Abstract |
The pathophysiological mechanisms of migraine are not yet very well understood. The gene CACNA1A, coding for the alpha 1A subunit of neuronal P/Q-type Ca2+ channels is mutated in the rare Mendelian inherited variant, familial hemiplegic migraine. This finding suggests a role for disturbed neuronal Ca2+ influx and/or homeostasis in the pathophysiology of migraine. It has stimulated in vitro electrophysiological investigations into the function of mutant human and mouse P/Q-type channels at cell bodies and synapses. A complex picture has emerged from this work, showing that different CACNA1A mutations lead to different effects on Ca2+ channel behavior and that synaptic transmission may become affected. We will review these studies and discuss the possible implications for the understanding of migraine pathophysiology.
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Authors | J J Plomp, A M van den Maagdenberg, P C Molenaar, R R Frants, M D Ferrari |
Journal | Current opinion in investigational drugs (London, England : 2000)
(Curr Opin Investig Drugs)
Vol. 2
Issue 9
Pg. 1250-60
(Sep 2001)
ISSN: 1472-4472 [Print] England |
PMID | 11717812
(Publication Type: Journal Article, Review)
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Chemical References |
- Calcium Channels, P-Type
- Calcium Channels, Q-Type
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Topics |
- Animals
- Calcium Channels, P-Type
(genetics, physiology)
- Calcium Channels, Q-Type
(genetics, physiology)
- Electrophysiology
- Hemiplegia
(etiology, physiopathology)
- Humans
- Mice
- Migraine Disorders
(genetics, physiopathology)
- Mutation
(genetics)
- Synapses
(physiology)
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