CGRP Receptor Antagonism and Migraine

Lars Edvinsson, Tony W. Ho

Research output: Contribution to journalArticlepeer-review

Abstract

Calcitonin gene-related peptide (CGRP) is expressed throughout the central and peripheral nervous systems, consistent with control of vasodilatation, nociception, motor function, secretion, and olfaction. αCGRP is prominently localized in primary spinal afferent C and AΔ fibers of sensory ganglia, and βCGRP is the main isoform in the enteric nervous system. In the CNS there is a wide distribution of CGRP-containing neurons, with the highest levels occurring in striatum, amygdala, colliculi, and cerebellum. The peripheral projections are involved in neurogenic vasodilatation and inflammation, and central release induces hyperalgesia. CGRP is released from trigeminal nerves in migraine. Trigeminal nerve activation results in antidromic release of CGRP to cause non-endothelium-mediated vasodilatation. At the central synapses in the trigeminal nucleus caudalis, CGRP acts postjunctionally on second-order neurons to transmit pain signals centrally via the brainstem and midbrain to the thalamus and higher cortical pain regions. Recently developed CGRP receptor antagonists are effective at aborting acute migraine attacks. They may act both centrally and peripherally to attenuate signaling within the trigeminovascular pathway.

Original languageEnglish (US)
Pages (from-to)164-175
Number of pages12
JournalNeurotherapeutics
Volume7
Issue number2
DOIs
StatePublished - Apr 1 2010

Keywords

  • CGRP
  • CGRP receptor antagonists
  • Migraine
  • trigeminovascular

ASJC Scopus subject areas

  • Pharmacology
  • Clinical Neurology
  • Pharmacology (medical)

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