Scientists at the University of North Carolina School of Medicine have discovered that a peptide called CGRP interferes with the flow of cerebrospinal fluid through the lymphatic vessels in the brain, thus contributing to pain during migraine attacks. Research results published In the Journal of Clinical Investigation (JCI).
Some studies have shown that during migraine attacks, the number of CGRP protein molecules, which interact with sensory neurons in the meninges to transmit pain signals, increases. To find out exactly how CGRP triggers pain, scientists conducted an experiment involving two groups of mice.
The first group included genetically modified rodents that were immune to the effects of CGRP. The second group of rodents served as controls; no changes were made to their genomes. All rodents were placed in a double room, one part of which was brightly lit and the other part was darkened. The mice with the inactivated CGRP peptide felt more comfortable in bright light, while the rodents in the control group expressed a desire to hide in the shadows. The scientists explained that bright light is known to trigger migraines in humans.
Using cell culture techniques, the researchers analyzed how the specialized protein BE-cadherin is distributed in the space between individual cells lining lymphatic vessels. This protein helps hold lymphatic endothelial cells together and controls how much fluid, such as spinal fluid, can pass between them and enter the vessels.
Scientists discovered that in the presence of CGRP, lymphatic endothelial cells form peculiar lines made of the protein VE-cadherin, which prevents fluid from passing between them. They suggested that migraine is caused by the inability of cerebrospinal fluid to exit the brain’s meningeal lymphatic vessels, preventing the organ’s protective covering from being “patrolled” by immune cells.
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