ReviewThe Journal of physiology2010
Insights into migraine mechanisms and CaV2.1 calcium channel function from mouse models of familial hemiplegic migraine.
Review in The Journal of physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
25 citing papers in PubMed, 61 citations in OpenAlex.
- Trial
- Calcium Ions in the Physiology and Pathology of the Central Nervous System.International journal of molecular sciences · 2024Review
- Transcriptional profile changes caused by noise-induced tinnitus in the cochlear nucleus and inferior colliculus of the rat.Annals of medicine · 2024Article
- Complex effects on CaScientific reports · 2022Article
- Cerebro-Cerebellar Networks in Migraine Symptoms and Headache.Frontiers in pain research (Lausanne, Switzerland) · 2022Review
- Ankyrin B and Ankyrin B variants differentially modulate intracellular and surface Cav2.1 levels.Molecular brain · 2019Article
- Hypocalcemia and Vitamin D Deficiency amongst Migraine Patients: A Nationwide Retrospective Study.Medicina (Kaunas, Lithuania) · 2019Article
- Pathophysiology of Migraine: A Disorder of Sensory Processing.Physiological reviews · 2017Review
- Abnormal synaptic Ca(2+) homeostasis and morphology in cortical neurons of familial hemiplegic migraine type 1 mutant mice.Annals of neurology · 2015Article
- Malan syndrome: Sotos-like overgrowth with de novo NFIX sequence variants and deletions in six new patients and a review of the literature.European journal of human genetics : EJHG · 2015Review
- How voltage-gated calcium channels gate forms of homeostatic synaptic plasticity.Frontiers in cellular neuroscience · 2014Review
- ATP P2X3 receptors and neuronal sensitization.Frontiers in cellular neuroscience · 2013Review
- Cortical spreading depression as a target for anti-migraine agents.The journal of headache and pain · 2013Review
- Article
- Article
- Sodium channels, the electrogenisome and the electrogenistat: lessons and questions from the clinic.The Journal of physiology · 2012Review
- Effects of familial hemiplegic migraine type 1 mutation T666M on voltage-gated calcium channel activities in trigeminal ganglion neurons.Journal of neurophysiology · 2012Article
- Synaptic release and extracellular actions of Zn2+ limit propagation of spreading depression and related events in vitro and in vivo.Journal of neurophysiology · 2012Article
- In vivo evidence that TRAF4 is required for central nervous system myelin homeostasis.PloS one · 2012Article
- Unequal gains of function are a headache for migraine mechanisms.The Journal of physiology · 2012Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Migraine is a very common disabling brain disorder with unclear pathogenesis. A subtype of migraine with aura (familial hemiplegic migraine type 1: FHM1) is caused by mutations in CaV2.1 (P/Q-type) Ca2+ channels. This review describes the functional consequences of FHM1 mutations in knockin mouse models carrying the mild R192Q or severe S218L mutations in the orthologous gene. The FHM1 knockin mice show allele dosage-dependent gain-of-function of neuronal P/Q-type Ca2+ current, reflecting activation of mutant channels at lower voltages, and allele dosage- and sex-dependent facilitation of induction and propagation of cortical spreading depression (CSD), the phenomenon that underlies migraine aura. Gain-of-function of neuronal Ca2+ current, facilitation of CSD and post-CSD motor deficits were larger in S218L than R192Q knockin mice, in correlation with the more severe human S218L phenotype. Enhanced cortical excitatory neurotransmission, due to increased action potential-evoked Ca2+ influx and increased probability of glutamate release at pyramidal cell synapses, but unaltered inhibitory neurotransmission at fast-spiking interneuron synapses, were demonstrated in R192Q knockin mice. Evidence for a causative link between enhanced glutamate release and CSD facilitation was obtained. The data from FHM1 mice strengthen the view of CSD as a key player in the pathogenesis of migraine, give insight into CSD mechanisms and point to episodic disruption of excitation-inhibition balance and neuronal hyperactivity as the basis for vulnerability to CSD ignition in migraine.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.