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Migraine: Calcium Channels and Glia
Marta Kowalska1, Michał Prendecki1, Thomas Piekut1
1Laboratory of Neurobiology, Department of Neurology, Poznan University of Medical Sciences, 49 Przybyszewskiego St., 60-355 Poznan, Poland.
International Journal of Molecular Sciences
|April 3, 2021
Summary
Migraine involves the trigeminovascular system (TGVS) and CGRP release. Aberrant neuron-glia interactions, particularly in familial hemiplegic migraine type 1 (FHM1), are key to understanding migraine with aura.
Area of Science:
- Neurology
- Neuroscience
- Molecular Biology
Background:
- Migraine is a prevalent neurological disorder affecting 11% of adults.
- Clinical subtypes include migraine with aura and migraine without aura.
- The neurovascular theory implicates trigeminovascular system (TGVS) activation and neuropeptide release (e.g., CGRP) in headache pathogenesis.
Purpose of the Study:
- To review neuron-glia interactions in migraine pathogenesis.
- To focus on these interactions in familial hemiplegic migraine type 1 (FHM1).
Main Methods:
- Review of existing literature on migraine mechanisms.
- Focus on studies involving familial hemiplegic migraine (FHM) models.
- Examination of the role of CACNA1A mutations in FHM1.
Main Results:
- Cortical spreading depression (CSD), responsible for aura, involves aberrant neuron-glia interactions.
- FHM1, caused by CACNA1A mutations, provides a model to study these interactions.
- The α1A subunit of the P/Q-type voltage-gated calcium channel is implicated.
Conclusions:
- Neuron-glia interactions are crucial in the pathophysiology of migraine with aura.
- Understanding these interactions in FHM1 offers insights into migraine mechanisms.
- Targeting these pathways may offer novel therapeutic strategies for migraine.
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