Cortical spreading depression as a site of origin for migraine: Role of CGRP

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Abstract
Premise: Migraine is a complex neurologic disorder that leads to significant disability, yet remains poorly understood. Problem: One potential triggering mechanism in migraine with aura is cortical spreading depression, which can activate the trigeminal nociceptive system both peripherally and centrally in animal models. A primary neuropeptide of the trigeminal system is calcitonin gene-related peptide, which is a potent vasodilatory peptide and is currently a major therapeutic target for migraine treatment. Despite the importance of both cortical spreading depression and calcitonin gene-related peptide in migraine, the relationship between these two players has been relatively unexplored. However, recent data suggest several potential vascular and neural connections between calcitonin gene-related peptide and cortical spreading depression. Conclusion: This review will outline calcitonin gene-related peptide-cortical spreading depression connections and propose a model in which cortical spreading depression and calcitonin gene-related peptide act at the intersection of the vasculature and cortical neurons, and thus contribute to migraine pathophysiology.
Funding Information
  • U.S. Department of War (W81XWH-16-1-0071)
  • U.S. Department of War (W81XWH-16-1-0211)
  • National Institute of Neurological Disorders and Stroke (NS075599)
  • U.S. Department of Veterans Affairs (1I01RX002101)

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