulation during migraine attacks, and GRP injection 
in migraineurs results in migraine-like attacks. Most importantly, two 
chemically unrelated CGRP-receptor antagonists, the parenteral agent, 
olcegepant, and the orally available telcagepant demonstrated efficacy in the 
treatment of migraine attacks, thus supporting CGRP as an important mediator in 
migraine.