AI Article Synopsis
- Classical migraine patients experience an aura characterized by temporary neurological symptoms before headaches, linked to a phenomenon called cortical spreading depression (CSD).
- This study reveals that cerebrospinal fluid (CSF) enters the trigeminal ganglion, allowing communication between the brain and trigeminal cells.
- After CSD occurs, about 11% of proteins in the CSF change, leading to an increase in proteins that can activate trigeminal neurons, potentially explaining the connection between aura and migraine headaches.
Article Abstract
Classical migraine patients experience aura, which is transient neurological deficits associated with cortical spreading depression (CSD), preceding headache attacks. It is not currently understood how a pathological event in cortex can affect peripheral sensory neurons. In this study, we show that cerebrospinal fluid (CSF) flows into the trigeminal ganglion, establishing nonsynaptic signaling between brain and trigeminal cells. After CSD, ~11% of the CSF proteome is altered, with up-regulation of proteins that directly activate receptors in the trigeminal ganglion. CSF collected from animals exposed to CSD activates trigeminal neurons in naïve mice in part by CSF-borne calcitonin gene-related peptide (CGRP). We identify a communication pathway between the central and peripheral nervous system that might explain the relationship between migrainous aura and headache.
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| http://dx.doi.org/10.1126/science.adl0544 | DOI Listing |
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