期刊
BIOCHIMICA ET BIOPHYSICA ACTA-BIOMEMBRANES
卷 1828, 期 7, 页码 1655-1665出版社
ELSEVIER
DOI: 10.1016/j.bbamem.2012.11.012
关键词
Calcium channel; Migraine; Spreading depression; Channelopathy; Trigeminal ganglion; Cerebral cortex
资金
- University of Padova (Strategic Project: Physiopathology of Signaling in Neuronal Tissue)
- Fondazione Cariparo (Excellence Project: Calcium Signaling in Health and Disease)
- Telethon-Italy [GGP06234]
Missense mutations in CACNA1A, the gene that encodes the pore-forming alpha(1) subunit of human voltage-gated Ca(v)2.1 (P/Q-type) calcium channels, cause a rare form of migraine with aura (familial hemiplegic migraine type 1: FHM1). Migraine is a common disabling brain disorder whose key manifestations are recurrent attacks of unilateral headache that may be preceded by transient neurological aura symptoms. This review, first, briefly summarizes current understanding of the pathophysiological mechanisms that are believed to underlie migraine headache, migraine aura and the onset of a migraine attack, and briefly describes the localization and function of neuronal Ca(v)2.1 channels in the brain regions that have been implicated in migraine pathogenesis. Then, the review describes and discusses i) the functional consequences of FHM1 mutations on the biophysical properties of recombinant human Ca(v)2.1 channels and native Ca(v)2.1 channels in neurons of knockin mouse models carrying the mild R192Q or severe S218L mutations in the orthologous gene, and ii) the functional consequences of these mutations on neurophysiological processes in the cerebral cortex and trigeminovascular system thought to be involved in the pathophysiology of migraine, and the insights into migraine mechanisms obtained from the functional analysis of these processes in FHM1 knockin mice. This article is part of a Special Issue entitled: Calcium channels. (c) 2012 Elsevier B.V. All rights reserved.
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