Evidence from human models of migraine as well as other lines of research suggest a putative model for the genesis of migraine attacks.1 Within vascular smooth muscle cells of cephalic arteries, migraine-inducing substances act through intracellular second messengers including cyclic adenosine monophosphate (cAMP) or cyclic guanosine monophosphate (cGMP) to eventually cause the opening of ATP-sensitive potassium (KATP) channels or large-conductance Ca2+-activated K+ (BKCa) channels. This release of potassium from vascular smooth muscle cells and subsequently vasodilation. The efflux of potassium might activate adjacent perivascular nerve fibers to trigger the perception of migraine pain.
AMP = Adenosine Monophosphate; ATP = Adenosine Triphosphate; CGRP = Calcitonin Gene-Related Peptide; GMP = Guanosine Monophosphate; GTP = Guanosine Triphosphate; NO = Nitric Oxide; PACAP-38 = Pituitary Adenylate Activating Polypeptide-38; PDE-3; Phosphodiesterase-3; PDE-5; Phosphodiesterase-5; PKA = Protein Kinase A; PKG = Protein Kinase G.
Related content
Migraine is a prevalent neurological disorder characterized by recurrent and disabling attacks of moderate to severe headache
Migraine affects an estimated 1.1 billions worldwide and ranks as the 2nd leading cause of disability, while being the leading among young adults.
In human models of migraine, a suspected pharmacological migraine trigger is administered either orally or via infusion to a participant with migraine or a healthy volunteer, typically within a double-blinded, randomized, placebo-controlled design