More than one billion people worldwide suffer from migraines every yearand a quarter of them experience auras, those warning signs that appear before or during a migraine, such as bright lights, nonexistent sounds or a tingling sensation.
For years, scientists have searched understand how these auras are connected to migraines. Now, a recent study in mice may have found the answer, opening up new possibilities for treating this debilitating condition.
A team of researchers has identified a New pathway between the brain and peripheral nerves that could explain this connection. This finding, published July 4 in the journal Science, details how the The brain communicates with the peripheral nerves through a group of neurons known as the trigeminal ganglion.
This set of cells transmits signals from the nerves of the face and jaw to the brain, connecting around the brain stem.
The key: cortical spreading depression
Migraine auras are linked to “cortical spreading depression,” waves of abnormal activity that travel through the brain and temporarily shut down certain neurons. These waves release chemicals into the cerebrospinal fluid (CSF), which surrounds and protects the brain. But the question remains: How do these chemicals activate pain nerves?
The study reveals that CSF and molecules within it can escape from the brain through the trigeminal ganglion, allowing these molecules to reach peripheral nerves and trigger pain.
To reach this conclusion, the researchers used genetically modified mice whose neurons glow in the presence of calcium, a crucial element for the transmission of electrical signals in the brain. Looking at the trigeminal ganglion, they injected a tracer into the brains of the mice to track the flow of CSF and activated the neurons by introducing a substance that allows calcium to flow.
CSF appeared in the trigeminal ganglion about four minutes after injection, followed by a significant increase in calcium-driven activity. This provided direct evidence that CSF can transport molecules out of the brain through this channel.
Implications for the treatment of migraines
This discovery has important implications for the treatment of migraines. The researchers showed that cortical spreading depression can increase CSF flow in the affected area, transporting more proteins and other molecules to the trigeminal ganglion than normal. Many of these proteins are responsible for pain and inflammation.
During the aura phase, proteins that can activate and sensitize sensory nerves are released, transporting them to the trigeminal ganglion and activating the nerves that mediate pain. Martin Kaag Rasmussen, study author and a postdoctoral fellow at the University of Copenhagen, explains that of the 12 identified proteins that activate pain nerves, only one, calcitonin gene-related peptide (CGRP), is a current target for migraine therapies. Drugs that block CGRP function alleviate migraine symptoms in about half of patients, leaving millions without effective treatment.
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